To see the other types of publications on this topic, follow the link: Inotropic.
Journal articles on the topic 'Inotropic'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'Inotropic.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Urquhart, Robert A., and Kenneth J. Broadley. "The indirect negative inotropic effects of the P1-receptor agonist, L-phenylisopropyladenosine, in guinea-pig isolated cardiac preparations: comparison with cromakalim." Canadian Journal of Physiology and Pharmacology 70, no. 6 (1992): 910–15. http://dx.doi.org/10.1139/y92-122.
Full textAbstract:
The possible mechanisms of the indirect negative inotropic responses to the P1-receptor agonist, L-phenylisopropyladenosine (L-PIA) were evaluated in electrically paced (2 Hz, 5 ms pulse width, voltage 50% above threshold) left atria and papillary muscles of guinea pigs. The responses were compared in naive tissues (direct effects) or after prestimulation with submaximal concentrations of either cAMP-dependent positive inotropes (isoprenaline or forskoiin) or the cAMP-independent inotrope Bay K 8644. Cumulative concentration – response curves were obtained in naive or prestimulated preparations for L-PIA or the potassium channel activator, cromakalim, for comparison. L-PIA and cromakalim exerted negative inotropy in naive atrial tissues, whereas only cromakalim was active in naive papillary muscles. In atria prestimulated with isoprenaline (31 nM) or forskolin (1.4 μM), the negative inotropy of L-PIA was enhanced compared with naive tissues. In contrast, prestimulation with Bay K 8644 (1 μM) exerted a significant functional antagonism of the response to L-PIA. In the case of cromakalim, prestimulation with isoprenaline exerted a functional antagonistic effect. In papillary muscles, an indirect negative inotropic effect of L-PIA was only seen in tissues prestimulated with the cAMP-dependent inotropes isoprenaline (31 nM) or forskolin (2.4 μM), and not in naive tissues or those prestimulated by Bay K 8644 (333 nM). As with atria, prestimulation with isoprenaline exerted a functional antagonistic effect on the response to cromakalim. These results suggest that the P1-receptor agonist, L-PIA, exerts its indirect negative inotropic effects in left atria by two mechanisms. One mechanism is common to the direct inhibition of naive tissues and an additional component is seen after prestimulation with cAMP-dependent positive inotropes. Where prestimulation is cAMP-independent, this component is absent and functional antagonism is observed. Similarly, the negative inotropic effect of the potassium channel activator, cromakalim, is cAMP-independent and functionally antagonized in both atria and papillary muscles by isoprenaline.Key words: L-phenylisopropyladenosine, atria, papillary muscles, guinea pig, cromakalim, isoprenaline, forskolin, Bay K 8644 prestimulation.
2
Bose, D., T. Kobayashi, R. A. Bouchard, and L. V. Hryshko. "Scattered light intensity fluctuation in the canine ventricular myocardium: correlation with inotropic drug effect." Canadian Journal of Physiology and Pharmacology 66, no. 9 (1988): 1232–38. http://dx.doi.org/10.1139/y88-203.
Full textAbstract:
Scattered light intensity fluctuation (SLIF) of coherent light by a strip of ventricular muscle during diastole is believed to be due to asynchronous cellular motion within the myocyte as a result of spontaneous release of Ca from the sarcoplasmic reticulum. Previous studies have shown a correlation between inotropic agents, such as ouabain and elevated extracellular Ca or decreased extracellular Na, and SLIF. The purpose of this study was to see if this correlation could be extended to other inotropic agents. The digitalis genin, ouabagenin, produces inotropy by increasing intracellular free Ca. In toxic concentrations the drug produces abnormal aftercontractions by spontaneous Ca release from the sarcoplasmic reticulum. On the other hand, the Ca channel agonist BAY k 8644 is also positively inotropic, but its effect is associated with a decrease in Ca release from the sarcoplasmic reticulum, manifested by conversion of "rest potentiation" to "rest depression." The effects of these inotropic agents on the power spectra of SLIF were dissimilar. Both frequency and amplitude of SLIF were increased after ouabagenin (1 μM), but these changes were most marked after the onset of toxicity, at which time contractility was decreased, rather than during the positive inotropic response. In contrast, BAY k 8644 (1 μM) decreased SLIF at all levels of inotropic response. The β-adrenoceptor stimulant drug, dobutamine, and the adenylate cyclase activator, forskolin, produced minimal increase in SLIF at inotropic concentrations but caused a large increase in SLIF only after the onset of toxicity. These results suggest that SLIF is a better indicator of intracellular Ca overload and toxic oscillatory contractions in the presence of an inotrope and not of increased inotropy, per se.
3
Wang, Guan-Ying, Diana T. McCloskey, Sally Turcato, Philip M. Swigart, Paul C. Simpson та Anthony J. Baker. "Contrasting inotropic responses to α1-adrenergic receptor stimulation in left versus right ventricular myocardium". American Journal of Physiology-Heart and Circulatory Physiology 291, № 4 (2006): H2013—H2017. http://dx.doi.org/10.1152/ajpheart.00167.2006.
Full textAbstract:
The left ventricle (LV) and right ventricle (RV) have differing hemodynamics and embryological origins, but it is unclear whether they are regulated differently. In particular, no previous studies have directly compared the LV versus RV myocardial inotropic responses to α1-adrenergic receptor (α1-AR) stimulation. We compared α1-AR inotropy of cardiac trabeculae from the LV versus RV of adult mouse hearts. As previously reported, for mouse RV trabeculae, α1-AR stimulation with phenylephrine (PE) caused a triphasic contractile response with overall negative inotropy. In marked contrast, LV trabeculae had an overall positive inotropic response to PE. Stimulation of a single subtype (α1A-AR) with A-61603 also mediated contrasting LV/RV inotropy, suggesting differential activation of multiple α1-AR-subtypes was not involved. Contrasting LV/RV α1-AR inotropy was not abolished by inhibiting protein kinase C, suggesting differential activation of PKC isoforms was not involved. However, contrasting LV/RV α1-AR inotropic responses did involve different effects on myofilament Ca2+ sensitivity: submaximal force of skinned trabeculae was increased by PE pretreatment for LV but was decreased by PE for RV. For LV myocardium, α1-AR-induced net positive inotropy was abolished by the myosin light chain kinase inhibitor ML-9. This study suggests that LV and RV myocardium have fundamentally different inotropic responses to α1-AR stimulation, involving different effects on myofilament function and myosin light chain phosphorylation.
4
Tanaka, Hikaru, Tomoyuki Matsuda, Mika Adachi та Koki Shigenobu. "Effect of sympathectomy on inotropic responsiveness to α-adrenoceptor stimulation in developing mouse myocardia". Canadian Journal of Physiology and Pharmacology 73, № 9 (1995): 1285–88. http://dx.doi.org/10.1139/y95-181.
Full textAbstract:
Effects of postnatal sympathectomy on inotropic responsiveness to α-adrenoceptor stimulation were examined in mouse myocardia to determine whether the developmental conversion of α-adrenoceptor-mediated inotropic responses from positive to negative is triggered by sympathetic innervation. Sympathectomy was performed chemically by consecutively administering 6-hydroxydopamine for 14 days after birth and confirmed by the absence of inotropic responses to tyramine. In newborn myocardia, phenylephrine, in the presence of propranolol, produced concentration-dependent positive inotropic responses. Three weeks after birth, phenylephrine, in the presence of propranolol, produced concentration-dependent negative inotropic responses, both in control and in sympathectomized myocardia; no difference was observed between the two groups of mice in the maximum decrease in contractile force produced by phenylephrine. The sensitivity (pD2 value) to phenylephrine was significantly higher in sympathectomized myocardia. In conclusion, sympathetic innervation of the mouse ventricular myocardium is not required for the developmental conversion of the α-adrenoceptor-mediated inotropic response from positive to negative.Key words: inotropism, α-adrenoceptor, supersensitivity, sympathetic innervation, development.
5
Vesoulis, Zachary A., Jessica Hao, Christopher McPherson, Nathalie M. El Ters, and Amit M. Mathur. "Low-frequency blood pressure oscillations and inotrope treatment failure in premature infants." Journal of Applied Physiology 123, no. 1 (2017): 55–61. http://dx.doi.org/10.1152/japplphysiol.00205.2017.
Full textAbstract:
The underlying mechanism as to why some hypotensive preterm infants do not respond to inotropic medications remains unclear. For these infants, we hypothesize that impaired vasomotor function is a significant factor and is manifested through a decrease in low-frequency blood pressure variability across regulatory components of vascular tone. Infants born ≤28 wk estimated gestational age underwent prospective recording of mean arterial blood pressure for 72 h after birth. After error correction, root-mean-square spectral power was calculated for each valid 10-min data frame across each of four frequency bands ( B1, 0.005–0.0095 Hz; B2, 0.0095–0.02 Hz; B3, 0.02–0.06 Hz; and B4, 0.06–0.16) corresponding to different components of vasomotion control. Forty infants (twenty-nine normotensive control and eleven inotrope-exposed) were included with a mean ± SD estimated gestational age of 25.2 ± 1.6 wk and birth weight 790 ± 211 g. 9.7/11.8 Million (82%) data points were error-free and used for analysis. Spectral power across all frequency bands increased with time, although the magnitude was 20% less in the inotrope-exposed infants. A statistically significant increase in spectral power in response to inotrope initiation was noted across all frequency bands. Infants with robust blood pressure response to inotropes had a greater increase compared with those who had limited or no blood pressure response. In this study, hypotensive infants who require inotropes have decreased low-frequency variability at baseline compared with normotensive infants, which increases after inotrope initiation. Low-frequency spectral power does not change for those with inotrope treatment failure, suggesting dysfunctional regulation of vascular tone as a potential mechanism of treatment failure. NEW & NOTEWORTHY In this study, we examine patterns of low-frequency oscillations in blood pressure variability across regulatory components of vascular tone in normotensive and hypotensive infants exposed to inotropic medications. We found that hypotensive infants who require inotropes have decreased low-frequency variability at baseline, which increases after inotrope initiation. Low-frequency spectral power does not change for those with inotrope treatment failure, suggesting dysfunctional regulation of vascular tone as a potential mechanism of treatment failure.
6
Nielsen, Dorthe Viemose, Malene Kærslund Hansen, Søren Paaske Johnsen, Mads Hansen, Karsten Hindsholm, and Carl-Johan Jakobsen. "Health Outcomes with and without Use of Inotropic Therapy in Cardiac Surgery." Anesthesiology 120, no. 5 (2014): 1098–108. http://dx.doi.org/10.1097/aln.0000000000000224.
Full textAbstract:
Abstract Background: Inotropes used to obtain short-term hemodynamic benefits in cardiac surgery may carry a risk of increased myocardial ischemia and adverse outcomes. This study investigated the association between intra- and postoperative use of inotropes and mortality and postoperative complications. Methods: A historic cohort study using prospective data from the Western Denmark Heart Registry on 6,005 consecutive cardiac surgery cases from three university hospitals. Propensity matching on pre- and intraoperative variables was used to identify a subgroup of patients receiving inotropic therapy (n = 1,170) versus comparable nonreceivers (n = 1,170) for outcome analysis. Results: Two thousand ninety-seven patients (35%) received inotropic therapy; 3,908 (65%) did not receive any inotropic or vasopressor support perioperatively. Among propensity-matched cohort including 2,340 patients 30-day mortality was 3.2% and 1-yr mortality was 7.6%. In the matched cohort, patients exposed to inotropes had a higher 30-day mortality (adjusted hazards ratio, 3.7; 95% CI, 2.1 to 6.5) as well as a higher 1-yr mortality rate (adjusted hazards ratio, 2.5; 95% CI, 1.8 to 3.5) compared with nonreceivers. Among propensity-matched, the following absolute events rates were observed: myocardial infarction 2.4%, stroke 2.8%, arrhythmia 35%, and renal replacement therapy 23.9%. Inotropic therapy was independently associated with postoperative myocardial infarction (adjusted odds ratio, 2.1; 95% CI, 1.4 to 3.0), stroke (adjusted odds ratio, 2.4; 95% CI, 1.4 to 4.3), and renal replacement therapy (adjusted odds ratio, 7.9; 95% CI, 3.8 to 16.4). Conclusion: Use of intra- and postoperative inotropes was associated with increased mortality and major postoperative morbidity.
7
Gomes, Clara, Caíque Bueno Terhoch, Silvia Moreira Ayub-Ferreira, et al. "Prognosis and risk stratification in patients with decompensated heart failure receiving inotropic therapy." Open Heart 5, no. 2 (2018): e000923. http://dx.doi.org/10.1136/openhrt-2018-000923.
Full textAbstract:
ObjectivesThe prognostic significance of transient use of inotropes has been sufficiently studied in recent heart failure (HF) populations. We hypothesised that risk stratification in these patients could contribute to patient selection for advanced therapies.MethodsWe analysed a prospective cohort of adult patients admitted with decompensated HF and ejection fraction (left ventricular ejection fraction (LVEF)) less than 50%. We explored the outcomes of patients requiring inotropic therapy during hospital admission and after discharge.ResultsThe study included 737 patients, (64.0% male), with a median age of 58 years (IQR 48–66 years). Main aetiologies were dilated cardiomyopathy in 273 (37.0%) patients, ischaemic heart disease in 195 (26.5%) patients and Chagas disease in 163 (22.1%) patients. Median LVEF was 26 % (IQR 22%–35%). Inotropes were used in 518 (70.3%) patients. In 431 (83.2%) patients, a single inotrope was administered. Inotropic therapy was associated with higher risk of in-hospital death/urgent heart transplant (OR=10.628, 95% CI 5.055 to 22.344, p<0.001). At 180-day follow-up, of the 431 patients discharged home, 39 (9.0%) died, 21 (4.9%) underwent transplantation and 183 (42.4%) were readmitted. Inotropes were not associated with outcome (death, transplant and rehospitalisation) after discharge.ConclusionsInotropic drugs are still widely used in patients with advanced decompensated HF and are associated with a worse in-hospital prognosis. In contrast with previous results, intermittent use of inotropes during hospitalisation did not determine a worse prognosis at 180-day follow-up. These data may add to prognostic evaluation in patients with advanced HF in centres where mechanical circulatory support is not broadly available.
8
Varma, Daya R., Hansjorg Rindt, Sylvain Chemtob та Shree Mulay. "Mechanism of the negative inotropic effects of α1-adrenoceptor agonists on mouse myocardium". Canadian Journal of Physiology and Pharmacology 81, № 8 (2003): 783–89. http://dx.doi.org/10.1139/y03-071.
Full textAbstract:
This study was done to identify the mechanism of the α1-adrenoceptor (AR) mediated negative inotropic effects of phenylephrine (PE) on adult mouse myocardium. As reported by others, we also found that the nonselective α1AR agonist PE produced a negative inotropic effect on ventricular strips from adult mice that was inhibited by the α1AAR antagonist 5-methylurapidil (5MU) but not by the α1BAR antagonist chloroethylclonidine (CEC) or the α1DAR antagonist BMY 7378. The selective α1AAR agonist A61603 also produced a negative inotropic effect, which was antagonized by 5MU. Phorbol 12,13-dibutyrate (activator of all PKC isoforms) mimicked the negative inotropic responses to PE and A61603. The negative inotropic effects of PE were inhibited by bisindolylmaleimide (inhibitor of all PKC isoforms) but not by Gö 6976 (inhibitor of Ca2+-dependant PKC). Rottlerin, an inhibitor of Ca2+-independent PKCδ, antagonized the negative inotropic effects of PE and A61603. PE and A61603 increased the translocation of PKCδ, which was prevented by rottlerin. These data suggest that the α1AR-mediated negative inotropy on adult mouse myocardium is signaled by Ca2+-independent PKCδ.Key words: phorbol 12,13-dibutyrate, 5-methylurapidil, BMY 7378, chloroethylclolidine, Ca2+-dependant PKC isoforms, α1A-adrenoceptor.
9
Sakai, Mari, Tokiko Suzuki, Kengo Tomita, et al. "Diminished responsiveness to dobutamine as an inotrope in mice with cecal ligation and puncture-induced sepsis: attribution to phosphodiesterase 4 upregulation." American Journal of Physiology-Heart and Circulatory Physiology 312, no. 6 (2017): H1224—H1237. http://dx.doi.org/10.1152/ajpheart.00828.2016.
Full textAbstract:
Dobutamine has been used in septic shock for many years as an only inotrope, but its benefit has been questioned. We weighed the effects of dobutamine and milrinone as inotropes in mice with cecal ligation and puncture (CLP)-induced polymicrobial sepsis. CLP-induced septic mice exhibited significant cardiac inflammation, as indicated by greatly increased mRNAs of proinflammatory cytokines and robust infiltration of inflammatory cells in the ventricular myocardium. Elevations of plasma cardiac troponin-I showed cardiac injury in CLP mice. Noninvasive echocardiographic assessment of cardiac function revealed that despite preserved left ventricular function in the presence of fluid replacement, the dobutamine inotropic response was significantly impaired in CLP mice compared with sham-operated controls. By contrast, milrinone exerted inotropic effects in sham-operated and CLP mice in an equally effective manner. Surface expression levels of β1-adrenoceptors and α-subunits of three main G protein families in the myocardium were unaffected by CLP-induced sepsis. Plasma cAMP levels were significantly elevated in both sham-operated and CLP mice in response to milrinone but only in sham-operated controls in response to dobutamine. Of phosphodiesterase (PDE) isoforms, PDE4D, but not PDE3A, both of which are responsible for cardiac cAMP hydrolysis, was significantly upregulated in CLP mouse myocardium. We define a novel mechanism for the impaired responsiveness to dobutamine as an inotrope in sepsis, and understanding the role of PDE4D in modulating cardiac functional responsiveness in sepsis may open the potential of a PDE4D-targeted therapeutic option in septic patients with low cardiac output who have a need for inotropic support. NEW & NOTEWORTHY Advisability of the usefulness of dobutamine in septic shock management is limited. Here, we reveal that the effect of dobutamine as a positive inotrope is impaired in mice with cecal ligation and puncture-induced sepsis without changes in cardiac β1-adrenoceptor signaling as a result of cAMP breakdown achieved by upregulated phosphodiesterase 4D.
10
Todaka, Koji, Jie Wang, Geng-Hua Yi, et al. "Effect of BAY y 5959 on myocardial function and metabolism in normal and failing hearts." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 5 (1998): H1560—H1568. http://dx.doi.org/10.1152/ajpheart.1998.274.5.h1560.
Full textAbstract:
BAY y 5959 is a dihydropyridine derivative with positive inotropic actions mediated by a direct increase in intracellular calcium. We characterized the direct myocardial actions of this new agent in hearts isolated from seven normal dogs and from five dogs with repeated coronary microembolization-induced heart failure. Inotropic actions of BAY y 5959 were accompanied by little effect on duration of contraction and by prolongation of the monophasic action potential (MAP); in contrast, isoproterenol decreased contraction and MAP durations. Whereas inotropic responsiveness to isoproterenol was blunted in embolized hearts, these actions of BAY y 5959 were relatively preserved in the heart failure state. Isoproterenol increased heart rate, whereas BAY y 5959 had little effect. Changes in coronary vascular resistance also decreased similarly for isoproterenol and BAY y 5959. Finally, for comparable inotropy, increases in myocardial oxygen consumption were similar for isoproterenol and for BAY y 5959. In summary, preserved inotropic responsiveness and lack of positive chronotropic actions are two clinically favorable features of this type of inotropic agents compared with a typical β-adrenergic agonist.
11
Nagashima, M., Y. Hattori, Y. Akaishi, et al. "Alpha 1-adrenoceptor subtypes mediating inotropic and electrophysiological effects in mammalian myocardium." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 4 (1996): H1423—H1432. http://dx.doi.org/10.1152/ajpheart.1996.271.4.h1423.
Full textAbstract:
Stimulation of alpha 1-adrenoceptors produces a positive inotropic effect in rat and rabbit ventricular myocardium via different mechanisms, the prolongation of action potential duration (APD) exclusively in the former and an increase in myofibrillar Ca2+ sensitivity in large part in the latter. This study was designed to determine whether the two inotropic mechanisms are mediated by different alpha 1-adrenoceptor subtypes. In rat papillary muscles, the positive inotropic effect and APD prolongation induced by phenylephrine (in the presence of propranolol) were inhibited by WB-4101, but not affected by chlorethylclonidine (CEC). WB-4101, but not CEC, blocked the phenylephrine-induced inhibition of the transient outward current (Ito) in rat ventricular cells. On the other hand, WB-4101 and CEC each antagonized the positive inotropic effect of phenylephrine in rabbit papillary muscles. However, the phenylephrine-induced APD prolongation observed in rabbit papillary muscles was blocked only by WB-4101. These results indicate that the WB-4101 sensitive alpha 1-adrenoceptor subtype mediates the positive inotropism that is correlated with the APD prolongation resulting from Ito reduction, whereas the CEC-sensitive subtype mediates the positive inotropism that is probably associated with increased myofibrillar Ca2+ sensitivity. Radioligand binding studies with [3H] prazosin showed a similar ratio of alpha 1A-to alpha 1B-adrenoceptor subtypes in rat and rabbit ventricular myocardium, implying that the different degree of contribution of each action mechanism to the overall inotropic effect in the two species cannot be explained by distribution of the alpha 1-adrenoceptor subtypes.
12
Latimer, Abigail, Natalie D. Pope, and Jessica M. McFarlin. "“I Just Feel Like I Always Did”: Inotropic Dependency at End of Life." American Journal of Hospice and Palliative Medicine® 37, no. 7 (2019): 497–502. http://dx.doi.org/10.1177/1049909119886302.
Full textAbstract:
Background: Patients not considered for mechanical circulatory support or heart transplant may be dependent on inotropic therapy at end of life. End-of-life conversations in advanced heart failure can be challenging for providers, but guidelines recommend frequent goals-of-care conversations when inotropes are used as a palliative treatment. The purpose of this study was to identify aspects of care pertinent for health-care professionals working with patients in end-stage heart failure who are receiving continuous inotropic support. Methods: Qualitative analysis was used to examine 3 audio-recorded semistructured interviews with 1 patient, her family, and her cardiologist. The selected patient was an older adult, diagnosed with advanced heart failure, and dependent on continuous inotropic therapy with no other advanced treatment options available. Results: The analysis revealed that (1) reliance on others, (2) contending with uncertainty, and (3) deciding when to discontinue inotropic support were identified as themes central to the patient’s and provider’s experience. Conclusion: This study offers insight into how to best support and communicate with patients having advanced heart failure who are dependent on continuous inotropic therapy at end of life.
13
Fellahi, Jean-Luc, Marc-Olivier Fischer, Georges Daccache, Jean-Louis Gerard, and Jean-Luc Hanouz. "Positive Inotropic Agents in Myocardial Ischemia–Reperfusion Injury." Anesthesiology 118, no. 6 (2013): 1460–65. http://dx.doi.org/10.1097/aln.0b013e31828f4fc3.
Full textAbstract:
Abstract Positive inotropic agents should be used judiciously when managing surgical patients with acute myocardial ischemia–reperfusion injury, as use of these inotropes is not without potential adverse effects.
14
Shrestha, Jarina, Shashi Panday, and Ranju Gurung. "Knowledge Regarding Administration of Inotropic Drugs Among Nurses Working in Selected Hospitals, Kathmandu." International Journal of Health Sciences and Research 13, no. 11 (2023): 189–94. http://dx.doi.org/10.52403/ijhsr.20231124.
Full textAbstract:
Background: Cardiovascular diseases (CVDs) are the leading cause of death globally. An estimated 17.9 million people died from CVDs in 2019; representing 32% of all global deaths. An Inotrope is a medium that adjusts the power or efforts of muscle constrictions. Inotropic drugs help in improving cardiac output, easing respiratory congestion and improving the quality of cardiac muscle contraction and tissue perfusion. Method/ Material: A descriptive cross-sectional design was adopted for the study. Non probability purposive sampling technique was used to select the 113 nurses. Descriptive statistics like mean, median, frequency and standard deviation for calculating frequency and percentage and inferential statistics such as chi square test or fisher exact was used to determine the association between knowledge and selected variables. Result: The majority 65.5% of the participants had inadequate level of knowledge followed by more than one third 34.5% had moderate knowledge and none 0% of the participants had adequate knowledge regarding administration of inotropic drugs. There is association between level of knowledge regarding administration of inotropic drugs and selected socio demographic variables among participants in the study. After the analysis through chi-square test or fisher exact test, level of knowledge regarding administration of inotropic drugs was found to be significantly associated with educational qualification (p=0.028) and working unit (p=0.035) Conclusion: Nurses have inadequate knowledge about administration of inotropic drugs. Therefore, concerned authorities of hospital and intervention makers should be focused to train or educate nurses on administration of inotropic drugs which will ultimately leads to delivery of quality health services. Key words: Knowledge, Administration of Inotropic drugs, Nurse
15
Bing, O. H., N. L. Hague, C. L. Perreault, et al. "Thyroid hormone effects on intracellular calcium and inotropic responses of rat ventricular myocardium." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 3 (1994): H1112—H1121. http://dx.doi.org/10.1152/ajpheart.1994.267.3.h1112.
Full textAbstract:
To examine the mechanisms by which thyroid hormone modulates the inotropic state of rat myocardium, we studied the effects of thyroid state on isolated rat left ventricular papillary muscle function and intracellular calcium transients in the baseline state and in response to calcium and isoproterenol. Marked differences in contractile state of papillary muscles from hypothyroid and thyroid hormone-treated rats seen under baseline conditions (1.0 mM bath calcium, 30 degrees C, stimulation rate 12/min) do not appear to be due to differences in intracellular calcium concentration ([Ca2+]i) or to changes in myofilament calcium sensitivity but correlate with shifts in myosin isozyme distribution. In response to superimposed inotropic interventions (calcium, 0.625-5.0 mM, or isoproterenol, 10(-8)-10(-6) M), myocardial thyroid state modulates peak [Ca2+]i and inotropy, both of which are increased in thyroid hormone-treated relative to hypothyroid myocardium. The change in inotropy appears to be proportional to peak [Ca2+]i, whether mediated directly by calcium or as a result of beta-adrenergic stimulation. Thus, whereas baseline differences between hypothyroid and thyroid hormone-treated myocardium appear to be due to differences in myosin isozymes and presumed changes in adenosinetriphosphatase activity and cross-bridge cycling, superimposed inotropic responses appear to be mediated by changes in [Ca2+]i.
16
Garlid, Keith D., Paolo E. Puddu, Philippe Pasdois, et al. "Inhibition of cardiac contractility by 5-hydroxydecanoate and tetraphenylphosphonium ion: a possible role of mitoKATP in response to inotropic stress." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 1 (2006): H152—H160. http://dx.doi.org/10.1152/ajpheart.01233.2005.
Full textAbstract:
This study investigates the role of the mitochondrial ATP-sensitive K+ channel (mitoKATP) in response to positive inotropic stress. In Langendorff-perfused rat hearts, inotropy was induced by increasing perfusate calcium to 4 mM, by adding 80 μM ouabain or 0.25 μM dobutamine. Each of these treatments resulted in a sustained increase in rate-pressure product (RPP) of ∼60%. Inhibition of mitoKATP by perfusion of 5-hydroxydecanoate (5-HD) or tetraphenylphosphonium before induction of inotropic stress resulted in a marked attenuation of RPP. Inhibition of mitoKATP after induction of stress caused the inability of the heart to maintain a high-work state. In human atrial fibers, the increase in contractility induced by dobutamine was inhibited 60% by 5-HD. In permeabilized fibers from the Langendorff-perfused rat hearts, inhibition of mitoKATP resulted, in all cases, in an alteration of adenine nucleotide compartmentation, as reflected by a 60% decrease in the half-saturation constant for ADP [ K1/2 (ADP)]. We conclude that opening of cardiac mitoKATP is essential for an appropriate response to positive inotropic stress and propose that its involvement proceeds through the prevention of stress-induced decrease in mitochondrial matrix volume. These results indicate a physiological role for mitoKATP in inotropy and, by extension, in heart failure.
17
Lee, C. O. "200 years of digitalis: the emerging central role of the sodium ion in the control of cardiac force." American Journal of Physiology-Cell Physiology 249, no. 5 (1985): C367—C378. http://dx.doi.org/10.1152/ajpcell.1985.249.5.c367.
Full textAbstract:
Digitalis has been used therapeutically for two centuries, but the mechanism by which it enhances the ability of cardiac muscle to produce force (the positive inotropic effect) has not been fully elucidated. The major controversy concerns the question of whether the inhibition of the Na+-K+ pump by digitalis, particularly at low (therapeutic) concentrations, increases the intracellular Na+ concentration and thus is causally related to the positive inotropic effect. Na+-selective microelectrodes, introduced recently, have made it possible to measure small changes in intracellular Na+ activity (aiNa) in beating preparations of cardiac muscle and, in particular, to follow the exact time course of change in both aiNa and contractile force during the positive inotropic effect of digitalis. It has been demonstrated that digitalis at low and high concentrations produces a parallel increase in aiNa and in contractile force during the onset of its effect; washout of the drug results in a parallel and complete recovery of aiNa and contractile force. Additional strong evidence for a correlation between the pump inhibition and digitalis inotropy is the fact that the magnitude of increase in aiNa and contractile force produced by digitalis depends on the level of aiNa and therefore on the rate of Na+ extrusion by the Na+-K+ pump. The study on the quantitative relationship between aiNa and contractile force reveals that the force of contraction is a power function of aiNa, such that a small rise in aiNa produces a significant increase in contractile force. Direct measurements of aiNa and intracellular free Ca2+ during digitalis inotropy strongly support the hypothesis that an increase in aiNa raises intracellular Ca2+ via Na+-Ca2+ exchange, thus producing the positive inotropic effect. In conclusion, the recent data available from the simultaneous and continuous measurements of aiNa and contractile force strongly indicate that the inhibition of the Na+-K+ pump is causally related to the positive inotropic effect of digitalis on cardiac muscle.
18
Cowley, Patrick M., Guanying Wang, Audrey N. Chang та ін. "The α1A-adrenergic receptor subtype mediates increased contraction of failing right ventricular myocardium". American Journal of Physiology-Heart and Circulatory Physiology 309, № 5 (2015): H888—H896. http://dx.doi.org/10.1152/ajpheart.00042.2015.
Full textAbstract:
Dysfunction of the right ventricle (RV) is closely related to prognosis for patients with RV failure. Therefore, strategies to improve failing RV function are significant. In a mouse RV failure model, we previously reported that α1-adrenergic receptor (α1-AR) inotropic responses are increased. The present study determined the roles of both predominant cardiac α1-AR subtypes (α1A and α1B) in upregulated inotropy in failing RV. We used the mouse model of bleomycin-induced pulmonary fibrosis, pulmonary hypertension, and RV failure. We assessed the myocardial contractile response in vitro to stimulation of the α1A-subtype (using α1A-subtype-selective agonist A61603) and α1B-subtype [using α1A-subtype knockout mice and nonsubtype selective α1-AR agonist phenylephrine (PE)]. In wild-type nonfailing RV, a negative inotropic effect of α1-AR stimulation with PE (force decreased ≈50%) was switched to a positive inotropic effect (PIE) with bleomycin-induced RV injury. Upregulated inotropy in failing RV occurred with α1A-subtype stimulation (force increased ≈200%), but not with α1B-subtype stimulation (force decreased ≈50%). Upregulated inotropy mediated by the α1A-subtype involved increased activator Ca2+ transients and increased phosphorylation of myosin regulatory light chain (a mediator of increased myofilament Ca2+ sensitivity). In failing RV, the PIE elicited by the α1A-subtype was appreciably less when the α1A-subtype was stimulated in combination with the α1B-subtype, suggesting functional antagonism between α1A- and α1B-subtypes. In conclusion, upregulation of α1-AR inotropy in failing RV myocardium requires the α1A-subtype and is opposed by the α1B-subtype. The α1A subtype might be a therapeutic target to improve the function of the failing RV.
19
Vivien, Benoit, Jean-Luc Hanouz, Pierre-Yves Gueugniaud, Yves Lecarpentier, Pierre Coriat, and Bruno Riou. "Myocardial Effects of Halothane and Isoflurane in Hamsters with Hypertrophic Cardiomyopathy." Anesthesiology 87, no. 6 (1997): 1406–16. http://dx.doi.org/10.1097/00000542-199712000-00020.
Full textAbstract:
Background The effects of halothane and isoflurane on myocardial contraction and relaxation in diseased myocardium are not completely understood. Methods The effects of equianesthetic concentrations of halothane and isoflurane on inotropy and lusitropy in left ventricular papillary muscles of healthy hamsters and those with genetically induced cardiomyopathy (strain BIO 14.6) were investigated in vitro (29 degrees C; pH 7.40; Ca2+ 2.5 mM; stimulation frequency, 3/min) in isotonic and isometric conditions. Results Halothane induced a negative inotropic effect that was greater in cardiomyopathic than in healthy hamsters (1.5 vol%, active isometric force (AF): 19 +/- 8% vs. 28 +/- 11% of control values; P &lt; 0.05). Isoflurane induced a negative inotropic effect that was greater in cardiomyopathic than in healthy hamsters (2.0 vol%, AF: 64 +/- 13% vs. 75 +/- 11% of control values; P &lt; 0.01). However, the negative inotropic effects of halothane and isoflurane were not different for cardiomyopathic or healthy hamsters when their concentrations were corrected for minimum alveolar concentration (MAC) values in each strain. Halothane induced a negative lusitropic effect under low load, which was more important in cardiomyopathic hamsters, suggesting a greater impairment in calcium uptake by the sarcoplasmic reticulum. In contrast, isoflurane induced a moderate positive lusitropic effect under low load in healthy but not in cardiomyopathic hamsters. Halothane and isoflurane induced no significant lusitropic effect under high load. Conclusions Halothane and isoflurane had greater negative inotropic effects in cardiomyopathic than in healthy hamsters. Nevertheless, no significant differences in their inotropic effects were noted when concentrations were correlated as a multiple of MAC in each strain.
20
Bozhinovska, Marija, Gordana Taleska, Andrej Fabian, and Maja Å oÅ¡tariÄ. "The Role of Levosimendan in Patients with Decreased Left Ventricular Function Undergoing Cardiac Surgery." Open Access Macedonian Journal of Medical Sciences 4, no. 3 (2016): 510–16. http://dx.doi.org/10.3889/oamjms.2016.071.
Full textAbstract:
The postoperative low cardiac output is one of the most important complications following cardiac surgery and is associated with increased morbidity and mortality. The condition requires inotropic support to achieve adequate hemodynamic status and tissue perfusion. While catecholamines are utilised as a standard therapy in cardiac surgery, their use is limited due to increased oxygen consumption. Levosimendan is calcium sensitising inodilatator expressing positive inotropic effect by binding with cardiac troponin C without increasing oxygen demand. Furthermore, the drug opens potassium ATP (KATP) channels in cardiac mitochondria and in the vascular muscle cells, showing cardioprotective and vasodilator properties, respectively. In the past decade, levosimendan demonstrated promising results in treating patients with reduced left ventricular function when administered in peri- or post- operative settings. In addition, pre-operative use of levosimendan in patients with severely reduced left ventricular ejection fraction may reduce the requirements for postoperative inotropic support, mechanical support, duration of intensive care unit stay as well as hospital stay and a decrease in post-operative mortality. However, larger studies are needed to clarify clinical advantages of levosimendan versus conventional inotropes.
21
King, Caitlin E., Elizabeth J. Thompson, Henry P. Foote, et al. "An evidence-based review of the use of vasoactive and inotropic medications in post-operative paediatric patients after cardiac surgery with cardiopulmonary bypass from 2000 to 2020." Cardiology in the Young 30, no. 12 (2020): 1757–71. http://dx.doi.org/10.1017/s1047951120004151.
Full textAbstract:
AbstractBackground:Infants with moderate-to-severe CHD frequently undergo cardiopulmonary bypass surgery in childhood. Morbidity and mortality are highest in those who develop post-operative low cardiac output syndrome. Vasoactive and inotropic medications are mainstays of treatment for these children, despite limited evidence supporting their use.Methods:To help inform clinical practice, as well as the conduct of future trials, we performed a systematic review of existing literature on inotropes and vasoactives in children after cardiac surgery using the PubMed and EMBASE databases. We included studies from 2000 to 2020, and the patient population was defined as birth – 18 years of age. Two reviewers independently reviewed studies to determine final eligibility.Results:The final analysis included 37 papers. Collectively, selected studies reported on 12 different vasoactive and inotropic medications in 2856 children. Overall evidence supporting the use of these drugs in children after cardiopulmonary bypass was limited. The majority of studies were small with 30/37 (81%) enrolling less than 100 patients, 29/37 (78%) were not randomised, and safety and efficacy endpoints differed widely, limiting the ability to combine data for meta-analyses.Conclusion:Vasoactive and inotropic support remain critical parts of post-operative care for children after cardiopulmonary bypass surgery. There is a paucity of data for the selection and dosing of vasoactives and inotropes for these patients. Despite the knowledge gaps that remain, numerous recent innovations create opportunities to rethink the conduct of clinical trials in this high-risk population.
22
Lampé, Nóra, Dániel Priksz, Tamás Erdei, et al. "Negative Inotropic Effect of BGP-15 on the Human Right Atrial Myocardium." Journal of Clinical Medicine 9, no. 5 (2020): 1434. http://dx.doi.org/10.3390/jcm9051434.
Full textAbstract:
Cardiovascular morbidity and mortality carry great socioeconomic burden worldwide that mandates the development of new, efficacious therapeutic agents with limited adverse effects. O-(3-piperidino-2-hydroxy-1-propyl) nicotinic acid amidoxime (BGP-15) is a known, well-tolerable drug candidate that exerts beneficial effects in several disease models. As BGP-15 has a significant structural similarity with propranolol, it arose that BGP-15 might also have a direct effect on the heart. Thus, in the present work, we investigated the effect of BGP-15 and propranolol on the contractility of isolated, paced, human right atrial samples (obtained from patients undergone open-heart surgery), with or without previous isoproterenol (ISO) stimulation (evoking an indirect or direct effect, respectively). We found that both BGP-15 and propranolol exerted direct as well as indirect negative inotropic effects on the atrial myocardium, reaching similar maximal response. However, BGP-15 had considerably smaller potency than propranolol regarding both types of negative inotropy. In addition, BGP-15, in contrast to propranolol, had a significantly greater indirect negative inotropic effect on samples exhibiting strong response to ISO. Moreover, the indirect negative inotropic effect of BGP-15 was significantly greater on samples derived from diabetic patients than on samples obtained from non-diabetic ones. Our results suggest that the enhanced ISO sensitivity is associated with the diabetic state, and BGP-15 exerts greater negative inotropic effect on the human atrial myocardium in both conditions (as compared to the atrial tissue that is not ISO oversensitive and/or diabetic). Additionally, the negative inotropic effects of BGP-15 and propranolol seem to be mediated by in part different molecular pathways in the atrial myocardium.
23
McCann, Patrick, and Paul J. Hauptman. "Inotropic Therapy." Medical Clinics of North America 96, no. 5 (2012): 943–54. http://dx.doi.org/10.1016/j.mcna.2012.07.004.
Full text
24
Brown, Ricardo A., Prashant Bhasin, Adedapo O. Savage, and Joseph C. Dunbar. "Chronic verapamil treatment attenuates the negative inotropic effect of ethanol in diabetic rat myocardium." Canadian Journal of Physiology and Pharmacology 72, no. 9 (1994): 1013–18. http://dx.doi.org/10.1139/y94-141.
Full textAbstract:
It is well established that cardiomyopathy is a consistent feature of diabetic myocardium and that alcohol consumption increases the risk of cardiovascular disease among diabetic subjects. The objective of this investigation was to determine whether acute or chronic verapamil treatment attenuates the negative inotropic effect of ethanol (EtOH) in the diabetic rat heart. Wistar rats were made diabetic with streptozotocin (55 mg/kg, iv). Left-ventricular papillary muscles, from normal and diabetic (8 weeks) rats, were superfused with Tyrode's solution at 30 °C while driven at 0.5 Hz. A subgroup of diabetic and normal animals received daily injections of verapamil (8 mg/kg, ip; 8 weeks), whereas muscles from untreated animals were exposed to verapamil (2 μM) in vitro. Peak tension developed (PTD), time to peak tension (TPT), time to 90% relaxation (RT90), and the maximum velocities of tension development (+VT) and decay (−VT) were determined in the absence and presence of clinically relevant concentrations of EtOH (80–240 mg/dL, i.e., 17.4–52.1 mM). Ethanol at 80 mg/dL reduced PTD, + VT, and −VT only in preparations from diabetic animals. Higher concentrations of EtOH (120–240 mg/dL) decreased PTD, TPT, +VT, and −VT. The negative inotropic effect of EtOH (240 mg/dL) was attenuated only in diabetic myocardium chronically treated with verapamil, whereas acute verapamil treatment potentiated the negative inotropic effect of EtOH in both normal and diabetic myocardium. Thus, chronic verapamil therapy diminishes the negative inotropic effect of EtOH in diabetic myocardium and acute verapamil treatment exaggerates it. Altered expression of membrane-bound calcium channels may be involved in the negative inotropic response to EtOH in long-term diabetes.Key words: ethanol, papillary muscle, inotropism, myocardium, force of contraction, diabetes mellitus.
25
Flenner, Frederik, Nicole Arlt, Mahtab Nasib та ін. "In Vitro Negative Inotropic Effect of Low Concentrations of Bupivacaine Relates to Diminished Ca2+ Sensitivity but Not to Ca2+ Handling or β-Adrenoceptor Signaling". Anesthesiology 128, № 6 (2018): 1175–86. http://dx.doi.org/10.1097/aln.0000000000002180.
Full textAbstract:
Abstract Background Systemic toxicity of local anesthetics is predominantly complicated by their myocardial toxicity. Especially long-acting local anesthetics exert a negative inotropic effect that has been described at lower concentrations than defined for blockade of myocardial ion channels. We evaluated the negative inotropic effect of bupivacaine at a concentration described for clinical toxicity testing the hypothesis that negative inotropy is a result of reduced Ca2+ sensitivity rather than blockade of ion channels. Methods We simultaneously measured force development and action potentials in guinea pig right papillary muscles (n = 5 to 7). L-type Ca2+ currents (n = 8 to 16) and Ca2+ transients (n = 10 to 11) were measured in isolated cardiomyocytes. Sensitivity of myofilaments to Ca2+ was assessed in skinned fibers (n = 10). Potential effects of bupivacaine on 3′,5′-cyclic adenosine monophosphate concentrations were measured using Förster Resonance Energy Transfer (n = 12 to 14) microscopy. Results Bupivacaine reduced force in a concentration-dependent manner from 173 ± 119 µN at baseline to 28 ± 13 µN at 300 µM (mean ± SD). At concentrations giving half-maximum negative inotropic effects (5 µM), the maximum upstroke velocity of action potentials, as a surrogate of sodium channel activity, was unaffected. Maximum positive inotropic effects of isoprenaline were also reduced to 50%. Neither basal nor isoprenaline-induced 3′,5′-cyclic adenosine monophosphate accumulation, L-type Ca2+ currents, or Ca2+ transients were affected by 5 µM bupivacaine, but this concentration significantly decreased Ca2+ sensitivity of myofilaments, changing the negative logarithm of the half-maximum effective Ca2+ concentrations from 5.66 to 5.56 –log[M]. Conclusions We provide evidence that the negative inotropic effect of bupivacaine may be caused mainly by a reduction in myofilament sensitivity to Ca2+.
26
Reibel, D. K., M. A. Holahan, and C. E. Hock. "Effects of dietary fish oil on cardiac responsiveness to adrenoceptor stimulation." American Journal of Physiology-Heart and Circulatory Physiology 254, no. 3 (1988): H494—H499. http://dx.doi.org/10.1152/ajpheart.1988.254.3.h494.
Full textAbstract:
The effect of dietary fish oil on cardiac function and responsiveness to alpha- and beta-adrenergic receptor agonists was examined in isolated perfused rat hearts. Rats were fed either a standard laboratory diet (SD) or diets containing 5% corn oil (CO) or 5% menhaden oil (MO) for 4 wk. When perfused as working preparations at varying preloads and afterloads, the peak aortic pressures, aortic outputs, and coronary flows were comparable in hearts of rats fed the three experimental diets. Inotropic responsiveness to phenylephrine was examined by infusing graded doses of the drug into the heart while monitoring changes in the rate of left ventricular pressure development (+dP/dt). Prior to phenylephrine administration +dP/dt was not different among the three groups of hearts. However, at each dose of phenylephrine employed, delta +dP/dt was approximately 50% less in hearts of rats fed MO when compared with either SD or CO. Thus cardiac inotropic responsiveness to this alpha-agonist was reduced by dietary fish oil. In contrast, cardiac inotropic responsiveness to isoproterenol was not altered with MO feeding. The data demonstrate that dietary fish oil results in alterations in alpha- but not beta-adrenoceptor mediated changes in cardiac inotropy.
27
Siedlecka, U., M. Arora, T. Kolettis, et al. "Effects of clenbuterol on contractility and Ca2+ homeostasis of isolated rat ventricular myocytes." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 5 (2008): H1917—H1926. http://dx.doi.org/10.1152/ajpheart.00258.2008.
Full textAbstract:
Clenbuterol, a compound classified as a β2-adrenoceptor (AR) agonist, has been employed in combination with left ventricular assist devices (LVADs) to treat patients with severe heart failure. Previous studies have shown that chronic administration of clenbuterol affects cardiac excitation-contraction coupling. However, the acute effects of clenbuterol and the signaling pathway involved remain undefined. We investigated the acute effects of clenbuterol on isolated ventricular myocyte sarcomere shortening, Ca2+ transients, and L-type Ca2+ current and compared these effects to two other clinically used β2-AR agonists: fenoterol and salbutamol. Clenbuterol (30 μM) produced a negative inotropic response, whereas fenoterol showed a positive inotropic response. Salbutamol had no significant effects. Clenbuterol reduced Ca2+ transient amplitude and L-type Ca2+ current. Selective β1-AR blockade did not affect the action of clenbuterol on sarcomere shortening but significantly reduced contractility in the presence of fenoterol and salbutamol ( P < 0.05). Incubation with 2 μg/ml pertussis toxin significantly reduced the negative inotropic effects of 30 μM clenbuterol. In addition, overexpression of inhibitory G protein (Gi) by adenoviral transfection induced a stronger clenbuterol-mediated negative inotropic effect, suggesting the involvement of the Gi protein. We conclude that clenbuterol does not increase and, at high concentrations, significantly depresses contractility of isolated ventricular myocytes, an effect not seen with fenoterol or salbutamol. In its negative inotropism, clenbuterol predominantly acts through Gi, and the consequent downstream signaling pathways activation may explain the beneficial effects observed during chronic administration of clenbuterol in patients treated with LVADs.
28
Zima, Endre, Dimitrios Farmakis, Piero Pollesello, and John T. Parissis. "Differential effects of inotropes and inodilators on renal function in acute cardiac care." European Heart Journal Supplements 22, Supplement_D (2020): D12—D19. http://dx.doi.org/10.1093/eurheartj/suaa091.
Full textAbstract:
Abstract Pathological interplay between the heart and kidneys is widely encountered in heart failure (HF) and is linked to worse prognosis and quality of life. Inotropes, along with diuretics and vasodilators, are a core medical response to HF but decompensated patients who need inotropic support often present with an acute worsening of renal function. The impact of inotropes on renal function is thus potentially an important influence on the choice of therapy. There is currently relatively little objective data available to guide the selection of inotrope therapy but recent direct observations on the effects of levosimendan and milrinone on glomerular filtration favour levosimendan. Other lines of evidence indicate that in acute decompensated HF levosimendan has an immediate renoprotective effect by increasing renal blood flow through preferential vasodilation of the renal afferent arterioles and increases in glomerular filtration rate: potential for renal medullary ischaemia is avoided by an offsetting increase in renal oxygen delivery. These indications of a putative reno-protective action of levosimendan support the view that this calcium-sensitizing inodilator may be preferable to dobutamine or other adrenergic inotropes in some settings by virtue of its renal effects. Additional large studies will be required, however, to clarify the renal effects of levosimendan in this and other relevant clinical situations, such as cardiac surgery.
29
Fulton, B., M. Pertwee, R. Latimer, et al. "The inotropic effectsof piroxinone — a new inotropic vasodilating agent." Journal of Cardiothoracic Anesthesia 4, no. 6 (1990): 100. http://dx.doi.org/10.1016/0888-6296(90)90171-b.
Full text
30
Kurobane, Itsuo, Dhirendra L. Nandi, and George T. Okita. "Association of the positive inotropic action of ouabain with a second species of digitalis receptors." Canadian Journal of Physiology and Pharmacology 63, no. 5 (1985): 476–86. http://dx.doi.org/10.1139/y85-083.
Full textAbstract:
Studies were conducted to determine whether Na–K ATPase or a second species of digitalis receptors in canine cardiac sarcolemma membrane preparations is associated with the positive inotropic action of nontoxic concentrations of ouabain. [3H]ouabain association and dissociation experiments using highly enriched sarcolemma preparations from canine ventricle indicate the presence of two species of ouabain binding receptors. Ouabain binding to Na–K ATPase of the sarcolemma preparation requires supporting ligands and is characterized by fast association and very slow dissociation in vitro. The second species of digitalis receptor does not require supporting ligands for ouabain binding and is characterized by slow association and fast dissociation. To determine which species of digitalis receptor is associated with the positive inotropic action of digitalis, ouabain washout experiments were conducted using various isolated canine myocardial preparations. Washout of the positive inotropic effects of 1.2–2.4 × 10−7 M ouabain gave half-life values of 1.5–2.0 h for the various myocardial preparations. [3H]ouabain dissociation from the second species of digitalis receptors gave half-life values of 1.7–1.8 h, whereas dissociation from the sarcolemma Na–K ATPase gave half-life values of 8.9–9.3 h for the various sarcolemma preparations utilized. Therefore, based on similarities in half-life values between ouabain inotropy and [3H]ouabain dissociation from the second class of digitalis receptors, it is postulated that the positive inotropic action of digitalis glycosides is associated with the second species of digitalis receptors in the sarcolemma and not with the digitalis inhibitory receptor of Na–K ATPase for nontoxic concentrations of digitalis.
31
Nagao, Kazuya, Takao Kato, Hidenori Yaku, et al. "Current use of inotropes according to initial blood pressure and peripheral perfusion in the treatment of congestive heart failure: findings from a multicentre observational study." BMJ Open 12, no. 1 (2022): e053254. http://dx.doi.org/10.1136/bmjopen-2021-053254.
Full textAbstract:
ObjectivesCurrent guidelines restrict the use of inotropes for the treatment for heart failure (HF) unless the patients are hypotensive or hypoperfused because of safety concerns. This study sought to characterise the contemporary real-world use of inotropes and associated long-term outcomes according to systolic blood pressure (sBP) and perfusion status.DesignA multicentre prospective cohort study.SettingThis study was nested from the Kyoto Congestive Heart Failure registry, which included consecutive Japanese patients admitted for HF.ParticipantsWe categorised 3995 patients into two groups: sBP ≥90 mm Hg and warm profile group, and sBP <90 mm Hg or cold profile group. In each group, patients were stratified across the use of inotropes within 24 hours of hospital presentation.Primary and secondary outcomesThe primary outcome was all-cause death throughout follow-up. Secondary outcomes included cardiovascular death throughout follow-up, all-cause death during index hospitalisation and after discharge, and HF hospitalisation.ResultsA total of 793 patients (20%) presented with sBP <90 mm Hg or cold profile, whereas 3202 patients had sBP ≥90 mm Hg and warm profile; 276 patients (35%) in the sBP <90 mm Hg/cold group and 312 patients (10%) in the sBP ≥90 mm Hg/warm group received initial inotropic treatment. Adjusted excess risk of inotrope use relative to no inotrope for the primary outcome measure was significant in the sBP ≥90 mm Hg/warm group (adjusted HR), 1.36; 95% CI 1.09 to 1.72, p=0.006) but not in the sBP <90 mm Hg/cold group (adjusted HR, 1.28, 95% CI 0.96 to 1.69, p=0.09). Risk for postdischarge all-cause death and HF hospitalisation was not significantly different between the patients with inotropes and no inotropes in both groups.ConclusionInotrope use in the absence of hypotension and hypoperfusion is still common, but associated with a worse long-term prognosis.Trial registration numberUMIN000015238.
32
Nassar, Mazen Alaadeen, Lama Hisham Bedaiwi, Tariq Omar Ali, et al. "Role of inotropes and vasopressors therapy in the intensive care unit." International Journal Of Community Medicine And Public Health 10, no. 1 (2022): 459. http://dx.doi.org/10.18203/2394-6040.ijcmph20223574.
Full textAbstract:
Vasopressors and inotropes are often administered to critically ill patients in intensive care unit for the management and treatment of haemodynamic impairment, heart failure, septic and cardiogenic shock, trauma among certain other diseases. In patients with shock, vasopressors and inotropes are used to induce vasoconstriction or enhance cardiac contractility. Vasopressors induces vasoconstriction, which causes systemic vascular resistance, leading to increase in mean arterial pressure and elevates organ perfusion. While inotropes raise cardiac output, which helps maintain mean arterial pressure and body perfusion. Due to a decreased risk of side effects compared to other catecholamine vasopressors, norepinephrine is considered a first-line vasopressor titrated to attain an optimal arterial pressure. An inotrope such as dobutamine may be given to raise cardiac output to a sufficient level to fulfil tissue demand if tissue and organ perfusion still is not enough. Due to their strengthening effect on cardiac contractility, inotropes have been utilized in the care of patients with heart failure for decades, particularly for patients with systolic dysfunction, or heart failure with reduced ejection fraction. Along with their beneficial inotropic impact, they also have chronotropic and peripheral vascular effects. For patients with severely reduced cardiac output and peripheral organ hypoperfusion, they are most frequently employed in intensive care unit. Along with their benefits they are also associated with certain considerate side-effects. The purpose of this research is to review the available information about role of inotropes and vasopressors therapy in the intensive care unit.
33
Moura, André Luiz de, Stephen Hyslop, Dora M. Grassi-Kassisse та Regina C. Spadari. "Functional β2-adrenoceptors in rat left atria: effect of foot-shock stress". Canadian Journal of Physiology and Pharmacology 95, № 9 (2017): 999–1008. http://dx.doi.org/10.1139/cjpp-2016-0622.
Full textAbstract:
Altered sensitivity to the chronotropic effect of catecholamines and a reduction in the β1/β2-adrenoceptor ratio have previously been reported in right atria of stressed rats, human failing heart, and aging. In this report, we investigated whether left atrial inotropism was affected by foot-shock stress. Male rats were submitted to 3 foot-shock sessions and the left atrial inotropic response, adenylyl cyclase activity, and β-adrenoceptor expression were investigated. Left atria of stressed rats were supersensitive to isoprenaline when compared with control rats and this effect was abolished by ICI118,551, a selective β2-receptor antagonist. Schild plot slopes for the antagonism between CGP20712A (a selective β1-receptor antagonist) and isoprenaline differed from unity in atria of stressed but not control rats. Atrial sensitivity to norepinephrine, as well as basal and forskolin- or isoprenaline-stimulated adenylyl cyclase activities were not altered by stress. The effect of isoprenaline on adenylyl cyclase stimulation was partially blocked by ICI118,551 in atrial membranes of stressed rats. These findings indicate that foot-shock stress equally affects inotropism and chronotropism and that β2-adrenoceptor upregulation contributes to the enhanced inotropic response to isoprenaline.
34
Ali, Insha, and Masood Ahmad Sheikh. "PRE-EXPERIMENTAL STUDY TO ASSESS THE EFFECTIVENESS OF A STRUCTURED TEACHING PROGRAM ON KNOWLEDGE REGARDING THE ADMINISTRATION OF SELECTED INOTROPIC DRUGS AMONG THE STAFF NURSES IN SELECTED HOSPITAL KASHMIR." International Journal of Advanced Research 9, no. 02 (2021): 604–9. http://dx.doi.org/10.21474/ijar01/12488.
Full textAbstract:
Nowadays we are observing there are enough number of cardiovascular patients and also day by day their ratio is getting increased at huge number because Cardiovascular diseases are the number one cause of death globally, taking an estimated 17.9 million lives each year. Cardiovascular diseases are a group of disorders of the heart and blood vessels and include coronary heart disease and other conditions. Four out of five deaths are due to heart attacks and strokes and one third of these deaths occur prematurely in people under 70 years of age. Individual at risk may demonstrate raised blood pressure, glucose, and lipids as well as overweight and obesity. These can all be easily measured in primary care facilities. Identifying those at high risk of cardiovascular diseases and ensuring they receive appropriate treatment and can prevent premature deaths. For those conditions inotropic drugs play a vital role in rehablitating the cardiovascular disease patients. Inotropic state is most commonly used in reference to various drugs that affect the strength of contraction of heart muscle. Inotropic drugs are the medicines that change the force of hearts contractions. There are two kinds of inotropes namely positive which strengthen the force of heart beat and negative inotropes which weaken the force of heartbeat. So inotropic drugs are the commonly drugs used to treat cardiovascular conditions. Therefore in view of this pre-experimental one group pre-test post-test research design study was conducted to as assess the effectiveness of a structured teaching program on knowledge regarding the administration of inotropic drugs among the staff nurses in selected hospital of Kashmir for which 60 subjects were selected by simple random sampling technique. After data collection structured knowledge questionnaire was used to assess the knowledge among subjects. The data was analyzed by descriptive and inferential statistics by using chi-square and t-test. The findings revealed that in posttest majority of the study subjects 6(10%) had excellent knowledge, 53(88.3%) had good knowledge, 1(1.7%) had average and none had below average knowledge with posttest mean score 26.15 standard deviation 3.019 with mean percentage 63.78 and mean difference 12.97. Study concludes that null hypothesis was rejected because there was gain in knowledge among staff nurses after imparting structured teaching programme. The study also concluded that null hypothesis was accepted because there was statistically no significant association between selected variable (professional qualification, working experience, place of posting, and in-service education programme attended) at p> 0.001 of staff nurses with their pre-test knowledge scores at 0.05 level of significance.
35
Gupta, Kishore, Dhiren Shah, and Dhaval Naik. "Levosimendan: evolution over last two decades." International Journal of Advances in Medicine 9, no. 3 (2022): 376. http://dx.doi.org/10.18203/2349-3933.ijam20220446.
Full textAbstract:
Levosimendan was maiden agent at the time of its emergence, promoting inotropy mainly through calcium sensitization of cardiac troponin C (cTnC). Levosimendan seems a lucrative option but has not demonstrated a clear superiority to other inotropes in well-designed trials. We searched the PubMed database and reviewed the pertinent studies published till 2021 and summarized various trials/studies to come to a consensus regarding its indications in cardiac patients. Patients with decompensated heart failure requiring inotropic support and receiving beta-blockers represent most widely accepted indication. Levosimendan infusions are increasingly used to facilitate extracorporeal membrane oxygenation (ECMO) weaning and avoiding hospitalizations in patients with end-stage heart failure. Levosimendan doesn’t seem to have long term survival benefit in ventricular dysfunction patients undergoing surgery. The evidence supporting the role in right ventricular failure is not well-established. These lines of evidence require further investigation and their clinical significance needs to be evaluated in specifically designed prospective trials.
36
Nandkeolyar, Shuktika, Tanya Doctorian, Gary Fraser, et al. "Predictors of In-hospital Mortality in Cardiogenic Shock Patients on Vasoactive or Inotropic Support." Clinical Medicine Insights: Cardiology 15 (January 2021): 117954682110494. http://dx.doi.org/10.1177/11795468211049449.
Full textAbstract:
Background: Though controversial, the short-duration in-patient use of inotropes in cardiogenic shock (CS) remain an ACC/AHA Class IIa indication, and are frequently used in the initial treatment of CS. We evaluated in-patient mortality and effect on mortality risk of commonly used vasoactive inotropic medications for the medical management of SCAI stage B and C cardiogenic shock patients in a tertiary care cardiac care unit: dobutamine, dopamine, milrinone, and norepinephrine. Methods: We retrospectively evaluated 342 patients who received dobutamine, milrinone, dopamine, norepinephrine or a combination of these medications for SCAI stage B and C cardiogenic shock. Cox proportional hazards were used to form longitudinal mortality predictions. Results: Overall in-patient mortality was 18%. Each 1 µg/kg/minute increase in dobutamine independently corresponded to a 15% increase in risk of mortality. High dose dobutamine >3 µg/kg/minute is associated with 3-fold increased risk compared to ⩽3 µg/kg/minute ( P < .001). Use of milrinone, norepinephrine, and dopamine were not independently associated with mortality. Conclusion: We demonstrate that the overall in-hospital mortality of SCAI stage B and C cardiogenic shock patients medically managed on inotropes was not in excess of prior studies. Dobutamine was independently associated with mortality, while other vasoactive inotropic medications were not. Inotropes remain a feasible method of managing SCAI stage B and C cardiogenic shock.
37
Hedia, Sara Mokhtar Abdelaal, Manal Ezzat Badawy, Hamed Mohamed Elsharkawy, and Sara Mohamed Elashry. "The Relationship between Inotrope Use and Intraventricular Hemorrhage in Preterm Neonates." Asian Journal of Pediatric Research 14, no. 12 (2024): 84–88. https://doi.org/10.9734/ajpr/2024/v14i12413.
Full textAbstract:
In preterm newborns, intraventricular haemorrhage (IVH) may be preceded by erroneous hemodynamic alterations in cerebral circulation. Neonatal hypotension requiring use of inotropes was found to be the significantly risk factors in IVH. Reduced use of inotropic medications (such dopamine or epinephrine), which have been linked to the development of IVH, and a reduced incidence of hypotension, may be linked to the increased intravascular volume.
38
Gueugniaud, Pierre-Yves, Jean-Luc Hanouz, Jean-Marc Martino, Yves Lecarpentier, Pierre Coriat, and Bruno Riou. "Interaction of Halogenated Anesthetics with Dobutamine in Rat Myocardium." Anesthesiology 90, no. 6 (1999): 1663–70. http://dx.doi.org/10.1097/00000542-199906000-00023.
Full textAbstract:
Background Halogenated anesthetics potentiate the positive inotropic effects of alpha- and beta-adrenoceptor stimulations, but their interactions with dobutamine remain unknown. Methods The effects of halothane, isoflurane, sevoflurane, and desflurane (1 and 2 minimum alveolar concentration) on the inotropic responses induced by dobutamine (10(-8)-10(-4) M) were studied in rat left ventricular papillary muscles in vitro. Inotropic effects were studied under low (isotony) and high (isometry) loads. The authors also studied the lusitropic effects in isotonic (R1) and isometric (R2) conditions. Data are the mean percentage of baseline +/- SD. Results Dobutamine induced a positive inotropic effect (active isometric force: 185+/-36%, P &lt; 0.001) and a positive lusitropic effect under low load (R1: 78+/-9%, P &lt; 0.001), but not under high load (R2: 95+/-21%, not significant). Halothane, isoflurane, and sevoflurane did not modify the positive inotropic effect of dobutamine. Even in the presence of alpha-adrenoceptor blockade, isoflurane did not potentiate the positive inotropic effect of dobutamine. Desflurane significantly enhanced the positive inotropic effect of dobutamine (active isometric force: 239+/-35%, P &lt; 0.001), but this potentiation was abolished by pretreatment with reserpine. In contrast to halothane, isoflurane, sevoflurane, and desflurane did not significantly modify the lusitropic effects of dobutamine. Conclusions Halogenated anesthetics, except desflurane, did not modify the positive inotropic effects of dobutamine. Desflurane enhanced the positive inotropic effect of dobutamine, but this effect was related to the desflurane-induced release in intramyocardial catecholamine stores.
39
Colleti, José, and Werther Brunow de Carvalho. "Vasoactive-Inotropic Score." Pediatric Critical Care Medicine 18, no. 10 (2017): 1003. http://dx.doi.org/10.1097/pcc.0000000000001270.
Full text
40
Leone, Marc, Jacques Alban??se, and Claude Martin. "Positive inotropic stimulation." Current Opinion in Critical Care 8, no. 5 (2002): 395–403. http://dx.doi.org/10.1097/00075198-200210000-00005.
Full text
41
Archer, N. "Which inotropic agent?" Current Paediatrics 4, no. 2 (1994): 102–5. http://dx.doi.org/10.1016/0957-5839(94)90061-2.
Full text
42
Cingolani, Horacio E. "Inotropic agents. Introduction." Journal of Molecular and Cellular Cardiology 24 (May 1992): 83. http://dx.doi.org/10.1016/0022-2828(92)90276-6.
Full text
43
Sun, Yan-ting, Li-hong Wang, and Yun-tai Yao. "Vasoactive-inotropic agents in pediatric patients undergoing cardiac surgery: A single-center retrospective study." Medicine 104, no. 18 (2025): e42333. https://doi.org/10.1097/md.0000000000042333.
Full textAbstract:
This study aimed to retrospectively summarize the use of vasoactive-inotropic agents in pediatric patients undergoing cardiac surgery at Fuwai Hospital. A total of 401 patients who met the screening criteria were enrolled in this study between April and June 2021 at Fuwai Hospital. We retrospectively summarized the current practices for vasoactive-inotropic agent use across different ages, Risk Adjustment in Cardiac Surgery 1 (RACHS-1) categories, and among various anesthesiologists. Intraoperatively, milrinone was the most commonly used inotrope (327 patients, 81.6%), followed by dopamine (274, 68.3%), dobutamine (263, 65.4%), epinephrine (67, 16.7%), and isoprenaline (11, 2.7%). Vasopressin was mainly administered during the pediatric intensive care unit period, with the highest use rate on postoperative day (POD)-1 (16/401, 3.9%). Furthermore, a combination of dopamine, dobutamine, and milrinone was administered by 52.1% of anesthesiologists intraoperatively and by 30.2% of pediatric intensivists on POD 1. Milrinone, dopamine, and dobutamine were selected by most anesthesiologists (13/14, 92.9%), and their usage rates among different anesthesiologists ranged from 66.67% to 92.68%, 52.94% to 89.66%, and 46.18% to 86.21%, respectively. Moreover, their use in category 4 surgeries was significantly higher than in category 1 to 3 surgeries. Milrinone, dopamine, and dobutamine were the most commonly used vasoactive-inotropic agents, while the other agents represented the diversity of medications used during both the intra- and postoperative periods in pediatric cardiac surgery at Fuwai Hospital.
44
Osthoff, Mirjam, Christine Bernsmeier, Stephan C. Marsch, and Patrick R. Hunziker. "Levosimendan as Treatment Option in Severe Verapamil Intoxication: A Case Report and Review of the Literature." Case Reports in Medicine 2010 (2010): 1–3. http://dx.doi.org/10.1155/2010/546904.
Full textAbstract:
Cardiovascular shock due to verapamil intoxication is often refractory to standard resuscitation methods. Recommended therapy includes prevention of further absorption of the drug, inotropic therapy, calcium gluconate, and hyperinsulinemia/euglycemia therapy. Often further measures are needed such as ventricular pacing or mechanical circulatory support. Still, mortality remains high. Levosimendan, an inotropic agent, that enhances myofilament response to calcium, increases myocardial contraction and could therefore be beneficial in verapamil intoxication. Here, we report the case of a 60-year-old patient with clinically severe verapamil poisoning who presented with shock, bradycardia, and sopor. Standard therapy including high-dose inotropes failed to ameliorate the signs of intoxication. But additional therapy with levosimendan led to rapid improvement. Based on this observation, the literature is reviewed focusing on utilization of levosimendan in the treatment of calcium channel blocker overdose. We suggest to consider levosimendan as additional treatment option in patients with cardiovascular shock due to verapamil intoxication that are refractory to standard management.
45
Karmazyn, M., and M. P. Moffat. "Positive inotropic effects of low concentrations of leukotrienes C4 and D4 in rat heart." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 4 (1990): H1239—H1246. http://dx.doi.org/10.1152/ajpheart.1990.259.4.h1239.
Full textAbstract:
We examined the effects of leukotrienes (LT) B4, C4, D4, and E4 (0.010-2.5 ng/ml) on contractile and coronary function in isolated rat hearts. Concentration-dependent effects were examined either by the cumulative addition of LTs or by addition of specific concentrations to individual preparations. Neither LTB4 nor LTE4 produced myocardial or coronary effects at any concentration, irrespective of addition protocol. At 0.010 ng/ml, both LTC4 and LTD4 produced an increase in force that was associated with a 30% elevation in coronary pressure. Further cumulative addition of either leukotriene resulted in a negative inotropic effect and a further increase in coronary pressure. In contrast, following single additions of LTC4 or LTD4 (0.01-0.50 ng/ml) a positive inotropic effect and an increased coronary pressure were observed. LTC4 or LTD4 at 0.5 ng/ml produced a negative inotropic effect in hearts pretreated with 0.01 ng/ml of LTD4 or LTC4, respectively. Reversal of this addition protocol resulted in a negative inotropic effect of either 0.01 ng/ml LTD4 or LTC4. Verapamil and nifedipine significantly attenuated the positive inotropic and coronary constricting effect of 0.5 ng/ml LTC4 and LTD4. The addition of either LT following BAY K 8644 resulted in a negative inotropic effect, in contrast to the positive inotropic influence seen with leukotriene alone. Our results demonstrate a positive inotropic effect of low concentrations of LTC4 and LTD4 concomitant with coronary artery constriction, a phenomenon determined by leukotriene addition protocols and suggestive of LTC4/LTD4 receptor interaction. The effects of calcium channel antagonists and BAY K 8644 on the inotropic response suggest a leukotriene-mediated activation of the calcium channel resulting in increased intracellular calcium concentrations.
46
Temma, Kyosuke, Hiroshi Kondo, and Tai Akera. "Developmental changes in inotropic actions of neurotoxins observed in ventricular muscle of rat heart." Canadian Journal of Physiology and Pharmacology 69, no. 4 (1991): 494–500. http://dx.doi.org/10.1139/y91-074.
Full textAbstract:
Developmental changes in functions of myocardial sodium channels were examined from inotropic effects of several neurotoxins in ventricular muscle preparations obtained from prenatal (20–22 day gestation) or adult (3–4 months old) rat hearts. Tetrodotoxin caused a negative inotropic effect in low concentrations and a loss of muscle responsiveness to electrical stimulation in high concentrations in preparations obtained from either prenatal or adult rat heart. The tetrodotoxin concentration that caused a 50% decrease in developed tension was higher in prenatal rats. Anemonia sulcata toxin, Androctonus australis toxin, veratridine, and Centruroides sculpturatus toxin all produced positive inotropic effects in adult rat heart. The effects were largest with A. sulcata and A. australis toxins, intermediate with veratridine, and smallest with C. sculpturatus toxin. Prenatal heart required higher concentrations of either veratridine, or A. sulcata or A. australis toxins to produce comparable positive inotropic effects. With C. sculpturatus toxin, no significant positive inotropic effect was observed in prenatal heart muscle preparations. These results indicate that cardiac sodium channels undergo significant functional changes during development and that negative and positive inotropic effects of neurotoxins resulting from inhibition and enhancement of fast Na+ channels reflect developmental changes in the cardiac sodium channels.Key words: sodium channels, sodium channel toxins, cardiac inotropic agents.
47
Ahmad, Tanjeev, Shamitha A. Manohar, Jason D. Stencel, and Thierry H. Le Jemtel. "Dobutamine in the Management of Advanced Heart Failure." Journal of Clinical Medicine 13, no. 13 (2024): 3782. http://dx.doi.org/10.3390/jcm13133782.
Full textAbstract:
Background: The potential harm and clinical benefits of inotropic therapy in patients with decompensated heart failure with reduced ejection fraction or advanced heart failure were debated for three decades. Nonetheless, confronted with a dismal quality of life in the last months to years of life, continuous home inotropic therapy has recently gained traction for palliative therapy in patients who are not candidates for left ventricular mechanical circulatory support or heart transplantation. Methods: As continuous inotropic therapy is only considered for patients who experience symptomatic relief and display objective evidence of improvement, clinical equipoise is no longer present, and randomized controlled trials are hard to conduct. Results: We first outline the transient use of inotropic therapy in patients with decompensated heart failure with reduced ejection fraction and emphasize the hemodynamic requisite for inotropic therapy, which is a demonstration of a low cardiac output through a low mixed venous oxygen saturation. Lastly, we review the current experience with the use of home inotropic therapy in patients who are not candidates or are awaiting mechanical circulatory support or heart transplantation. Conclusions: Evidence-based clinical data are needed to guide inotropic therapy for refractory decompensated heart failure with reduced ejection fraction in patients who are ineligible or awaiting mechanical circulatory support or heart transplantation.
48
Hanouz, Jean-Luc, Bruno MD Riou, Laurent Massias, Yves Lecarpentier та Pierre Coriat. "Interaction of Halothane with α- and β-Adrenoceptor Stimulations in Rat Myocardium". Anesthesiology 86, № 1 (1997): 147–59. http://dx.doi.org/10.1097/00000542-199701000-00019.
Full textAbstract:
Background Halothane induces negative inotropic and lusitropic effects in myocardium. It has been suggested that halothane potentiates beta-adrenoceptor stimulation. However, its effects on the inotropic response to alpha-adrenoceptor stimulation and its effects on the lusitropic effects of alpha- and beta-adrenoceptor stimulation are unknown. Methods The effects of halothane (0.5 and 1 minimum alveolar concentration [MAC]) on the inotropic responses induced by phenylephrine (10(-8) to 10(-4) M) and isoproterenol (10(-8) to 10(-4) M) were studied in rat left ventricular papillary muscles in vitro (in Krebs-Henseleit solution at 29 degrees C, pH 7.40, with 0.5 mM calcium and stimulation frequency at 12 pulses/min). The lusitropic effects were studied in isotonic (R1) and isometric (R2) conditions. Results One MAC halothane induced a negative inotropic effect (54 +/- 3%, P &lt; 0.05), increased R1 (109 +/- 3%, P &lt; 0.05), and decreased R2 (88 +/- 2%, P &lt; 0.05). In control groups, phenylephrine (137 +/- 7%, P &gt; 0.05) and isoproterenol (162 +/- 6%, P &lt; 0.05) induced a positive inotropic effect. Halothane did not significantly modify the positive inotropic effect of calcium, suggesting that it did not modify the inotropic reserve of papillary muscles. In contrast, 1 MAC halothane enhanced the positive inotropic effects of phenylephrine (237 +/- 19%, P &lt; 0.05) and isoproterenol (205 +/- 11%, P &lt; 0.05). Halothane did not modify the lusitropic effect of phenylephrine under high or low load. In contrast, 1 MAC halothane impaired the positive lusitropic effect of isoproterenol under low load (P &lt; 0.05), whereas it did not modify the positive lusitropic effect of isoproterenol under high load. Conclusions At clinically relevant concentrations, halothane potentiated the positive inotropic effects of both alpha- and beta-adrenoceptor stimulation. Furthermore, halothane alters the positive lusitropic-effect of beta-adrenoceptor stimulation under low load.
49
DAR, FN, A. YUNUS, and MN NIAZ. "RELATIONSHIP OF POST-OPERATIVE INOTROPIC USE AND MORTALITY IN CABG PATIENTS WITH RADIAL GRAFTS." Biological and Clinical Sciences Research Journal 2023, no. 1 (2023): 422. http://dx.doi.org/10.54112/bcsrj.v2023i1.422.
Full textAbstract:
This retrospective analysis aimed to assess the effect of post-operative use of inotropic support on the long-term mortality rates of coronary artery bypass graft (CABG) patients who had undergone radial grafts. Inotropic drugs are frequently administered to improve heart function after surgery, but their impact on long-term survival is still controversial. The primary objective was to compare the 10-year mortality rates between patients who received post-operative inotropic support (Group A) and those who did not (Group B). We also sought to determine whether inotropic infusion correlated with improved or worsened long-term survival. A total of 80 participants were retrospectively analyzed, with Group A consisting of 18 individuals who received inotropic support and Group B comprising 62 individuals without such support. Demographic and clinical characteristics, including age, gender, comorbidities, clinical parameters, ejection fraction, New York Heart Association (NYHA) functional class, and 10-year mortality rates, were assessed and compared between the two groups. Kaplan-Meier survival analysis was done to assess the survival benefits. The analysis revealed no significant difference in 10-year mortality rates between Group A and Group B, with an insignificant p-value of 0.987. The Kaplan-Meier survival analysis and log-rank test further supported this finding, indicating no significant relationship between the absence of inotropic infusion and increased survival chances. These results suggest that post-operative inotropic support may not significantly influence long-term survival. Inotropic infusion may not be necessary for improving or worsening 10-year survival rates in surgical patients. While this retrospective analysis provides valuable insights, further research, particularly larger prospective studies, and randomized controlled trials, is needed to validate these findings and offer more conclusive guidance regarding the use of inotropic agents in post-operative care.
50
Haleen, Stephen J., Robert P. Steffen, and Ronald E. Weishaar. "Species differences in the positive inotropic response to DPI 201-106, a novel cardiotonic agent." Canadian Journal of Physiology and Pharmacology 67, no. 11 (1989): 1460–63. http://dx.doi.org/10.1139/y89-235.
Full textAbstract:
The positive inotropic activity of the novel cardiotonic DPI 201-106 was investigated in rat and guinea pig isolated hearts. For comparative purposes, the adenylate cyclase stimulant forskolin and the sodium channel agonist veratridine were also evaluated in both species. DPI 201-106 and veratridine produced greater inotropic effects in rat hearts than in guinea pig hearts, whereas forskolin produced comparable effects. In both species the inotropic response to DPI 201-106 and veratridine, but not forskolin, was reversed by the sodium channel antagonist tetrodotoxin. These results confirm that the positive inotropic effect of DPI 201-106 is due to stimulation of the sodium channel and demonstrate for the first time that species differences exist in the inotropic response to this novel cardiotonic drug.Key words: cardiac muscle, contractility, cardiotonic drug, sodium channel, isolated heart.