Relevant bibliographies by topics / Positive inotropic effect

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Academic literature on the topic 'Positive inotropic effect'

Author: Grafiati
Published: 11 December 2022
Last updated: 19 July 2025

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Journal articles on the topic "Positive inotropic effect"

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.

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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.
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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.

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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.
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3

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.

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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.
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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.

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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 < 0.001) and a positive lusitropic effect under low load (R1: 78+/-9%, P < 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 < 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.
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Rustamov, Shavkat Yu, Inoyat Z. Jumayev, Sadriddin N. Boboev, Eldor B. Ibragimov, Pulat B. Usmanov, and Sherzod N. Zhurakulov. "Description of the Mechanism of Positive Inotropic Action of the Isoquinoline Alkaloid F-18." Cardiology Research and Reports 3, no. 3 (2021): 01–04. http://dx.doi.org/10.31579/2692-9759/023.

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This study evaluated the mechanism of inotropic effect of an isoquinoline alkaloid derivative, 1-(2´-bromine-4´,5´-dimethoxyphenyl)-6,7-dimethoxy-1,2,3,4- tetrahydroisoquinoline (F-18) using electrically stimulated rat left ventricular papillary muscle of rat. The F-18 alkaloid have been shown to have positive inotropic effect on papillary muscle contraction activity, IC50 value -14,6 µM. Са2+L-channel blocker - nifedipine was used in experiments. Inotropic effects of F-18 isoquinoline alkaloid on cardiomyocytes were suggested, based on results obtained in experiments carried in cardiomyocytes SR Ca2+- transport systems modulation.
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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.

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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.
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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.

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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.
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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.

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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 < 0.05), increased R1 (109 +/- 3%, P < 0.05), and decreased R2 (88 +/- 2%, P < 0.05). In control groups, phenylephrine (137 +/- 7%, P > 0.05) and isoproterenol (162 +/- 6%, P < 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 < 0.05) and isoproterenol (205 +/- 11%, P < 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 < 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.
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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.

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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.
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Endou, M., Y. Hattori, N. Tohse, and M. Kanno. "Protein kinase C is not involved in alpha 1-adrenoceptor-mediated positive inotropic effect." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 1 (1991): H27—H36. http://dx.doi.org/10.1152/ajpheart.1991.260.1.h27.

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This study was performed to determine whether activation of protein kinase C is responsible for the positive inotropic effect of alpha 1-adrenoceptor stimulation in rat papillary muscle. In the presence of 1 microM propranolol, phenylephrine (10 microM) produced triphasic inotropic response that was accompanied by prolongation of action potential duration (APD) and hyperpolarization of membrane potential. Phorbol 12,13-dibutyrate (PDBu, 0.1 microM) abolished the negative inotropic effect of phenylephrine and apparently resulted in enhancement of the positive inotropic effect. PDBu also attenuated the phenylephrine-induced hyperpolarization without affecting the APD prolongation. However, such changes were not observed with 12-O-tetradecanoylphorbol-13-acetate (TPA, 0.1 microM). Neither PDBu nor TPA increased the force of contraction or prolonged APD similar to phenylephrine. The protein kinase C inhibitor 1-(5-isoquinolinylsulfonyl)-2-methyl-piperazine (H 7, 10 microM) did not suppress the changes induced by PDBu, and more importantly H 7 did not affect the inotropic and electrophysiological effects of phenylephrine. Both TPA and PDBu significantly inhibited the phenylephrine-induced phosphoinositide hydrolysis as measured by [3H]inositol monophosphate, and these inhibitory effects were eliminated in the presence of H 7. Our results provide an argument against a role of protein kinase C activation in the alpha 1-adrenoceptor-mediated inotropic and electrophysiological effects.
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Dissertations / Theses on the topic "Positive inotropic effect"

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Weintraub, Joe͏̈lle. "Les hétérosides cardiotoniques : propriétés pharmacologiques et mécanisme de leur action inotrope positive." Paris 5, 1988. http://www.theses.fr/1988PA05P057.

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Chamberland, Caroline. "Action inotrope positive de l'apéline liée à l'augmentation de l'amplitude du courant sodique dans les myocytes cardiaque de chien." Mémoire, Université de Sherbrooke, 2008. http://savoirs.usherbrooke.ca/handle/11143/3965.

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L'apéline est l'agoniste du récepteur APJ-R (putative angiotensin II receptor like), récepteur couplé aux protéines G. Exprimée dans le coeur de plusieurs espèces dont l'homme, l'apéline joue un rôle important dans le système cardiovasculaire. L'apéline a un effet inotrope positif sur le coeur. Szokodi et al. ont démontré que cet effet était dû à l'activation de la cascade PLC-PKC et que les échangeurs sodium-hydrogène (NHE) et sodium-calcium (NCX) étaient impliqués. Ils ont également démontré que l'augmentation de la force contractile du myocarde n'était pas due à l'augmentation du courant calcique de type L (I[indice inférieur CaL]). Nous proposons que l'augmentation de la contractilité est due à un effet de l'apéline sur le courant sodique rapide (I[indice inférieur Na]). Matériel et Méthodes. La localisation du récepteur APJ-R fut faite par immunofluorescence sur des myocytes isolés du ventricule gauche de chien. Les mesures du courant sodique sur ces mêmes cellules furent faites par la méthode de patch-clamp en configuration cellule entière en voltage imposé. L'apéline 13 et l'apéline 17 furent perfusées à des concentrations de 100 nM pendant 20 minutes pour évaluer leurs effets sur le courant sodique. Résultats. Le récepteur APJ-R est localisé sur la membrane sarcoplasmique des myocytes au niveau des bandes Z, une structure clé pour la contraction, ce qui nous indique que la localisation du récepteur est propice à la modulation de la contraction cardiaque. L'apéline 13 et l'apéline 17 augmentent I[indice inférieur Max] du courant sodique de 39% et 61% respectivement comparativement au contrôle. En plus de l'augmentation du courant sodique, les deux formes d'apéline déplacent l'activation du canal sodique de -6,8 mV et -8,6 mV pour l'apéline 13 et 17 comparativement à la condition contrôle. Ce déplacement de l'activation vers des potentiels plus négatifs augmente l'excitabilité des myocytes cardiaques et pourrait ainsi moduler la contraction cardiaque. L'inactivation du canal sodique n'est pas modifiée par la présence des deux formes d'apéline. L'apéline ne modifie donc pas la disponibilité du canal en fonction du voltage. Le temps de réactivation est significativement augmenté par la présence d'apéline 13 et 17 ce qui a pour effet d'augmenter la période réfractaire au niveau du coeur. Conclusion. Le récepteur APJ est bien présent au niveau des bandes Z des myocytes suggérant son implication dans la contraction cardiaque. Nos résultats sur le courant sodique démontrent pour la première fois que l'apéline affecte significativement ce courant et que cette augmentation du courant sodique pourrait être responsable de l'augmentation de la contraction cardiaque par l'apéline.
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Kania, Sebastian Martin Albert [Verfasser], Rolf [Akademischer Betreuer] Wachter, Wolfram-Hubertus [Gutachter] Zimmermann, and Wolfgang [Gutachter] Krick. "Der positiv inotrope Effekt von Insulin am menschlichen Myokard / Sebastian Martin Albert Kania. Betreuer: Rolf Wachter. Gutachter: Wolfram-Hubertus Zimmermann ; Wolfgang Krick." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2016. http://d-nb.info/1105759962/34.

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Klenowski, Paul Mark. "Molecular and structural requirements of the ß1L-adrenoceptor." Thesis, Queensland University of Technology, 2012.

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Noradrenaline which occurs naturally in the body binds to beta-adrenoceptors on the heart, causing the heart to beat faster and with greater force in response to increased demand. This enables the heart to provide oxygenated blood to vital organs. Prolonged overstimulation by noradrenaline can be harmful to the heart and lead to the progression of heart disease. In these circumstances beta-adrenoceptors are blocked with drugs called beta-blockers. Beta-blockers block the effects of noradrenaline by binding to the same site on the beta-adrenoceptor. Some beta-blockers such as CGP12177 can also cause increases in heart rate. Therefore it was proposed that CGP12177 could bind in a different place to noradrenaline. The aim of this study was to determine where CGP12177 binds to on the beta-adrenoceptor. The results have revealed a separate binding site named beta-1-low. These results may lead to the development of improved -blockers for the management of heart conditions.
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Potter, Tetyana [Verfasser]. "Hemmung der Alpha-1-beta-1-Isoform der Na,K-ATPase aber fehlender positiv inotroper Effekt von 8-Methoxycoumestrol im humanen Myokard – neue Aspekte in der Pharmakologie der Herzglykoside / Tetyana Potter." Köln : Deutsche Zentralbibliothek für Medizin, 2010. http://d-nb.info/1007870699/34.

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Kania, Sebastian Martin Albert. "Der positiv inotrope Effekt von Insulin am menschlichen Myokard." Doctoral thesis, 2016. http://hdl.handle.net/11858/00-1735-0000-0028-8773-0.

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Mahnecke, Nina [Verfasser]. "Bedeutung der Myosin-Leichtketten-Kinase für den alpha1-adrenergen positiv inotropen Effekt im Herzmuskel / vorgelegt von Nina Mahnecke." 2008. http://d-nb.info/991706714/34.

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Books on the topic "Positive inotropic effect"

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Arrigo, Mattia, and Alexandre Mebazaa. Positive inotropes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0035.

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Inotropic agents are substances used to improve cardiac output and end-organ perfusion in severe forms of acute heart failure. However, inappropriate use of inotropic agents may be associated with severe adverse effects and death. Despite clear indications to restrict their use to acute heart failure patients presenting with signs of end-organ hypoperfusion, the current use of inotropes is very frequent and often unnecessary. This chapter reviews mechanisms of action of current and future inotropes (including catecholamines, phosphodiesterase-III inhibitors, calcium sensitizers, cardiac myosin activators, and istaroxime) and discusses their clinical use in acute heart failure.
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Schwarte, Lothar A., Stephan A. Loer, J. K. Götz Wietasch, and Thomas W. L. Scheeren. Cardiovascular drugs in anaesthetic practice. Edited by Michel M. R. F. Struys. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0019.

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Anaesthetists should be familiar with currently available cardiovascular drugs used to maintain cardiovascular stability and achieve haemodynamic goals in surgical patients. The first part of this chapter summarizes antihypertensive agents, and the second part discusses positive inotropic drugs and vasopressors, which can be used perioperatively. Selection of vasoactive agents should be guided by the therapeutic goal (e.g. decreasing or increasing blood pressure or blood flow) and the underlying pathophysiology. Choice of catecholamines in a given situation should be based on the desired effects, that is, goals that can be monitored. Generally speaking, it is easier to affect blood pressure than cardiac output, and how to optimize regional and microcirculatory blood flow remains uncertain. Regardless of the chosen intervention, its haemodynamic effects should be closely monitored and always evaluated against the clinical effects. Recent developments include the definition of haemodynamic goals (goal-directed therapy) and clinical end-points, which seem to decrease morbidity and mortality, regardless of the goals defined and interventions used. With regard to mortality, use of inotropic agents has been associated with adverse outcomes, whereas the use of vasodilators has not. Inotropes in combination with vasodilators have the highest mortality.
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Erdmann, E., R. Jacob, and W. Schaper. Cardiac Glycoside Receptors and Positive Inotropy: Evidence for More Than One Receptor? Symposium, Munich, October 26-29 1983. Steinkopff, Dietrich, 2013.

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Book chapters on the topic "Positive inotropic effect"

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Baan, Jan, and Enno T. van der Velde. "Ventricular Pressure-Volume Relations Demonstrate Positive Inotropic Effect of Increased Arterial Impedance." In Cardiac Mechanics and Function in the Normal and Diseased Heart. Springer Japan, 1989. http://dx.doi.org/10.1007/978-4-431-67957-8_18.

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Raasmaja, Atso, Antti Talo, Heimo Haikala, Erkki Nissinen, Inge-Britt Lindén, and Pentti Pohto. "Biochemical Properties of OR-1259 - A Positive Inotropic and Vasodilatory Compound with an Antiarrhythmic Effect." In Excitation-Contraction Coupling in Skeletal, Cardiac, and Smooth Muscle. Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3362-7_63.

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Scholz, Hasso. "Introduction: Mechanisms of positive inotropic effects." In Inotropic Stimulation and Myocardial Energetics. Steinkopff, 1989. http://dx.doi.org/10.1007/978-3-662-07908-9_1.

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Schmitz, Wilhelm, C. Kohl, J. Neumann, H. Scholz, and J. Scholz. "On the mechanism of positive inotropic effects of alpha-adrenoceptor agonists." In Inotropic Stimulation and Myocardial Energetics. Steinkopff, 1989. http://dx.doi.org/10.1007/978-3-662-07908-9_4.

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Norota, Ikuo, and Masao Endoh. "Pharmacological characteristics of endothelin receptors in the rabbit ventricular myocardium: The nonselective endothelin receptor antagonist PD 145065 antagonizes the positive inotropic effect of endothelin-3 but not of endothelin-1." In Biochemical Mechanisms in Heart Function. Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1279-6_9.

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Erlemeier, H. H., and W. Bleifeld. "Effects of Different Positive Inotropic Drugs in Congestive Heart Failure." In Heart Failure Mechanisms and Management. Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-58231-8_21.

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Sasayama, Shigetake, Akira Matsumori, Sigeo Matsui, Tetsuo Shioi, and Takehiko Yamada. "Immunomodulating Effects as New Aspects of a Positive Inotropic Agent." In Molecular and Cellular Mechanisms of Cardiovascular Regulation. Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-65952-5_32.

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Brown, Lindsay, B. Lorenz, and E. Erdmann. "Additive and non-additive positive inotropic effects in human and guinea-pig myocardium." In Cardiac Glycosides 1785–1985. Steinkopff, 1986. http://dx.doi.org/10.1007/978-3-662-11292-2_26.

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Khatter, Jagdish C., Moses Agbanyo, Deepak Bose, and Robert J. Hoeschen. "An endogenous positive inotropic factor (EPIF) from porcine heart: Its effects on sarcoplasmic reticular (SR) Ca2+ metabolism." In The Cellular Basis of Cardiovascular Function in Health and Disease. Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5765-4_21.

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Arrigo, Mattia, and Alexandre Mebazaa. "Positive inotropes." In ESC CardioMed. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0035_update_001.

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Inotropic agents are substances used to improve cardiac output and end-organ perfusion in severe forms of acute heart failure. However, inappropriate use of inotropic agents may be associated with severe adverse effects and death. Despite clear indications to restrict their use to acute heart failure patients presenting with signs of end-organ hypoperfusion, the current use of inotropes is very frequent and often unnecessary. This chapter reviews mechanisms of action of current and future inotropes (including catecholamines, phosphodiesterase-III inhibitors, calcium sensitizers, cardiac myosin activators, and istaroxime) and discusses their clinical use in acute heart failure.
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Conference papers on the topic "Positive inotropic effect"

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Neumann, Joachim, Britt Hofmann, Uwe Kirchhefer, and Ulrich Gergs. "Positive inotropic effects of dexmedetomidine in the human atrium." In ASPET 2024 Annual Meeting Abstract. American Society for Pharmacology and Experimental Therapeutics, 2024. http://dx.doi.org/10.1124/jpet.468.960520.

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Haarmann, W., and H. Weisenberger. "LACK OF CORRELATION BETWEEN INTRAPLATELET cAMP INCREASE AND SYSTEMIC CIRCULATORY EFFECTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644532.

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Compounds inhibiting platelet function by acting on platelet cAMP metabolism usually also have effects on the circulatory system, i.e. they decrease systemic blood pressure (bp) and are positive inotropic. For several compounds selected because of their distinct platelet inhibitory effects, the influence on these parameters in animals and on the cAMP metabolism in human platelets was determined.Inotropic effects and bp were measured via an indwelling catheter in anestetised cats after i.v. application of the test compounds. The inhibition of platelet PDEs was measured in freeze-thaw homogenates of human platelets using 3H-cAMP as substrate. Intraplatelet cAMP changes were measured by prelabelling the ATP pool with 3H-adenine and isolation of 3H-cAMP. Linear regression analysis of the drug concentrations causing a doubling of intraplatelet cAMP levis and the % difference in bp or the % difference in dp/dt, resp., by i.v. application of 0.3 mg/kg test compound yielded the following results:cAMP vs % diff. bp : r=0.02, N=18cAMP vs % diff. dp/dt: r = 0.02 , N = 15In contrast to a good correlation between intraplatelet cAMP levels and inhibition of platelet function tests, no obvious relationship was seen between cAMP and decrease in bp and positive initropic effects. It is not known whether the lack of correlation could be due to a different drug access to platelets and the bp regulatory system.A biochemical parameter, i.e. intraplatelet cAMP increase by inhibition of PDEs correlates reasonably well with the inhibition of platelet function tests. This parameter is not useful, however, to predict the effects on the heart and the circulatory system.
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