Journal articles: 'Langendorff-perfused rabbit heart'

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Gralinski, M. R., S. C. Black, L. F. Stancato, K. S. Kilgore, P. A. Campau, J. L. Park, M. J. Ozeck, W. B. Pratt, and B. R. Lucchesi. "Heat stress protects the perfused rabbit heart from complement-mediated injury." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 2 (August 1, 1996): H571—H578. http://dx.doi.org/10.1152/ajpheart.1996.271.2.h571.

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We determined if heat stress induction of heat shock protein (HSP) 70 modulates complement activation in an experimental model of xenograft rejection. Male New Zealand White rabbits were heat stressed (core body temperature to 42 degrees C for 15 min; n = 9). Control rabbits (n = 13) were not exposed to heat stress. Hearts were removed 18 h later and perfused by the Langendorff method. After equilibration, human plasma (source of human complement) was added to the perfusion medium. Hemodynamic variables recorded during perfusion with human plasma were improved in hearts from heat-stressed animals compared with control hearts. Assembly of the soluble membrane attack complex was reduced in the interstitial fluid effluent from the heat-stressed hearts. Electron microscopic evidence of ultrastructural changes was attenuated in the hearts from heat-stressed rabbits. Myocardial tissue from heat-stressed animals exhibited an increase in inducible HSP 70 that was virtually absent in the hearts of control rabbits. Previous whole body hyperthermia protects the rabbit heart against the detrimental effects of heterologous plasma, suggesting that heat-stress induction of HSP 70 limits the extent of complement activation by a discordant vascularized tissue (xenograft). Induction of heat stress proteins by the donor organ might be an important mechanism affecting the outcome of xenograft transplants.

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Kuzmin, V. S., Yu V. Egorov, and L. V. Rozenshtraukh. "Electrhopysiological Effect of the Polyamine Spermine in Normoxic and Ischemic Ventricular Myocardium." Kardiologiia 59, no. 3 (April 13, 2019): 43–51. http://dx.doi.org/10.18087/cardio.2019.3.10240.

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Cytoplasmic polyamines (PA) are involved in control of many cellular functions and are well known as regulators of so called inward-rectifier potassium ion channels. Nevertheless, functional significance of extracellular PA in the heart is poorly elucidated. Aim of this study was to study effects of endogenous PA spermine in the ventricular myocardium. Effects of the extracellular spermine were investigated in isolated multicellular preparations of rabbit and rat ventricular myocardium. Langendorff-perfused isolated rat and rabbit hearts were also used. Action potential (APs) duration and pattern of excitation in ventricular myocardium were estimated using standard microelectrode technique and optical mapping. Functional refractory periods were assessed in Langendorff perfused hearts with the help of programmedelectrical stimulation of the ventricle. In this study extracellular PA spermine (0.1–5 mM) induced shortening of the APs in multicellular preparations of rat ventricular myocardium registered using sharp microelectrode technique. However, spermine caused only weak effect in preparations of ventricular myocardium from rabbit heart: highest tested concentration of spermine (5 mM) induced 4.7 % APs shortening. Similarly, 0.1–1 mM of spermine was unable to alter substantially ventricular effective refractory periods in isolated perfused rabbit hearts. In two animal species tested (rat and rabbit) 0.1–1 mM of spermine failed to affect conduction velocity and activation pattern in ventricles of isolated Langendorff-perfused hearts under normoxia. However, in the rat no-flow model of ischemia-reperfusion extracellular spermine improved conduction of excitation in ventricles. Our results allow suggesting that extracellular spermine can prevent ischemia-induced proarrhythmic changes in ventricular myocardium probably due to reduction of calcium accumulation, but this effect is significant only when PA is applied in millimolar concentrations. Also, potential anti-ischemic effect of the PA may be species specific.

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Mischke, Karl, Markus Zarse, Christian Knackstedt, and Patrick Schauerte. "Rate Control in Atrial Fibrillation by Cooling: Effect of Temperature on Dromotropy in Perfused Rabbit Hearts." Cardiology Research and Practice 2011 (2011): 1–4. http://dx.doi.org/10.4061/2011/162984.

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Background. Cooling has emerged as a therapeutic option in critically ill patients (especially after cardiac resuscitation) and might also have a negative dromotropic effect in atrial fibrillation. We sought to determine the impact of cooling on electrophysiologic properties of Langendorff-perfused rabbit hearts.Methods and Results. In 20 isolated Langendorff-perfused rabbit hearts, the temperature of the tissue bath was changed between 17 and 42°C. With decreasing temperature, significant increases of the spontaneous sinus cycle length, decreases of the mean ventricular heart rate during atrial fibrillation, and relevant increases of atrial and ventricular refractory periods were observed (ANOVAP<.01).Conclusions. Cardiac hypothermia leads to a significant drop of mean ventricular heart rate during atrial fibrillation. Negative chronotropy and dromotropy induced by moderate cardiac hypothermia might be a feasible therapeutic approach in patients with hemodynamically relevant tachyarrhythmias in a CCU/ICU setting.

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Neuber, Johanna U., Andrei G. Pakhomov, and Christian W. Zemlin. "Electroporation safety factor of 300 nanosecond and 10 millisecond defibrillation in Langendorff-perfused rabbit hearts." PLOS ONE 16, no. 9 (September 24, 2021): e0257287. http://dx.doi.org/10.1371/journal.pone.0257287.

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Aims Recently, a new defibrillation modality using nanosecond pulses was shown to be effective at much lower energies than conventional 10 millisecond monophasic shocks in ex vivo experiments. Here we compare the safety factors of 300 nanosecond and 10 millisecond shocks to assess the safety of nanosecond defibrillation. Methods and results The safety factor, i.e. the ratio of median effective doses (ED50) for electroporative damage and defibrillation, was assessed for nanosecond and conventional (millisecond) defibrillation shocks in Langendorff-perfused New Zealand white rabbit hearts. In order to allow for multiple shock applications in a single heart, a pair of needle electrodes was used to apply shocks of varying voltage. Propidium iodide (PI) staining at the surface of the heart showed that nanosecond shocks had a slightly lower safety factor (6.50) than millisecond shocks (8.69), p = 0.02; while PI staining cross-sections in the electrode plane showed no significant difference (5.38 for 300 ns shocks and 6.29 for 10 ms shocks, p = 0.22). Conclusions In Langendorff-perfused rabbit hearts, nanosecond defibrillation has a similar safety factor as millisecond defibrillation, between 5 and 9, suggesting that nanosecond defibrillation can be performed safely.

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Morgan, Eric E., Zhichuan Li, Cory Stebal, Aude Belliard, Glen Tennyson, Bijan Salari, Keith D. Garlid, and Sandrine V. Pierre. "Preconditioning by Subinotropic Doses of Ouabain in the Langendorff perfused Rabbit Heart." Journal of Cardiovascular Pharmacology 55, no. 3 (March 2010): 234–39. http://dx.doi.org/10.1097/fjc.0b013e3181ce5e14.

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Salbaş, K., G. Akgün, G. Pamīr, and T. Gürel. "Interaction between Beta-Blockers and Contrast Media during Intracoronary Administration in Rabbit Heart." Acta Radiologica 35, no. 1 (January 1994): 70–76. http://dx.doi.org/10.1177/028418519403500115.

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The effects of ionic, meglumine sodium diatrizoate (Urografin 76) and nonionic, iohexol contrast media were examined in the absence and presence of propranolol, a beta-blocker having nonspecific membrane stabilizing action and atenolol, a beta-blocker lacking nonspecific membrane stabilizing action on Langendorff-perfused rabbit hearts. Contrast medium, 0.7 ml, was injected into the aortic root in the absence and presence of 10−7 and 10−5 M beta-blocker to observe the changes in resting tension, force of contraction, rate of contraction, heart rate and PR interval. Beta-blockers and contrast media interact in affecting myocardial contractility, heart rate and atrioventricular conduction. The interaction is milder when the beta-blocker lacks membrane stabilizing activity and the contrast medium is nonionic.

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Guillon, Jean Michel, Michel Roche, Veronique Ballet, and Michel Doubovetzky. "Electrocardiographic effects of moxifloxacin, quinidine and quinimax on a langendorff-perfused rabbit heart model." Journal of Pharmacological and Toxicological Methods 62, no. 2 (September 2010): e37. http://dx.doi.org/10.1016/j.vascn.2010.11.126.

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Laycock, Sarra, Neal Appleton, Anouska Godier, and Kirsty Macfarlane. "FREQUENCY-DEPENDENT EFFECTS OF PRO-ARRHYTHMIC COMPOUNDS IN THE LANGENDORFF-PERFUSED ISOLATED RABBIT HEART." Journal of Pharmacological and Toxicological Methods 56, no. 2 (September 2007): e52. http://dx.doi.org/10.1016/j.vascn.2007.02.104.

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Klair, Sarbjit S., James B. Louttit, and Peter A. Charlton. "Atrial natriuretic factor in the Langendorff perfused coronary vasculature of the rabbit isolated heart." Life Sciences 45, no. 25 (January 1989): 2477–83. http://dx.doi.org/10.1016/0024-3205(89)90014-3.

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Vosyliute, Ruta, Arvydas Matiukas, Irma Martišienė, Jonas Jurevičius, Antanas Navalinskas, Rimantas Treinys, Regina Mačianskienė, and Arkady M. Pertsov. "Illumination-Induced Changes in Action Potential during Optical Mapping in Langendorff-Perfused Rabbit Heart." Biophysical Journal 104, no. 2 (January 2013): 337a. http://dx.doi.org/10.1016/j.bpj.2012.11.1875.

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ZARSE, MARKUS, CHRISTOPH STELLBRINK, EVANGELIA ATHANATOU, JENS ROBERT, ULRICH SCHOTTEN, and PETER HANRATH. "Verapamil Prevents Stretch-Induced Shortening of Atrial Effective Refractory Period in Langendorff-Perfused Rabbit Heart." Journal of Cardiovascular Electrophysiology 12, no. 1 (January 2001): 85–92. http://dx.doi.org/10.1046/j.1540-8167.2001.00085.x.

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12

Shirakawa, Makoto, Hajime Imura, and Takashi Nitta. "Propofol Protects the Immature Rabbit Heart against Ischemia and Reperfusion Injury: Impact on Functional Recovery and Histopathological Changes." BioMed Research International 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/601250.

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The general anesthetic propofol protects the adult heart against ischemia and reperfusion injury; however, its efficacy has not been investigated in the immature heart. This work, for the first time, investigates the cardioprotective efficacy of propofol at clinically relevant concentrations in the immature heart. Langendorff perfused rabbit hearts (7–12 days old) were exposed to 30 minutes’ global normothermic ischemia followed by 40 minutes’ reperfusion. Left ventricular developed pressure (LVDP) and coronary flow were monitored throughout. Lactate release into coronary effluent was measured during reperfusion. Microscopic examinations of the myocardium were monitored at the end of reperfusion. Hearts were perfused with different propofol concentrations (1, 2, 4, and 10 μg/mL) or with cyclosporine A, prior to ischemic arrest and for 20 minutes during reperfusion. Propofol at 4 and 10 μg/mL caused a significant depression in LVDP prior to ischemia. Propofol at 2 μg/mL conferred significant and maximal protection with no protection at 10 μg/mL. This protection was associated with improved recovery in coronary flow, reduced lactate release, and preservation of cardiomyocyte ultrastructure. The efficacy of propofol at 2 μg/mL was similar to the effect of cyclosporine A. In conclusion, propofol at a clinically relevant concentration is cardioprotective in the immature heart.

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Gibbs, C. L., and G. Kotsanas. "Factors regulating basal metabolism of the isolated perfused rabbit heart." American Journal of Physiology-Heart and Circulatory Physiology 250, no. 6 (June 1, 1986): H998—H1007. http://dx.doi.org/10.1152/ajpheart.1986.250.6.h998.

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Basal metabolism has been measured in isolated whole hearts from rabbits and compared with myothermic and polarographic measurements on isolated papillary muscles. Hearts were perfused at constant pressure (Langendorff method) using a modified Krebs-Henseleit solution (KH) with glucose as substrate. Higher levels of basal O2 consumption (MVO2) and coronary flow (CF) were observed when arrest was induced by calcium depletion (low Ca; 0.1 mM CaCl2, 10.0 mM KCl) rather than by potassium excess (high K; 30.0 mM KCl). The metabolic rate of high K arrested hearts was close to earlier myothermic estimates (J. Mol. Cell. Cardiol. 16: 953-962, 1984); polarographic values, however, were about twofold higher, and somewhat higher than the value obtained in low Ca arrested hearts. The addition of erythrocytes, albumin, or dextran significantly reduced CF but did not substantially alter basal MVO2. Basal metabolic rate was substrate- and O2 tension-dependent, and under all experimental conditions there was linear relationship between MVO2 and CF. Extrapolations to zero flow showed that the basal MVO2 values so obtained were similar in low Ca or high K and were not altered by the presence of erythrocytes. Our results show that there are several factors regulating basal metabolism.

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Black, Shawn C., S. Oluwole Fagbemi, Liguo Chi, Gregory S. Friedrichs, and Benedict R. Lucchesi. "Phorbol Ester-Induced Ventricular Fibrillation in the Langendorff-Perfused Rabbit Heart: Antagonism by Staurosporine and Glibenclamide." Journal of Molecular and Cellular Cardiology 25, no. 12 (December 1993): 1427–38. http://dx.doi.org/10.1006/jmcc.1993.1159.

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15

Tanhehco, Elaine J., Koji Yasojima, Patrick L. McGeer, Ruth A. Washington, and Benedict R. Lucchesi. "Free radicals upregulate complement expression in rabbit isolated heart." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 1 (July 1, 2000): H195—H201. http://dx.doi.org/10.1152/ajpheart.2000.279.1.h195.

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Both free radicals and complement activation can injure tissue. Our study determined whether free radicals alter complement production by the myocardium. Isolated hearts from New Zealand White rabbits were perfused on a Langendorff apparatus and exposed to xanthine (X; 100 μM) plus xanthine oxidase (XO; 8 mU/ml) (X/XO). The free radical-generating system significantly ( P < 0.05) increased C1q and also increased C1r, C3, C8, and C9 transcription compared with controls. Immunohistological examination revealed augmented membrane attack complex deposition on X/XO-treated tissue. X/XO-treated hearts also exhibited significant ( P < 0.05) increases in coronary perfusion pressure and left ventricular end-diastolic pressure and a decrease in left-ventricular developed pressure. N-(2-mercaptopropionyl)-glycine (3 mM), in conjunction with the superoxide dismutase mimetic SC-52608 (100 μM), significantly ( P < 0.05) reduced the upregulation of C1q, C1r, C3, C8, and C9 mRNA expression elicited by X/XO. The antioxidants also ameliorated the deterioration in function caused by X/XO. Local complement activation may represent a mechanism by which free radicals mediate tissue injury.

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Gustafson, Lori A., and Johannes H. G. M. Van Beek. "Measurement of the activation time of oxidative phosphorylation in isolated mouse hearts." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 6 (December 1, 2000): H3118—H3123. http://dx.doi.org/10.1152/ajpheart.2000.279.6.h3118.

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The purpose of this study was to develop a technique for determination of the dynamic regulation of oxidative myocardial metabolism in the mouse. The response time of myocardial oxygen consumption (MV˙o 2) to a step in heart rate was determined in Langendorff-perfused mouse hearts. We examined the effect of glucose-only perfusate and glucose combined with 1, 3, or 6 mM pyruvate. Left ventricular systolic pressure (LVSP) decreased, yet the rate-pressure product (RPP) and MV˙o 2 increased with upward steps in heart rate. Pyruvate increased LVSP, RPP, and MV˙o 2 at the lower concentrations; however, when 6 mM pyruvate was added, LVSP and RPP became depressed while MV˙o 2 remained elevated. The mean response time of oxygen consumption to a step in heart rate from 270 to 350 beats/min was 9.8 s ( n = 7) in the glucose-only perfused hearts. Perfusion with glucose plus 6 mM pyruvate decreased the response time to 5.3 s. These results are similar to those found in the rabbit heart and lay the groundwork for further examination of the dynamic regulation of oxidative myocardial metabolism in genetically altered mice. We concluded that the activation time of oxidative phosphorylation in the mouse is similar to that in larger species, despite the high mitochondrial content and natural heart rate of the mouse.

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Vejdani-Jahromi, Maryam, Mathew Nagle, Yang Jiang, Gregg E. Trahey, and Patrick D. Wolf. "A Comparison of Acoustic Radiation Force-Derived Indices of Cardiac Function in the Langendorff Perfused Rabbit Heart." IEEE Transactions on Ultrasonics, Ferroelectrics, and Frequency Control 63, no. 9 (September 2016): 1288–95. http://dx.doi.org/10.1109/tuffc.2016.2543026.

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Friedrichs, Gregory S., Liguo Chi, Shawn C. Black, Peter J. Manley, and Benedict R. Lucchesi. "Antiarrhythmic Agent, MS-551, Protects Against Pinacidil + Hypoxia-Induced Ventricular Fibrillation in Langendorff-Perfused Rabbit Isolated Heart." Journal of Cardiovascular Pharmacology 23, no. 1 (January 1994): 120–26. http://dx.doi.org/10.1097/00005344-199401000-00017.

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Martišienė, Irma, Jonas Jurevičius, Rūta Vosyliūtė, Antanas Navalinskas, Rimantas Treinys, Regina Mačianskienė, Rimantas Benetis, Arvydas Matiukas, and Arkady M. Pertsov. "Evolution of Action Potential Alternans in Rabbit Heart during Acute Regional Ischemia." BioMed Research International 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/951704.

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This study investigates the development of the spatiotemporal pattern of action potential alternans during acute regional ischemia. Experiments were carried out in isolated Langendorff-perfused rabbit heart using a combination of optical mapping and microelectrode recordings. The alternans pattern significantly changed over time and had a biphasic character reaching maximum at 6–9 min after occlusion. Phase I (3–11 minutes of ischemia) is characterized by rapid increase in the alternans magnitude and expansion of the alternans territory. Phase I is followed by gradual decline of alternans (Phase II) in both magnitude and territory. During both phases we observed significant beat-to-beat variations of the optical action potential amplitude (OAPA) alternans. Simultaneous microelectrode recordings from subepicardial and subendocardial layers showed that OAPA alternans coincided with intramural 2 : 1 conduction blocks. Our findings are consistent with the modeling studies predicting that during acute regional ischemia alternans can be driven by 2 : 1 conduction blocks in the ischemic region.

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Thakral, Anshul, Louis H. Stein, Mahesh Shenai, Boris I. Gramatikov, and Nitish V. Thakor. "Effects of anodal vs. cathodal pacing on the mechanical performance of the isolated rabbit heart." Journal of Applied Physiology 89, no. 3 (September 1, 2000): 1159–64. http://dx.doi.org/10.1152/jappl.2000.89.3.1159.

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Previous studies have suggested that anodal pacing enhances electrical conduction in the heart near the pacing site. It was hypothesized that enhanced conduction by anodal pacing would also enhance ventricular pressure in the heart. Left ventricular pressure measurements were made in isolated, Langendorff-perfused rabbit hearts by means of a Millar pressure transducer with the use of a balloon catheter fixed in the left ventricle. The pressure wave was analyzed for maximum pressure (Pmax) generated in the left ventricle and the work done by the left ventricle (Parea). Eight hearts were paced with monophasic square-wave pulses of varying amplitudes (2, 4, 6, and 8 V) with 100 pulses of each waveform delivered to the epicardium. Anodal stimulation pulses showed statistically significant improvement in mechanical response at 2, 4, and 8 V. Relative to unipolar cathodal pacing, unipolar anodal pacing improved Pmax by 4.4 ± 2.3 (SD), 5.3 ± 3.1, 3.5 ± 4.9, and 4.8 ± 1.9% at 2, 4, 6, and 8 V, respectively. Unipolar anodal stimulation also improved Parea by 9.0 ± 3.0, 12.0 ± 6.0, 10.1 ± 7.7, and 11.9 ± 6.0% at 2, 4, 6, and 8 V, respectively. Improvements in Pmax and Parea indicate that an anodally paced heart has a stronger mechanical response than does a cathodally paced heart. Anodal pacing might be useful as a novel therapeutic technology to treat mechanically impaired or failed hearts.

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Schwartz, D. D., J. L. Williams, and K. U. Malik. "Contribution of calcium to isoproterenol-stimulated lipolysis in the isolated perfused rabbit heart." American Journal of Physiology-Endocrinology and Metabolism 265, no. 3 (September 1, 1993): E439—E445. http://dx.doi.org/10.1152/ajpendo.1993.265.3.e439.

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The present study was performed to investigate the contribution of adenosine 3',5'-cyclic monophosphate (cAMP) and calcium to isoproterenol-stimulated lipolysis in the isolated rabbit heart perfused with Krebs-Henseleit buffer according to the method of Langendorff. Isoproterenol (0.05-1.5 nmol) increased glycerol output, left ventricular dP/dtmax, and heart rate but decreased coronary perfusion pressure. The phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (50 microM) failed to alter the basal or isoproterenol-induced increase in glycerol output, whereas cilostamide (5 microM) enhanced basal and inhibited isoproterenol-stimulated glycerol output. Inhibition of adenylyl cyclase with (phenylisopropyl)adenosine reduced isoproterenol-stimulated mechanical parameters but had no effect on basal or isoproterenol-stimulated glycerol output, whereas the cAMP analogue 8-(4-chlorophenylthio)-cAMP did not increase glycerol output but produced changes in mechanical parameters similar to isoproterenol. Decreasing perfusion fluid calcium concentration from 1.2 to 0.5 mM or infusion of the calcium channel antagonist diltiazem (23 microM) abolished the increase in glycerol output in response to isoproterenol. Activation of adenylyl cyclase with forskolin increased glycerol output, but the increase was abolished by reducing perfusion fluid calcium concentration or by diltiazem. These data suggest that, in the rabbit heart, isoproterenol-stimulated lipolysis appears to be mediated predominantly by calcium as a secondary metabolic response provided by the increase in mechanical activity.

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LUO, HAIJIAN, JUNQIANG SI, FENGJIE ZHANG, ZHENYU YANG, and RUXING WANG. "Cardiac inotropic rebound effect after washout of acetylcholine is associated with electrophysiological heterogeneity in Langendorff-perfused rabbit heart." Experimental and Therapeutic Medicine 7, no. 3 (January 15, 2014): 755–57. http://dx.doi.org/10.3892/etm.2014.1486.

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Quinn, T. Alexander, and Peter Kohl. "Comparing maximum rate and sustainability of pacing by mechanical vs. electrical stimulation in the Langendorff-perfused rabbit heart." EP Europace 18, suppl_4 (December 1, 2016): iv85—iv93. http://dx.doi.org/10.1093/europace/euw354.

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Focaccio, A., G. Ambrosio, I. Enea, R. Russo, P. Balestrieri, M. Chiariello, and M. Volpe. "Influence of O2 deprivation, reduced flow, and temperature on release of ANP from rabbit hearts." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 6 (June 1, 1995): H2352—H2357. http://dx.doi.org/10.1152/ajpheart.1995.268.6.h2352.

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The separate effects of hypoxia and ischemia on atrial natriuretic peptide (ANP) release were evaluated in Langendorff-perfused rabbit hearts. Heart rate, coronary flow, and atrial and ventricular volumes were kept constant. Hypoxia was induced for 20 min at room temperature in seven hearts and at 37 degrees C in a second group of seven hearts. A third group of eight hearts was subjected to global ischemia for 20 min by reducing coronary flow to 1 ml/min at room temperature. All hearts were reoxygenated/reperfused at 37 degrees C for 30 min. Hypoxia at 37 degrees C induced a significant increase in ANP release. In contrast, both room temperature hypoxia and ischemia were characterized by a significant decrease in ANP release, despite hemodynamic alterations similar to those recorded during hypoxia at 37 degrees C. Both reoxygenation and reperfusion induced a prompt reversal of the changes of ANP release observed during the period of oxygen deprivation. These data demonstrate that decreased oxygen availability and reduced coronary flow are not the primary factors affecting release of ANP during ischemia and that alterations of myocardial temperature may play a major role in this phenomenon.

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Giles, Abigail V., Junhui Sun, Armel N. Femnou, Sarah Kuzmiak-Glancy, Joni L. Taylor, Raul Covian, Elizabeth Murphy, and Robert S. Balaban. "Paradoxical arteriole constriction compromises cytosolic and mitochondrial oxygen delivery in the isolated saline-perfused heart." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 6 (December 1, 2018): H1791—H1804. http://dx.doi.org/10.1152/ajpheart.00493.2018.

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The isolated saline-perfused heart is used extensively to study cardiac physiology. Previous isolated heart studies have demonstrated lower tissue oxygenation compared with in vivo hearts based on myoglobin oxygenation and the mitochondrial redox state. These data, consistent with small anoxic regions, suggest that the homeostatic balance between work and oxygen delivery is impaired. We hypothesized that these anoxic regions are caused by inadequate local perfusion due to a paradoxical arteriole constriction generated by a disrupted vasoregulatory network. We tested this hypothesis by applying two exogenous vasodilatory agents, adenosine and cromakalim, to relax vascular tone in an isolated, saline-perfused, working rabbit heart. Oxygenation was monitored using differential optical transmission spectroscopy and full spectral fitting. Increases in coronary flow over control with adenosine (27 ± 4 ml/min) or cromakalim (44 ± 4 ml/min) were associated with proportional spectral changes indicative of myoglobin oxygenation and cytochrome oxidase (COX) oxidation, consistent with a decrease in tissue anoxia. Quantitatively, adenosine decreased deoxymyoglobin optical density (OD) across the wall by 0.053 ± 0.008 OD, whereas the reduced form of COX was decreased by 0.039 ± 0.005 OD. Cromakalim was more potent, decreasing deoxymyoglobin and reducing the level of COX by 0.070 ± 0.019 OD and 0.062 ± 0.019 OD, respectively. These effects were not species specific, as Langendorff-perfused mouse hearts treated with adenosine demonstrated similar changes. These data are consistent with paradoxical arteriole constriction as a major source of regional anoxia during saline heart perfusion. We suggest that the vasoregulatory network is disrupted by the washout of interstitial vasoactive metabolites in vitro. NEW & NOTEWORTHY Regional tissue anoxia is a common finding in the ubiquitous saline-perfused heart but is not found in vivo. Noninvasive optical techniques confirmed the presence of regional anoxia under control conditions and demonstrated that anoxia is diminished using exogenous vasodilators. These data are consistent with active arteriole constriction, occurring despite regional anoxia, generated by a disrupted vasoregulatory network. Washout of interstitial vasoactive metabolites may contribute to the disruption of normal vasoregulatory processes in vitro.

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WILLIAMS, Scott D., and Roberta A. GOTTLIEB. "Inhibition of mitochondrial calcium-independent phospholipase A2 (iPLA2) attenuates mitochondrial phospholipid loss and is cardioprotective." Biochemical Journal 362, no. 1 (February 8, 2002): 23–32. http://dx.doi.org/10.1042/bj3620023.

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Calcium-independent phospholipase A2 (iPLA2) is the predominant phospholipase A2 present in myocardium, and its pathophysiological role in acute myocardial infarction has been suggested by the rapid increase in membrane-associated iPLA2 activity during myocardial ischaemia and reperfusion (I/R). We therefore examined iPLA2 in mitochondrial fractions prepared from Langendorff-perfused adult rabbit hearts. Our studies indicate that iPLA2β is present in rabbit heart mitochondrial inner membranes with no apparent translocation during ischaemia, I/R or preconditioning. Mitochondrion-associated iPLA2 was catalytically competent and exhibited 2-, 3- and 2.5-fold increases in measured iPLA2 activity following ischaemia, I/R and preconditioning, respectively, when compared with the activity of iPLA2 measured in mitochondria from control hearts. Mitochondrial phospholipids are essential for maintaining the ordered structure and function of the organelle. I/R resulted in a rapid overall decrease in phosphatidylcholine and phosphatidylethanolamine glycerophospholipid species, as determined by electrospray ionization MS, that was partially alleviated by pretreatment of hearts with the iPLA2-specific inhibitor, bromoenol lactone (BEL). Pretreatment of I/R hearts with 10μM BEL significantly reduced the infarct size almost to that of continuously perfused hearts and was cardioprotective only when administered prior to ischaemia. Cardioprotection by BEL was reversed by the simultaneous perfusion of 100μM 5-hydroxydecanoate, implicating the mitochondrial KATP channel in BEL-mediated protection from I/R. Preconditioning also significantly reduced the infarct size in response to I/R but protection was lost by concurrent perfusion of 10μM arachidonic acid. Taken together, these data strongly implicate mitochondria-associated iPLA2 in the signal transduction of myocardial I/R injury.

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Efimov, Igor R., Felipe Aguel, Yuanna Cheng, Brian Wollenzier, and Natalia Trayanova. "Virtual electrode polarization in the far field: implications for external defibrillation." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 3 (September 1, 2000): H1055—H1070. http://dx.doi.org/10.1152/ajpheart.2000.279.3.h1055.

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We recently suggested that failure of implantable defibrillation therapy may be explained by the virtual electrode-induced phase singularity mechanism. The goal of this study was to identify possible mechanisms of vulnerability and defibrillation by externally applied shocks in vitro. We used bidomain simulations of realistic rabbit heart fibrous geometry to predict the passive polarization throughout the heart induced by external shocks. We also used optical mapping to assess anterior epicardium electrical activity during shocks in Langendorff-perfused rabbit hearts ( n= 7). Monophasic shocks of either polarity (10–260 V, 8 ms, 150 μF) were applied during the T wave from a pair of mesh electrodes. Postshock epicardial virtual electrode polarization was observed after all 162 applied shocks, with positive polarization facing the cathode and negative polarization facing the anode, as predicted by the bidomain simulations. During arrhythmogenesis, a new wave front was induced at the boundary between the two regions near the apex but not at the base. It spread across the negatively polarized area toward the base of the heart and reentered on the other side while simultaneously spreading into the depth of the wall. Thus a scroll wave with a ribbon-shaped filament was formed during external shock-induced arrhythmia. Fluorescent imaging and passive bidomain simulations demonstrated that virtual electrode polarization-induced scroll waves underlie mechanisms of shock-induced vulnerability and failure of external defibrillation.

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Brack, Kieran E., John H. Coote, and G. André Ng. "The effect of direct autonomic nerve stimulation on left ventricular force in the isolated innervated Langendorff perfused rabbit heart." Autonomic Neuroscience 124, no. 1-2 (January 2006): 69–80. http://dx.doi.org/10.1016/j.autneu.2005.11.005.

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Kettlewell, S., N. L. Walker, S. M. Cobbe, F. L. Burton, and G. L. Smith. "The electrophysiological and mechanical effects of 2,3-butane-dione monoxime and cytochalasin-D in the Langendorff perfused rabbit heart." Experimental Physiology 89, no. 2 (February 19, 2004): 163–72. http://dx.doi.org/10.1113/expphysiol.2003.026732.

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Ravelli, Flavia, and Maurits Allessie. "Effects of Atrial Dilatation on Refractory Period and Vulnerability to Atrial Fibrillation in the Isolated Langendorff-Perfused Rabbit Heart." Circulation 96, no. 5 (September 2, 1997): 1686–95. http://dx.doi.org/10.1161/01.cir.96.5.1686.

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Restivo, Mark, Dmitry O. Kozhevnikov, and Mohamed Boutjdir. "Optical mapping of activation patterns in an animal model of congenital heart block." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 4 (April 1, 2001): H1889—H1895. http://dx.doi.org/10.1152/ajpheart.2001.280.4.h1889.

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Congenital heart block (CHB) is associated with high mortality and affects children of mothers with autoantibodies (IgG) to ribonucleoproteins SSB/La and SSA/Ro. IgG from mothers of children with CHB (positive IgG) was used to assess activation patterns in both the right atrium (RA) and right ventricle (RV) of Langendorff-perfused young rabbit hearts. Optical action potentials (AP) were obtained by using a 124-site photodiode array with 4-[-[2-(di- n-butylamino)-6-naphthyl]vinyl]pyridinium. Optical APs were recorded to simultaneously image activation patterns from the RA and RV. Perfusion of positive IgG (800–1,200 μg/ml) resulted in sinus bradycardia and varying degrees of heart block. Activation maps revealed marked conduction delay at the sinoatrial junction but only minor changes in overall atrial and ventricular activation patterns. No conduction disturbances were seen in the presence of IgG from mothers with healthy children. In conclusion, besides atrioventricular (AV) block, positive IgG induces sinus bradycardia. These results establish that the sequelae of CHB are associated with impaired intrasinus and/or sinoatrial conduction. The findings raise the possibility that sinus bradycardia in the developing heart may indicate the potential for AV conduction disturbances.

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Eijgelshoven, M. H., J. B. Hak, J. H. Van Beek, and N. Westerhof. "Adaptation speed of cardiac mitochondrial oxygen consumption decreases with higher heart rate." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 6 (December 1, 1993): H1893—H1898. http://dx.doi.org/10.1152/ajpheart.1993.265.6.h1893.

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The purpose of the present study was to determine whether the mean response time of cardiac mitochondrial oxygen consumption after a step in metabolic demand is constant in heart muscle, as has already been found for skeletal muscle. The mean response time reflects the average delay between the change in ATP hydrolysis due to a heart rate step and mitochondrial ATP production. Isolated rabbit hearts with a water-filled balloon in the left ventricle were perfused according to Langendorff with a constant flow of Tyrode solution at 28 degrees C. The mean response time increased significantly from 7.6 s for a step in heart rate from 60 to 70 min-1 to 12.1 s for a step from 60 to 120 min-1. The mean response times for heart rate steps downward from 120 min-1 were all approximately 12 s, but for the step from 120 to 140 min-1 the response time was 16.8 s. These results demonstrate that the mean response time of cardiac mitochondrial oxygen consumption in most cases increases with heart rate. These findings are in contrast to those obtained in skeletal muscle, where the response time at which ATP synthesis adapts to a change in work load is constant.

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Gustafson, Lori A., and Keith Kroll. "Downregulation of 5′-nucleotidase in rabbit heart during coronary underperfusion." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 2 (February 1, 1998): H529—H538. http://dx.doi.org/10.1152/ajpheart.1998.274.2.h529.

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The hydrolysis of AMP to adenosine during acute coronary underperfusion is temporarily beneficial to myocardial survival yet may cause tissue injury during sustained underperfusion because of depletion of adenine nucleotides. We hypothesized that the enzyme mediating AMP hydrolysis, 5′-nucleotidase (5′-NT), is downregulated during sustained coronary underperfusion to prevent excessive loss of nucleotides. Langendorff-perfused rabbit hearts were subjected to two successive, identical 45-min periods of underperfusion (4–5% of baseline flow) separated by 20 min of reperfusion. Although coronary venous lactate efflux was comparable in the two periods, total coronary purine efflux during the second period of underperfusion was attenuated by 75%. Phosphorus nuclear magnetic resonance data showed that ATP fell 46% in the first period but fell only another 10% in the second period. Phosphocreatine levels fell comparably (75–78%) during both periods of underperfusion. Analysis using a mathematical model describing the kinetics of myocardial energetics revealed that the combined data set was best described by a lower activity of 5′-NT (52% decrease in maximal reaction velocity) during the second period of underperfusion. Additional time course experiments showed that the decrease in 5′-NT activity was slow in onset, requiring ∼20 min of underperfusion. The decrease in 5′-NT activity during sustained underperfusion may benefit tissue survival by limiting the depletion of myocardial adenine nucleotides. In conclusion, at the onset of coronary underperfusion, there is a high activity of 5′-NT, but later during sustained underperfusion, 5′-NT is downregulated, resulting in decreased AMP hydrolysis to adenosine.

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Garvey, J. L., E. G. Kranias, and R. J. Solaro. "Phosphorylation of C-protein, troponin I and phospholamban in isolated rabbit hearts." Biochemical Journal 249, no. 3 (February 1, 1988): 709–14. http://dx.doi.org/10.1042/bj2490709.

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Phosphorylation of myofibrillar and sacroplasmic-reticulum (SR) proteins was studied in Langendorff-perfused rabbit hearts subjected to various inotropic interventions. Stimulation of hearts with isoprenaline resulted in the phosphorylation of both troponin I (TnI) and C-protein in myofibrils and phospholamban in SR. Phosphorylation of phospholamban could be reversed by a 15 min perfusion with drug-free buffer, after a 1 minute pulse perfusion with isoprenaline, at which time the mechanical effects of isoprenaline stimulation had also been reversed. However, both TnI and C-protein remained phosphorylated at this time. Moreover, the inhibition of Ca2+ activation of the Mg2+-dependent ATPase (Mg-ATPase) activity associated with myofibrillar phosphorylation persisted in myofibrils prepared from hearts frozen after 15 min of washout of isoprenaline. To assess the contribution of C-protein phosphorylation in the decrease of Ca2+ activation of the myofibrillar Mg-ATPase activity, we reconstituted a regulated actomyosin system in which only C-protein was phosphorylated. In this system, C-protein phosphorylation did not contribute to the decrease in Ca2+ activation of Mg-ATPase activity, indicating that TnI phosphorylation is responsible for the diminished sensitivity of the myofibrils to Ca2+. These observations support the hypothesis that phospholamban phosphorylation plays a more dominant role than TnI or C-protein phosphorylation in the mechanical response of the mammalian heart to beta-adrenergic stimulation.

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Shimizu, Mikiko, Michael Tropak, Roberto J. Diaz, Fumiaki Suto, Harinee Surendra, Elena Kuzmin, Jing Li, et al. "Transient limb ischaemia remotely preconditions through a humoral mechanism acting directly on the myocardium: evidence suggesting cross-species protection." Clinical Science 117, no. 5 (August 3, 2009): 191–200. http://dx.doi.org/10.1042/cs20080523.

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rIPC (remote ischaemic preconditioning) is a phenomenon whereby short periods of ischaemia and reperfusion of a tissue or organ (e.g. mesentery, kidney) can protect a distant tissue or organ (e.g. heart) against subsequent, potentially lethal, ischaemia. We, and others, have shown that transient limb ischaemia can provide potent myocardial protection experimentally and clinically during cardiac surgery. Nonetheless, our understanding of the signal transduction from remote stimulus to local effect remains incomplete. The aim of the present study was to define the humoral nature of rIPC effector(s) from limb ischaemia and to study their local effects in isolated heart and cardiomyocyte models. Using a Langendorff preparation, we show that infarct size after coronary artery ligation and reperfusion was substantially reduced by rIPC in vivo, this stimulus up-regulating the MAPKs (mitogen-activating protein kinases) p42/p44, and inducing PKCε (protein kinase Cε) subcellular redistribution. Pre-treatment with the plasma and dialysate of plasma (obtained using 15 kDa cut-off dialysis membrane) from donor rabbits subjected to rIPC similarly protected against infarction. The effectiveness of the rIPC dialysate was abrogated by passage through a C18 hydrophobic column, but eluate from this column provided the same level of protection. The dialysate of rIPC plasma from rabbits and humans was also tested in an isolated fresh cardiomyocyte model of simulated ischaemia and reperfusion. Necrosis in cardiomyocytes treated with rIPC dialysate was substantially reduced compared with control, and was similar to cells pre-treated by ‘classical’ preconditioning. This effect, by rabbit rIPC dialysate, was blocked by pre-treatment with the opiate receptor blocker naloxone. In conclusion, in vivo transient limb ischaemia releases a low-molecular-mass (<15 kDa) hydrophobic circulating factor(s) which induce(s) a potent protection against myocardial ischaemia/reperfusion injury in Langendorff-perfused hearts and isolated cardiomyocytes in the same species. This cardioprotection is transferable across species, independent of local neurogenic activity, and requires opioid receptor activation.

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CHOU, CHUNG-CHUAN, MING-SHIEN WEN, HUI-LING LEE, PO-CHENG CHANG, HUNG-TA WO, SAN-JOU YEH, and DELON WU. "Dantrolene Suppresses Ventricular Ectopy and Arrhythmogenicity with Acute Myocardial Infarction in a Langendorff-Perfused Pacing-Induced Heart Failure Rabbit Model." Journal of Cardiovascular Electrophysiology 25, no. 4 (December 9, 2013): 431–39. http://dx.doi.org/10.1111/jce.12320.

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37

Chou, Chung-Chuan, Hui-Ling Lee, Po-Cheng Chang, Hung-Ta Wo, Ming-Shien Wen, and San-Jou Yeh. "Effects of Dantrolene on Arrhythmogenicity in Isolated Regional Ischemia-Reperfusion Rabbit Hearts with or without Pacing-Induced Heart Failure." BioMed Research International 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/532820.

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Dantrolene was reported to suppress ventricular fibrillation (VF) in failing hearts with acute myocardial infarction, but its antiarrhythmic efficacy in regional ischemia-reperfusion (IR) hearts remains debatable. Heart failure (HF) was induced by right ventricular pacing. The IR rabbit model was created by coronary artery ligation for 30 min, followed by reperfusion for 15 min in vivo in both HF and non-HF groups (n= 9 in each group). Simultaneous voltage and intracellular Ca2+(Cai) optical mapping was then performed in isolated Langendorff-perfused hearts. Electrophysiological studies were conducted and VF inducibility was evaluated by dynamic pacing. Dantrolene (10 μM) was administered after baseline studies. The HF group had a higher VF inducibility than the control group. Dantrolene had both antiarrhythmic (prolonged action potential duration (APD) and effective refractory period) and proarrhythmic effects (slowed conduction velocity, steepened APD restitution slope, and enhanced arrhythmogenic alternans induction) but had no significant effects on ventricular premature beat (VPB) suppression and VF inducibility in both groups. A higher VF conversion rate in the non-HF group was likely due to greater APD prolonging effects in smaller hearts compared to the HF group. The lack of significant effects on VPB suppression by dantrolene suggests that triggered activity might not be the dominant mechanism responsible for VPB induction in the IR model.

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Ellermann, Christian, Anja Kohnke, Dirk G. Dechering, Simon Kochhäuser, Florian Reinke, Michael Fehr, Lars Eckardt, and Gerrit Frommeyer. "Ranolazine Prevents Levosimendan-Induced Atrial Fibrillation." Pharmacology 102, no. 3-4 (2018): 138–41. http://dx.doi.org/10.1159/000490572.

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Objectives: Levosimendan is a calcium sensitizer that is used as positive inotropic drug in acute decompensated heart failure. An increased incidence of atrial fibrillation after levosimendan-treatment was observed in clinical and experimental studies. Due to the limited range of antiarrhythmic drugs, the aim of the present study was to assess potential antiarrhythmic effects of ranolazine in levosimendan-pretreated isolated rabbit hearts. Methods: Twelve rabbit hearts were excised and retrogradely perfused employing the Langendorff setup. Left and right atrial catheters were used to record monophasic action potentials and to obtain cycle length-dependent atrial action potential durations (aAPD90) and effective refractory periods (aERP). After obtaining baseline data, 0.5 µmol/L levosimendan was infused. Subsequently, 10 µmol/L ranolazine was administered. Results: Infusion of levosimendan led to a reduction of aAPD90 (–9 ms, p < 0.05) and aERP (–13 ms, p < 0.05). Additional treatment with ranolazine prolonged aAPD90 (+23 ms, p < 0.01) and aERP (+30 ms, p < 0.05). Under baseline conditions, a predefined pacing protocol induced 77 episodes of atrial fibrillation. Infusion of levosimendan enhanced the vulnerability to atrial fibrillation (132 episodes, p = 0.14). Further treatment with ranolazine had a significant antiarrhythmic effect (61 episodes, p < 0.05). Conclusions: In this study, ranolazine seems to prevent atrial fibrillation in levosimendan-pretreated hearts. Underlying mechanism is a prolongation of atrial repolarization and aERP.

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CASALEGGIO, A., A. CORANA, R. RANJAN, and N. V. THAKOR. "DIMENSIONAL ANALYSIS OF THE ELECTRICAL ACTIVITY IN FIBRILLATING ISOLATED HEARTS." International Journal of Bifurcation and Chaos 06, no. 08 (August 1996): 1547–61. http://dx.doi.org/10.1142/s0218127496000916.

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The dynamical behavior of the electrophysiological response at the epicardium of isolated Langendorff-perfused rabbit heart during different induced arrhythmic conditions is studied with the use of the correlation dimension D2 and Lyapunov exponents. Different conditions are investigated: normal sinus rhythm (NSR), normal sinus rhythm after ischemia (NSRI), and ventricular fibrillation with and without perfusion (VFWP and VF, respectively). Both single lead and simultaneous recordings from four leads are analyzed. The correlation dimensions during VF and VFWP are significantly higher than during NSR or NSRI, although low-dimensional attractors could not be clearly observed in VF and VFWP. Our conclusions are (a) that isolated hearts behave periodically during NSR, probably because the heart does not have to cope with time-varying demands either from the nervous system or from the metabolism; (b) during NSRI, spatially different regions of the heart show periodicities or chaotic behavior with low-dimensions, possibly due to electrophysiological inhomogeneity of the heart tissue; (c) during VF and VFWP, an intrinsic change in the dynamics seems to occur, and the heart behaves as a high-dimensional system, wherein VFWP signals show a greater spatial homogeneity than do VF signals. We propose a possible interpretation of the results in terms of the synchronization of cells by a pacemaker and desynchronization as a result of malignant arrhythmias.

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40

Magee, William P., Gayatri Deshmukh, Michael P. Deninno, Jill C. Sutt, Justin G. Chapman, and W. Ross Tracey. "Differing cardioprotective efficacy of the Na+/Ca2+ exchanger inhibitors SEA0400 and KB-R7943." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 3 (March 1, 2003): H903—H910. http://dx.doi.org/10.1152/ajpheart.00784.2002.

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KB-R7943 and SEA0400 are Na+/Ca2+ exchanger (NCX) inhibitors with differing potency and selectivity. The cardioprotective efficacy of these NCX inhibitors was examined in isolated rabbit hearts (Langendorff perfused) subjected to regional ischemia (coronary artery ligation) and reperfusion. KB-R7943 and SEA0400 elicited concentration-dependent reductions in infarct size (SEA0400 EC50: 5.7 nM). SEA0400 was more efficacious than KB-R7943 (reduction in infarct size at 1 μM: SEA0400, 75%; KB-R7943, 40%). Treatment with either inhibitor yielded similar reductions in infarct size whether administered before or after regional ischemia. SEA0400 (1 μM) improved postischemic recovery of function (±dP/d t), whereas KB-R7943 impaired cardiac function at ≥1 μM. At 5–20 μM, KBR-7943 elicited rapid and profound depressions of heart rate, left ventricular developed pressure, and ±dP/d t. Thus the ability of KB-R7943 to provide cardioprotection is modest and limited by negative effects on cardiac function, whereas the more selective NCX inhibitor SEA0400 elicits marked reductions in myocardial ischemic injury and improved ±dP/d t. NCX inhibition represents an attractive approach for achieving clinical cardioprotection.

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Patel, Vanlata H., Kieran E. Brack, John H. Coote, and G. André Ng. "A novel method of measuring nitric-oxide-dependent fluorescence using 4,5-diaminofluorescein (DAF-2) in the isolated Langendorff-perfused rabbit heart." Pflügers Archiv - European Journal of Physiology 456, no. 3 (January 5, 2008): 635–45. http://dx.doi.org/10.1007/s00424-007-0440-y.

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42

Robert, Emmanuelle, Jean E. de La Coussaye, Antoine G. M. Aya, Jean-Pierre Bertinchant, Anne Polge, Pascale Fabbro-Pèray, Christine Pignodel, and Jean-Jacques Eledjam. "Mechanisms of Ventricular Arrhythmias Induced by Myocardial Contusion." Anesthesiology 92, no. 4 (April 1, 2000): 1132–43. http://dx.doi.org/10.1097/00000542-200004000-00032.

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Background The aims of the Langendorff-perfused rabbit heart study were to evaluate the arrhythmogenic consequences of myocardial contusion and to determine the mechanism of arrhythmia. Methods Six hearts were in the control group, and 24 hearts (intact heart protocol) were submitted to one of four different contusion kinetic energies (75, 100, 150, or 200 millijoules [mJ]; n = 6). Occurrence of arrhythmia, of an electrically silent area (i.e., area with no electrical activity), and of line of fixed conduction block were reported before and for 1 h after contusion. In 16 hearts (frozen hearts) submitted to cryoprocedure and contusion impact of 100 or 200 mJ, ventricular conduction velocities, anisotropic ratio, wavelengths, ventricular effective refractory period, and its dispersion were measured before and for 1 h after contusion. Using high-resolution mapping, arrhythmias were recorded and analyzed. Results The intact heart study showed that the number and seriousness of contusion-induced arrhythmias increased with increasing contusion kinetic energy, as did the number of electrically silent areas (five of six ventricular fibrillations and five of six electrically silent areas at 200 mJ). In the frozen heart study, immediately after contusion ventricular effective refractory periods were shortened and dispersed, and wavelengths were also shortened. The arrhythmia analysis showed that all ventricular tachycardias but one were based on reentry developed around an electrically silent area or a line of fixed conduction block. Conclusions Myocardial contusion has direct arrhythmogenic effects, and the seriousness of arrhythmia increases with the level of contusion kinetic energy. The mechanism of arrhythmia was mainly based on reentrant circuit around a fixed obstacle.

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Jackson, W. F., A. Konig, T. Dambacher, and R. Busse. "Prostacyclin-induced vasodilation in rabbit heart is mediated by ATP-sensitive potassium channels." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 1 (January 1, 1993): H238—H243. http://dx.doi.org/10.1152/ajpheart.1993.264.1.h238.

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We tested the hypothesis that prostacyclin and its stable analogue iloprost act as agonists of ATP-sensitive potassium channels (KATP) to induce vasodilation of the coronary circulation. The selective blocker of KATP, glibenclamide, was used as a probe for vasodilation mediated by KATP in saline-perfused rabbit hearts (constant flow, Langendorff preparation). Glibenclamide (10-300 nM) significantly increased coronary perfusion pressure and inhibited vasodilation induced by iloprost (1-30 nM), prostacyclin (10 nM), adenosine (0.3 microM), and cromakalim (0.1 microM), a known agonist of KATP. This potassium channel antagonist also inhibited vasodilation of rabbit hearts in response to 10 nM bradykinin in the presence of an inhibitor of nitric oxide synthase (30 microM NG-nitro-L-arginine). Because bradykinin-induced vasodilation is mediated by prostacyclin released from endothelial cells when nitric oxide synthesis is inhibited, these data indicate that glibenclamide is also effective against endogenous prostacyclin. The inhibitory effects of glibenclamide were selective: vasodilation induced by sodium nitroprusside (1-10 microM) or acetylcholine (1 microM) were not inhibited by this potassium channel antagonist. In addition, basal and bradykinin-stimulated release of 6-ketoprostaglandin F1 alpha was not affected by this antagonist of KATP. Glibenclamide also did not inhibit the activation of adenylate cyclase, as indicated by its lack of effect on adenosine 3',5'-cyclic monophosphate accumulation induced by iloprost (10 nM-1 microM) in bovine coronary arterial segments, a tissue in which iloprost-induced vascular smooth muscle relaxation is inhibited by glibenclamide.(ABSTRACT TRUNCATED AT 250 WORDS)

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Nikolski, Vladimir P., Aleksandre T. Sambelashvili, and Igor R. Efimov. "Mechanisms of make and break excitation revisited: paradoxical break excitation during diastolic stimulation." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 2 (February 1, 2002): H565—H575. http://dx.doi.org/10.1152/ajpheart.00544.2001.

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10.1152/ajpheart.00544.2001. Onset and termination of electric stimulation may result in “make” and “break” excitation of the heart tissue. Wikswo et al. (30) explained both types of stimulations by virtual electrode polarization. Make excitation propagates from depolarized regions (virtual cathodes). Break excitation propagates from hyperpolarized regions (virtual anodes). However, these studies were limited to strong stimulus intensities. We examined excitation during weak near-threshold diastolic stimulation. We optically mapped electrical activity from a 4 × 4-mm area of epicardium of Langendorff-perfused rabbit hearts ( n = 12) around the pacing electrode in the presence ( n = 12) and absence ( n = 2) of 15 mM 2,3-butanedione monoxime. Anodal and cathodal 2-ms stimuli of various intensities were applied. We imaged an excitation wavefront with 528-μs resolution. We found that strong stimuli (×5 threshold) result in make excitation, starting from the virtual cathodes. In contrast, near-threshold stimulation resulted in break excitation, originating from the virtual anodes. Characteristic biphasic upstrokes in the virtual cathode area were observed. Break and make excitation represent two extreme cases of near-threshold and far-above-threshold stimulations, respectively. Both mechanisms are likely to contribute during intermediate clinically relevant strengths.

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Tsukube, T., J. D. McCully, K. R. Metz, C. U. Cook, and S. Levitsky. "Amelioration of ischemic calcium overload correlates with high-energy phosphates in senescent myocardium." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 1 (July 1, 1997): H418—H425. http://dx.doi.org/10.1152/ajpheart.1997.273.1.h418.

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Previously, we have shown that potassium and magnesium (K-Mg, 20 mM each) cardioplegia ameliorated cytosolic calcium ([Ca2+]i) accumulation and was associated with enhanced functional recovery after surgically induced global ischemia in the aged heart. K-Mg cardioplegia was also shown to enhance cytosolic cytochrome oxidase I activity and mRNA levels, suggesting that enhanced functional recovery may involve the preservation of high-energy phosphates. To investigate this hypothesis, 31P nuclear magnetic resonance was used to measure serial alterations in phosphocreatine (PCr), inorganic phosphate, nucleoside triphosphate (NTP), intracellular free magnesium (Mgf), and intracellular pH (pHi) in Langendorff-perfused, aged (135 wk) rabbit hearts during preischemia, global ischemia (30 min), and reperfusion (30 min). K-Mg cardioplegia retarded PCr depletion (P <0.05) and significantly enhanced NTP preservation (P < 0.05) during ischemia and reperfusion. K-Mg cardioplegia also attenuated the increase in Mgf during ischemia (P < 0.05). These results were correlated with amelioration of [Ca2+]i accumulation during ischemia and preservation of left ventricular function after reperfusion and suggest that optimal functional recovery from surgically induced ischemia is provided by K-Mg cardioplegia in the aged myocardium.

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Qu, Fujian, Fidel Zarubin, Brian Wollenzier, Vladimir P. Nikolski, and Igor R. Efimov. "The Gurvich waveform has lower defibrillation threshold than the rectilinear waveform and the truncated exponential waveform in the rabbit heart." Canadian Journal of Physiology and Pharmacology 83, no. 2 (February 1, 2005): 152–60. http://dx.doi.org/10.1139/y04-131.

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Implantable cardioverter defibrillator studies have established the superiority of biphasic waveforms over monophasic waveforms. However, external defibrillator studies of biphasic waveforms are not as widespread. Our objective was to compare the defibrillation efficacy of clinically used biphasic waveforms, i.e., truncated exponential, rectilinear, and quasi-sinusoidal (Gurvich) waveforms in a fibrillating heart model. Langendorff-perfused rabbit hearts (n = 10) were stained with a voltage-sensitive fluorescent dye, Di-4-ANEPPS. Transmembrane action potentials were optically mapped from the anterior epicardium. We found that the Gurvich waveform was significantly superior (p < 0.05) to the rectilinear and truncated exponential waveforms. The defibrillation thresholds (mean ± SE) were as follows: Gurvich, 0.25 ± 0.01 J; rectilinear-1, 0.34 ± 0.01 J; rectilinear-2, 0.33 ± 0.01 J; and truncated exponential, 0.32 ± 0.02 J. Using optically recorded transmembrane responses, we determined the shock-response transfer function, which allowed us to predict the cellular response to waveforms at high accuracy. The passive parallel resistor-capacitor model (RC-model) predicted polarization superiority of the Gurvich waveform in the myocardium with a membrane time constant (τm) of less than 2 ms. The finding of a lower defibrillation threshold with the Gurvich waveform in an in vitro model of external defibrillation suggests that the Gurvich waveform may be important for future external defibrillator designs.Key words: defibrillation, optical mapping, biphasic waveform, Gurvich waveform.

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Chorro, Francisco J., Isabel Trapero, Luis Such-Miquel, Francisca Pelechano, Luis Mainar, Joaquín Cánoves, Álvaro Tormos, et al. "Pharmacological modifications of the stretch-induced effects on ventricular fibrillation in perfused rabbit hearts." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 5 (November 2009): H1860—H1869. http://dx.doi.org/10.1152/ajpheart.00144.2009.

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Stretch induces modifications in myocardial electrical and mechanical activity. Besides the effects of substances that block the stretch-activated channels, other substances could modulate the effects of stretch through different mechanisms that affect Ca2+ handling by myocytes. Thirty-six Langendorff-perfused rabbit hearts were used to analyze the effects of the Na+/Ca2+ exchanger blocker KB-R7943, propranolol, and the adenosine A2 receptor antagonist SCH-58261 on the acceleration of ventricular fibrillation (VF) produced by acute myocardial stretching. VF recordings were obtained with two epicardial multiple electrodes before, during, and after local stretching in four experimental series: control ( n = 9), KB-R7943 (1 μM, n = 9), propranolol (1 μM, n = 9), and SCH-58261 (1 μM, n = 9). Both the Na+/Ca2+ exchanger blocker KB-R7943 and propranolol induced a significant reduction ( P < 0.001 and P < 0.05, respectively) in the dominant frequency increments produced by stretching with respect to the control and SCH-58261 series (control = 49.9%, SCH-58261 = 52.1%, KB-R7943 = 9.5%, and propranolol = 12.5%). The median of the activation intervals, the functional refractory period, and the wavelength of the activation process during VF decreased significantly under stretch in the control and SCH-58261 series, whereas no significant variations were observed in the propranolol and KB-R7943 series, with the exception of a slight but significant decrease in the median of the fibrillation intervals in the KB-R7943 series. KB-R7943 and propranolol induced a significant reduction in the activation maps complexity increment produced by stretch with respect to the control and SCH-58261 series. In conclusion, the electrophysiological effects responsible for stretch-induced VF acceleration in the rabbit heart are reduced by the Na+/Ca2+ exchanger blocker KB-R7943 and by propranolol but not by the adenosine A2 receptor antagonist SCH-58261.

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Tracey, W. Ross, Judith L. Treadway, William P. Magee, Jill C. Sutt, R. Kirk McPherson, Carolyn B. Levy, Donald E. Wilder, et al. "Cardioprotective effects of ingliforib, a novel glycogen phosphorylase inhibitor." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 3 (March 2004): H1177—H1184. http://dx.doi.org/10.1152/ajpheart.00652.2003.

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Interventions such as glycogen depletion, which limit myocardial anaerobic glycolysis and the associated proton production, can reduce myocardial ischemic injury; thus it follows that inhibition of glycogenolysis should also be cardioprotective. Therefore, we examined whether the novel glycogen phosphorylase inhibitor 5-Chloro- N-{(1 S,2 R)-3-[(3 R,4 S)-3,4-dihydroxy-1-pyrrolidinyl)]-2-hydroxy-3-oxo-1-(phenylmethyl)propyl}-1H-indole-2-carboxamide (ingliforib; CP-368,296) could reduce infarct size in both in vitro and in vivo rabbit models of ischemia-reperfusion injury (30 min of regional ischemia, followed by 120 min of reperfusion). In Langendorff-perfused hearts, constant perfusion of ingliforib started 30 min before regional ischemia and elicited a concentration-dependent reduction in infarct size; infarct size was reduced by 69% with 10 μM ingliforib. No significant drug-induced changes were observed in either cardiac function (heart rate, left ventricular developed pressure) or coronary flow. In open-chest anesthetized rabbits, a dose of ingliforib (15 mg/kg loading dose; 23 mg·kg–1·h–1 infusion) selected to achieve a free plasma concentration equivalent to an estimated EC50 in the isolated hearts (1.2 μM, 0.55 μg/ml) significantly reduced infarct size by 52%, and reduced plasma glucose and lactate concentrations. Furthermore, myocardial glycogen phosphorylase a and total glycogen phosphorylase activity were reduced by 65% and 40%, respectively, and glycogen stores were preserved in ingliforib-treated hearts. No significant change was observed in mean arterial pressure or rate-pressure product in the ingliforib group, although heart rate was modestly decreased postischemia. In conclusion, glycogen phosphorylase inhibition with ingliforib markedly reduces myocardial ischemic injury in vitro and in vivo; this may represent a viable approach for both achieving clinical cardioprotection and treating diabetic patients at increased risk of cardiovascular disease.

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49

Mačianskienė, Regina, Lauryna Pudžiuvelytė, Jurga Bernatonienė, Mantė Almanaitytė, Antanas Navalinskas, Rimantas Treinys, Inga Andriulė, and Jonas Jurevičius. "Antiarrhythmic Properties of Elsholtzia ciliata Essential Oil on Electrical Activity of the Isolated Rabbit Heart and Preferential Inhibition of Sodium Conductance." Biomolecules 10, no. 6 (June 23, 2020): 948. http://dx.doi.org/10.3390/biom10060948.

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Elsholtzia ciliata essential oil (E. ciliata) has been developed in Lithuania and internationally patented as exerting antiarrhythmic properties. Here we demonstrate the pharmacological effects of this herbal preparation on cardiac electrical activity. We used cardiac surface ECG and a combination of microelectrode and optical mapping techniques to track the action potentials (APs) in the Langendorff-perfused rabbit heart model during atrial/endo-/epi-cardial pacing. Activation time, conduction velocity and AP duration (APD) maps were constructed. E. ciliata increased the QRS duration and shortened QT interval of ECG at concentrations of 0.01–0.1 μL/mL, whereas 0.3 μL/mL (0.03%) concentration resulted in marked strengthening of changes. In addition, the E. ciliata in a concentration dependent manner reduced the AP upstroke dV/dtmax and AP amplitude as well as APD. A marked attenuation of the AP dV/dtmax and a slowing spread of electrical signals suggest the impaired functioning of Na+-channels, and the effect was use-dependent. Importantly, all these changes were at least partially reversible. Our results indicate that E. ciliata modulates cardiac electrical activity preferentially inhibiting Na+ conductance, which may contribute to its effects as a natural antiarrhythmic medicine.

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Ambrosio, G., W. E. Jacobus, M. C. Mitchell, M. R. Litt, and L. C. Becker. "Effects of ATP precursors on ATP and free ADP content and functional recovery of postischemic hearts." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 2 (February 1, 1989): H560—H566. http://dx.doi.org/10.1152/ajpheart.1989.256.2.h560.

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It has been proposed that administration of adenine nucleotide precursors might accelerate replenishment of myocardial ATP and "free" ADP, thus improving recovery of depressed contractility of postischemic hearts. To test this hypothesis, Langendorff-perfused rabbit hearts were subjected to 20 min of global ischemia and reperfused for 2 h with normal perfusate (n = 8) or perfusate containing 100 mumol/l of the ATP precursors adenosine (n = 8) or 5-amino-4-imidazolecarboxamide riboside (AICAriboside; n = 8). After reperfusion, developed pressure in untreated hearts averaged 70-80% of base line, whereas ATP content was reduced to approximately 70% of preischemic values. AICAriboside administration did not increase tissue ATP levels or contractility. However, in every heart that received adenosine during reperfusion, ATP content increased from a mean value of 65 +/- 4% of base line to 84 +/- 5% at the end of reperfusion (P less than 0.001). Free ADP also increased in adenosine-treated hearts from 40 to 50% of base line at the beginning of reperfusion, to normal levels by 60 min. However, no improvement in contractility was observed in the hearts that received adenosine. These results support the hypothesis that decreased availability of nucleotide precursors is responsible for depressed ATP levels in postischemic hearts; however, reduced ATP and free ADP levels may not be directly responsible for the depressed function of stunned myocardium.

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Journal articles on the topic 'Langendorff-perfused rabbit heart'

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