Antagonistic effects of ?-adrenoceptor blocking agents on arrhythmias, enzyme release, and myocardial necrosis in isolated rat hearts with coronary occlusion and reperfusion

Bernauer, W.; Ernenputsch, I

doi:10.1007/bf00168817

Cited by 32 publications

(19 citation statements)

References 29 publications

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“…Therefore, the occurrence of cardiac arrhythmias for up to 3 min was assigned the factor 2; 3-6 min was assigned the factor 4; 6 -10 min was assigned the factor 6; 10 -15 min was assigned the factor 8; 15-20 min was assigned the factor 10; 20 -25 min was assigned the factor 11; and 25-30 min was assigned the factor 12. Values ranging from 2 to 12 were obtained and were denoted as the arrhythmia severity index (ASI) (1,9).…”

Section: Methodsmentioning

confidence: 99%

Abolition of reperfusion-induced arrhythmias in hearts from thiamine-deficient rats

Oliveira¹,

Guatimosim²,

Castro³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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tensive work has been done regarding the impact of thiamine deprivation on the nervous system. In cardiac tissue, chronic thiamine deficiency is described to cause changes in the myocardium that can be associated with arrhythmias. However, compared with the brain, very little is known about the effects of thiamine deficiency on the heart. Thus this study was undertaken to explore whether thiamine deprivation has a role in cardiac arrhythmogenesis. We examined hearts isolated from thiamine-deprived and control rats. We measured heart rate, diastolic and systolic tension, and contraction and relaxation rates. Whole cell voltage clamp was performed in rat isolated cardiac myocytes to measure L-type Ca 2ϩ current. In addition, we investigated the global intracellular calcium transients by using confocal microscopy in the line-scan mode. The hearts from thiaminedeficient rats did not degenerate into ventricular fibrillation during 30 min of reperfusion after 15 min of coronary occlusion. The antiarrhythmogenic effects were characterized by the arrhythmia severity index. Our results suggest that hearts from thiamine-deficient rats did not experience irreversible arrhythmias. There was no change in L-type Ca 2ϩ current density. Inactivation kinetics of this current in Ca 2ϩ -buffered cells was retarded in thiamine-deficient cardiac myocytes. The global Ca 2ϩ release was significantly reduced in thiaminedeficient cardiac myocytes. The amplitude of caffeine-releasable Ca 2ϩ was lower in thiamine-deficient myocytes. In summary, we have found that thiamine deprivation attenuates the incidence and severity of postischemic arrhythmias, possibly through a mechanism involving a decrease in global Ca 2ϩ release.arrhythmia; calcium current; confocal microscopy THIAMINE DEFICIENCY CAUSES cardiovascular and neurological damage that presents clinically as beriberi. Thiamine pyrophosphate is an important cofactor in several vital enzymatic reactions involved in metabolism and energy production (34, 39). Following its uptake by the cell, thiamine rapidly undergoes pyrophosphorylation, yielding thiamine pyrophosphate, which is the active substance. Extensive work has been done regarding the impact of thiamine deprivation on the nervous system. However, very little is known about the effects of thiamine deficiency on the myocardium (5). Cappelli et al. (5) have shown evidence that supports the view that cardiac contractility is deeply affected in the rat by thiamine deficiency. Thiamine is also considered a clinically important factor in heart function, and its deficiency has been reported to cause heart failure (28, 33, 35). The general view that reperfusion of the ischemic myocardium exerts a beneficial effect by preventing the ischemiainduced changes in cardiac performance has been supported by a number of studies; however, reperfusion after a certain critical time has been shown to be deleterious to cardiac function (16). Intracellular Ca 2ϩ has an important role in heart function, and studies have been conducted to investigate pos...

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Section: Methodsmentioning

confidence: 99%

Abolition of reperfusion-induced arrhythmias in hearts from thiamine-deficient rats

Oliveira¹,

Guatimosim²,

Castro³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…A value of 0 to 12 was thus obtained in each experiment and is denoted as arrhythmia severity index (ASI). 12 To evaluate the role of cyclooxygenase products in the Ang-(1-7) effects, rats received indomethacin (5 mg/kg IP) plus heparin (400 IU IP). After 1 hour, the rats were decapitated, the thorax was opened, and the heart was dissected and perfused with KRS or KRS containing Ang-(1-7) (0.22 nmol/L, nϭ8).…”

Section: Methodsmentioning

confidence: 99%

Angiotensin-(1-7): Cardioprotective Effect in Myocardial Ischemia/Reperfusion

2001

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Abstract-In this study we evaluate the effects of angiotensin-(1-7) on reperfusion arrhythmias in isolated rat hearts. Rat hearts were perfused according to Langendorff technique and maintained in heated (37Ϯ1°C) and continuously gassed (95% O 2 /5% CO 2 ) Krebs-Ringer solution at constant pressure (65 mm Hg). The electrical activity was recorded with an ECG (bipolar). Local ischemia was induced by coronary ligation for 15 minutes. After ischemia, hearts were reperfused for 30 minutes. Cardiac arrhythmias were defined as the presence of ventricular tachycardia and/or ventricular fibrillation after the ligation of the coronary artery was released. Angiotensin II (0.20 nmol/L, nϭ10) produced a significant enhancement of reperfusion arrhythmias. On the other hand, Ang-(1-7) presented in the perfusion solution (0.22 nmol/L, nϭ11) reduced incidence and duration of arrhythmias. The antiarrhythmogenic effects of Ang-(1-7) was blocked by the selective Ang-(1-7) antagonist A-779 (2 nmol/L, nϭ9) and by indomethacin pretreatment (5 mg/kg IP, nϭ8) but not by the bradykinin B 2 antagonist HOE 140 (100 nmol/L, nϭ10) or by L-NAME pretreatment (30 mg/kg IP, nϭ8). These results suggest that the antiarrhythmogenic effect of low concentrations of Ang-(1-7) is mediated by a specific receptor and that release of endogenous prostaglandins .by Ang-(1-7) contributes to the alleviation of reversible and/or irreversible ischemia-reperfusion injury. Key Words: heart Ⅲ angiotensin II Ⅲ angiotensin antagonist Ⅲ renin-angiotensin system Ⅲ nitric oxide Ⅲ prostaglandins

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“…Therefore, the occurrence of cardiac arrhythmias for up to 5 min was assigned the factor 1, 10 min was assigned the factor 2, 15 min was assigned the factor 3, 20 min was assigned the factor 6, 25 min was assigned the factor 9, and 30 min was assigned the factor 12. A value of 0-12 was thus obtained in each experiment and is denoted "arrhythmia severity index" (ASI) (16,17). Data are reported as means ± SEM.…”

Section: Methodsmentioning

confidence: 99%

Effect of angiotensin-(1-7) on reperfusion arrhythmias in isolated rat hearts

Neves¹,

Almeida²,

Khosla³

et al. 1997

Braz J Med Biol Res

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There is increasing evidence that angiotensin-(1-7) (Ang-(1-7)) is an endogenous biologically active component of the renin-angiotensin system (RAS). In the present study, we investigated the effects of Ang-(1-7) on reperfusion arrhythmias in isolated rat hearts. Isolated rat hearts were perfused with two different media, i.e., Krebs-Ringer (2.52 mM CaCl 2 ) and low-Ca 2+ Krebs-Ringer (1.12 mM CaCl 2 ). In hearts perfused with Krebs-Ringer, Ang-(1-7) produced a concentration-dependent (27-210 nM) reduction in coronary flow (25% reduction at highest concentration), while only slight and variable changes in contraction force and heart rate were observed. Under the same conditions, angiotensin II (Ang II; 27 and 70 nM) produced a significant reduction in coronary flow (39% and 48%, respectively) associated with a significant increase in force. A decrease in heart rate was also observed. In low-Ca 2+ Krebs-Ringer solution, perfusion with Ang-(1-7) or Ang II at 27 nM concentration produced similar changes in coronary flow, contraction force and heart rate. In isolated hearts perfused with normal Krebs-Ringer, Ang-(1-7) produced a significant enhancement of reperfusion arrhythmias revealed by an increase in the incidence and duration of ventricular tachycardia and ventricular fibrillation (more than 30-min duration). The facilitation of reperfusion arrhythmias by Ang-(1-7) was associated with an increase in the magnitude of the decreased force usually observed during the postischemic period. The effects of Ang-(1-7) were abolished in isolated rat hearts perfused with low-Ca 2+ Krebs-Ringer. The effect of Ang II (27 nM) was similar but less pronounced than that of Ang-(1-7) at the same concentration. These results indicate that the heart is a site of action for Ang-(1-7) and suggest that this heptapeptide may be involved in the mediation of the cardiac effects of the RAS.

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Antagonistic effects of ?-adrenoceptor blocking agents on arrhythmias, enzyme release, and myocardial necrosis in isolated rat hearts with coronary occlusion and reperfusion

Cited by 32 publications

References 29 publications

Abolition of reperfusion-induced arrhythmias in hearts from thiamine-deficient rats

Abolition of reperfusion-induced arrhythmias in hearts from thiamine-deficient rats

Angiotensin-(1-7): Cardioprotective Effect in Myocardial Ischemia/Reperfusion

Effect of angiotensin-(1-7) on reperfusion arrhythmias in isolated rat hearts

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