The effect of ethanol on arrhythmias and myocardial necrosis in rats with coronary occlusion and reperfusion

Bernauer, W.

doi:10.1016/0014-2999(86)90047-6

Cited by 22 publications

(12 citation statements)

References 25 publications

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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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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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“…Although an excessive ethanol consumption is associated with cardiovascular diseases such as cardio-myopathies and arrhythmias [6,32], cardio-protective effects of ethanol has been reported in epidemiological studies and experimental (acute and chronic) animal models [2,13,16]. This study shows that ethanol, at a concentration tolerated in vivo, postpones uncoupling induced by LPC, a lysolipid which concentration increases shortly (i.e., 5-10 min) following cardiac ischemia.…”

Section: Discussionmentioning

confidence: 73%

“…Anti-fibrillatory effects of ethanol have also been reported [23,28]. Finally, cardio-protective effects (i.e., infarct size) of ethanol during ischemia and reperfusion/reoxygenation have been shown in anesthetized guinea pig and rat models [2,30], isolated perfused rat hearts [2] and cultures of neonate rat cardiomyocytes [40].…”

Section: Introductionmentioning

confidence: 96%

Ethanol protects against lysophosphatidylcholine-induced uncoupling of cardiac cell pairs

Daleau

2002

Pfl�gers Archiv European Journal of Physiology

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Moderate alcohol consumption is related to a reduction in cardiovascular deaths. Lysophosphatidylcholine (LPC) produces arrhythmias similar to those induced by ischemia most likely due to its uncoupling properties. We assessed effects of LPC in the presence of ethanol in cardiac myocyte pairs using the double whole-cell voltage-clamp technique. Ethanol 11, 22 and 44 mmol.l(-1) did not change junctional conductance for up to 25 min but postponed the time for total uncoupling induced by 20 micromol.l(-1) LPC from 11.3+/-3.0 min ( n=4), respectively, to 16.0+/-0.5 ( n=3; P=0.05), 20.5+/-1.9 min ( n=4; P<0.05) and 27.0+/-3.5 min ( n=3; P=0.01; mean+/-SEM). LPC-induced uncoupling which might occur during ischemia may be counteracted by ethanol.

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“…This statement is supported by the observation that LPC by itself can mimic several effects of ischemia: it can promote arrhythmias [33] and tissue damage [18]. In contrast, acute ethanol administration decreases arrhythmia and fibrillation during experimental ischemia-reperfusion [12], as well as decreasing tissue necrosis [4,12].…”

Section: Introductionmentioning

confidence: 75%

Ethanol delays and reverses lysophosphatidylcholine-induced calcium overload in neonatal rat heart cells

Gailis¹,

Lamarche²,

Boudriau³

et al. 2001

Pflügers Arch - Eur J Physiol

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Increased lysophosphatidylcholine (LPC) production by the ischemic heart is associated with tissue damage. In vitro, LPC produces an increase in cytosolic [Ca2+], usually followed by cell contracture and lysis. Since ethanol reportedly protect cells during ischemia-reperfusion, we wished to determine whether ethanol could protect heart cells against LPC-induced Ca2+ overload. Newborn rat heart cells in culture were loaded with Fura-2 and [Ca2+]i recorded in individual cells. The presence of 22 or 44 mM ethanol increased the time required for 10 microM x L-palmitoyl-LPC to produce maximal Ca2+ accumulation from 8.4+/-0.4 min (n=47) to 21.1+/-2.1 x min (n=32; P<0.01) and 23.8+/-1.8 min (n=10; P<0.01) respectively. The onset of the [Ca2+]i increase could be reversed partially by the addition of ethanol (44 or 88 mM). After the addition of 22 mM ethanol, the cells retained the Fura-2 three times longer than under control conditions. Ethanol (88 mM) decreased the critical micelle concentration of LPC, thus decreasing the LPC monomer concentration in this solution. La3+ also protected the cells against LPC but no further protection was afforded by the addition of ethanol. Our results suggest that ethanol concentrations commonly found in the blood of social drinkers protect heart cells against the deleterious effect of LPC.

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The effect of ethanol on arrhythmias and myocardial necrosis in rats with coronary occlusion and reperfusion

Cited by 22 publications

References 25 publications

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

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

Ethanol protects against lysophosphatidylcholine-induced uncoupling of cardiac cell pairs

Ethanol delays and reverses lysophosphatidylcholine-induced calcium overload in neonatal rat heart cells

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