Effects of Carbocromene on Ventricular Fibrillation during Acute Myocardial Ischemia in Anesthetized Dogs

Fiedler, Volker B.; Schneider, Siglinde; Nitz, Rolf-Eberhard

doi:10.1159/000137729

Cited by 6 publications

(4 citation statements)

References 8 publications

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“…In experimental animals, this instability can be measured by determining the ventricular fibrillation threshold (VFT) [12]. Previous experiments have shown that VFT decreases after acute coronary artery ligation in anaesthetized dogs, and that drugs which offer protective effects can alleviate the VFT reductions [5,11]. It was found in the present study that both ranitidine and cimetidine were effective in preventing the VFT decreases induced by LAD ligation in anaesthetized dogs, indicating their protective effects on ventricular vulnerability in canine hearts during acute coronary artery occlusion.…”

Section: Discussionmentioning

confidence: 99%

“…Ventricular fibrillation (VF) was produced with the technique of Fielder et al [11], with slight modifications. After the pericardium was opened, a plaque of platinum electrodes was sutured to the epicardial surface of the right ventricle near the conus arteriosus.…”

Section: Measurement Of Ventricular Fibrillation Thresholdmentioning

confidence: 99%

“…However, as rat hearts are generally believed to be less responsive than other mammalian hearts to histamine [8][9][10], more evidence is, therefore, required to confirm the protective effects of histamine H2-receptor antagonists against acute myocardial ischaemia in experimental animals. Coronary artery ligation in dogs has long been accepted as a useful model for producing experimental cardiac arrhythmias and for screening potential antiarrhythmic drugs [11]. In order to evaluate further the role of histamine in the production of early ventricular arrhythmias as well as the protective effects of H2-antihistamines during acute myocardial ischaemia, the present study examines the effects of ranitidine and cimetidine on the changes in ventricular fibrillation threshold and haemodynamics induced by acute coronary artery ligation in anaesthetized dogs.…”

Section: Introductionmentioning

confidence: 99%

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Cardiovascular effects of ranitidine and cimetidine during acute myocardial ischaemia in anaesthetized dogs

Dai

1986

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The effects of ranitidine and cimetidine on ventricular fibrillation threshold and haemodynamics were studied in pentobarbitone-anaesthetized dogs subjected to acute coronary artery ligation. These drugs did not significantly change the ventricular fibrillation threshold nor haemodynamics before coronary artery ligation, except for remarkable haemodynamic depression by ranitidine 1 mg/kg. Ligation of the left anterior descending coronary artery reduced the ventricular fibrillation threshold, decreased systemic and left ventricular pressures and myocardial contractility, and slightly increased heart rate. Pretreatment with ranitidine 0.25 or 1 mg/kg, or with cimetidine 2 mg/kg, significantly abolished the reductions in ventricular fibrillation threshold, but did not noticeably alter the haemodynamic changes. These findings further support the hypothesis that histamine release may contribute to the increased ventricular vulnerability resulting from acute myocardial ischaemia. However, the role of histamine in the haemodynamic responses to coronary artery ligation remains obscure.

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Section: Discussionmentioning

confidence: 99%

Section: Measurement Of Ventricular Fibrillation Thresholdmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cardiovascular effects of ranitidine and cimetidine during acute myocardial ischaemia in anaesthetized dogs

Dai

1986

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“…At the end of the 2 h reperfusion period, the LAD was re-occluded, and 1 ml of 1% Evans blue in phosphate-buffered saline was injected into the left ventricle of the beating heart, circulating the accessible vasculature, thereby leaving the area at risk (AAR) unstained (modified from (Fiedler et al, 1982;Ovize et al, 1994). After 2 min with perfusion of Evans blue, the heart was excised and frozen at −80°C overnight.…”

Section: Assessment Of Infarct Sizementioning

confidence: 99%

Effect of ischemic preconditioning and a Kv7 channel blocker on cardiac ischemia-reperfusion injury in rats

Corydon

Matchkov

Fais

et al. 2020

European Journal of Pharmacology

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Recently, we found cardioprotective effects of ischemic preconditioning (IPC), and from a blocker of KCNQ voltage-gated K + channels (K V 7), XE991 (10,10-bis(4-pyridinylmethyl)-9(10H)-anthracenone), in isolated rat hearts. The purpose of the present study was to investigate the cardiovascular effects of IPC and XE991 and whether they are cardioprotective in intact rats. In conscious rats, we measured the effect of the K V 7 channel blocker XE991 on heart rate and blood pressure by use of telemetry. In anesthetized rats, cardiac ischemia was induced by occluding the left coronary artery, and the animals received IPC (2 × 5 min of occlusion), XE991, or a combination. After a 2 h reperfusion period, the hearts were excised, and the area at risk and infarct size were determined. In both anesthetized and conscious rats, XE991 increased blood pressure, and the highest dose (7.5 mg/kg) of XE991 also increased heart rate, and 44% of conscious rats died. XE991 induced marked changes in the electrocardiogram (e.g., increased PR interval and prolonged QT C interval) without changing cardiac action potentials. The infarct size to area at risk ratio was reduced from 53 ± 2% (n = 8) in the vehicle compared to 36 ± 3% in the IPC group (P < 0.05, n = 9). XE991 (0.75 mg/kg) treatment alone or on top of IPC failed to reduce myocardial infarct size. Similar to the effect in isolated hearts, locally applied IPC was cardioprotective in intact animals exposed to ischemia-reperfusion. Systemic administration of XE991 failed to protect the heart against ischemia-reperfusion injury suggesting effects on the autonomic nervous system counteracting the cardioprotection in intact animals.

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Treatment of haemodynamic and electrocardiographic side-effects resulting from imipramine toxicity in rats and dogs

Fiedler¹,

Kettenbach²,

Göbel³

et al. 1985

Naunyn-Schmiedeberg's Arch. Pharmacol.

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This study was designed to analyze the effects of carbocromene and dipyridamole on the haemodynamic and electrocardiographic side-effects resulting from imipramine infusion in anaesthetised rats and dogs. Imipramine was infused at 1 mg/kg/min until cardiac failure and vascular collapse terminated the experiment at 21 +/- 2.3 min in rats and at 29.5 +/- 2.1 min in dogs. This was characterized by hypotension, bradycardia, intraventricular conduction delay, cardiac tachyarrhythmia and A-V block. Carbocromene (4 mg/kg i.v., followed by 80 micrograms/kg/min) protected the animals against heart failure. This was associated with delayed hypotension and negative inotropy, and lower incidence of heart block. Survival time increased to 37 +/- 1.5 min (P less than 0.05), and 54.2 +/- 2.6 min (P less than 0.02) in rats and dogs, respectively. Dipyridamole (0.5 mg/kg i.v., followed by 80 micrograms/kg/min) failed to decrease imipramine toxicity as judged by the haemodynamic and electrocardiographic parameters and did not alter survival time of imipramine controls. These results suggest that carbocromene is an effective treatment for imipramine-induced cardiovascular collapse and cardiac arrhythmias, the beneficial effects being largely due to metabolic and membrane stabilizing effects. Carbocromene has both therapeutic and prophylactic value and appears to be superior to dipyridamole therapy.

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Effects of Carbocromene on Ventricular Fibrillation during Acute Myocardial Ischemia in Anesthetized Dogs

Cited by 6 publications

References 8 publications

Cardiovascular effects of ranitidine and cimetidine during acute myocardial ischaemia in anaesthetized dogs

Cardiovascular effects of ranitidine and cimetidine during acute myocardial ischaemia in anaesthetized dogs

Effect of ischemic preconditioning and a Kv7 channel blocker on cardiac ischemia-reperfusion injury in rats

Treatment of haemodynamic and electrocardiographic side-effects resulting from imipramine toxicity in rats and dogs

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