Postcountershock Myocardial Damage after Pretreatment with Adrenergic and Calcium Channel Antagonists in Halothane‐anesthetized Dogs
作者:
David Gaba,
Samuel Metz,
Mervyn Maze,
期刊:
Anesthesiology
(OVID Available online 1985)
卷期:
Volume 62,
issue 5
页码: 610-614
ISSN:0003-3022
年代: 1985
出版商: OVID
关键词: Anesthesia: cardiovascular.;Heart: defibrillation.;Surgery: Cardiovascular.
数据来源: OVID
摘要:
Transthoracic electric countershock can cause necrotic myocardial lesions in humans as well as experimental animals. The authors investigated the effect on postcountershock myocardial damage of pretreatment with prazosin (0.1 mg/kg), an alpha-1 antagonist; L-metoprolol (0.5 mg/kg), a beta-1 antagonist, and verapamil (0.5 mg/kg), a calcium channel-blocking agent. Twenty dogs were anesthetized with halothane and given two transthoracic countershocks of 295 delivered joules each after drug or vehicle treatment. Myocardial injury was quantitated 24 h following countershock by measuring the uptake of technetium-99m pyrophosphate in the myocardium. Elevated technetium-99m pyrophosphate uptake occurred in visible lesions in most dogs regardless of drug treatment. For each of four parameters of myocardial damage there was no statistically significant difference between control animals and those treated with prazosin, metoprolol, or verapamil. These data suggest that adrenergic or calcium channel-mediated mechanisms are not involved in the pathogenesis of postcountershock myocardial damage.
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