FAILURE OF COUNTERSHOCK-TYPE PULSES INVITRO TO ADVERSELY ALTER MITOCHONDRIAL OXIDATIVE-PHOSPHORYLATION

被引：10

作者：

TROUTON, TG

BARRY, JJ

ALLEN, JD

ADGEY, AAJ

机构：

[1] Department of Physiology, The Queen's University, Regional Medical Cardiology Centre, Belfast, Northern Ireland

来源：

ANNALS OF EMERGENCY MEDICINE | 1992年 / 21卷 / 02期

关键词：

COUNTERSHOCK; MYOCARDIAL INJURY; MITOCHONDRIA;

D O I：

10.1016/S0196-0644(05)80146-5

中图分类号：

R4 [临床医学];

学科分类号：

1002 ; 100602 ;

摘要：

Study objective: The aim of the study was to investigate a potential mechanism of myocardial injury after DC countershock. The effect of countershock-type electrical discharges on rabbit heart mitochondrial oxygen consumption was measured in vitro using a novel respiration cell. Measurements and main results: Mitochondria were isolated from the hearts of adult Dutch and New Zealand White rabbits. Single rectangular shocks (voltage gradients 20 to 80 V/cm; 5 ms duration) caused no significant changes in state 3 oxygen consumption in standard incubation medium. Single and multiple defibrilator shocks (critically damped sine waveform; 5 ms duration) with peak voltage gradients of 242 to 659 V/cm similarly had no significant effect on state 3 oxygen consumption. Conclusion: At voltage gradients similar to and greater than those causing myocardial cell injury and necrosis, electrical discharges do not directly depress mitochondrial function. Therefore, the reduction in mitochondrial oxygen consumption observed following transthoracic shocks in vivo may invoke other mechanisms (eg. intracellular calcium influx, high circulating noradrenaline, or free radical formation in the intact heart).

引用

页码：132 / 136

页数：5

共 16 条

[1]

Resnekov, McDonald, Complications in 220 patients with cardiac dysrhythmias treated by phased direct current shock, and indications for electroconversion, Br Heart J, 29, pp. 926-936, (1967)

[2]

Weaver, Cobb, Copass, Et al., Ventricular defibrillation—A comparative trial using 175-J and 320-J shocks, N Engl J Med, 307, pp. 1101-1106, (1982)

[3]

Dunn, McComb, MacKenzie, Et al., Survival to leave hospital from ventricular fibrillation, Am Heart J, 112, pp. 745-751, (1986)

[4]

Dahl, Ewy, Thomas, Myocardial necrosis from direct current countershock, Circulation, 50, pp. 956-961, (1974)

[5]

Tacker, Van Vleet, Geddes, Electrocardiographic and serum enzyme alterations associated with cardiac alterations induced in dogs by single transthoracic damped sinusoidal defibrillator shocks of various strengths, Am Heart J, 98, pp. 185-193, (1979)

[6]

Gaba, Maxwell, Merlone, Et al., Internal countershock produces myocardial damage and lactate production without myocardial ischemia in anesthetized dogs, Anesthesiology, 66, pp. 477-482, (1987)

[7]

Trouton, Allen, Yong, Et al., Metabolic changes and mitochondrial dysfunction early following transthoracic countershock in dogs, PACE, 12, pp. 1827-1834, (1989)

[8]

Sordahl, Johnson, Blailock, Et al., The mitochondrion, Methods in Pharmacology, 1, pp. 247-286, (1971)

[9]

Gornall, Bardawill, David, Determination of serum proteins by means of the biuret reaction, J Biol Chem, 177, pp. 751-766, (1949)

[10]

Sobel, Jequier, Sjoerdsma, Et al., Effect of catecholamines and adrenergic blocking agents on oxidative phosphorylation in rat heart mitochondria, Circ Res, 19, pp. 1050-1061, (1966)

← 1 2 →