Caterine M R, Spencer K T, Pagan-Carlo L A, Smith R S, Buettner G R, Kerber R E
Cardiovascular Center, University of Iowa, Iowa City 52242, USA.
J Am Coll Cardiol. 1996 Nov 15;28(6):1598-609. doi: 10.1016/s0735-1097(96)00333-6.
We sought to demonstrate that direct current (DC) shocks to the heart generate free radicals.
Although it is a lifesaving maneuver, defibrillation is known to have myocardial toxicity. The mechanism of this toxicity is unknown. If DC shocks generate free radicals, free radicals could be a mechanism of myocardial injury.
In a canine model, DC shocks of 10 to 100 J were delivered to the epicardium of both beating and fibrillating hearts, and 200-J transthoracic shocks were administered in dogs with beating hearts. Ascorbate free radical (AFR) concentration was measured in arterial blood and blood continuously withdrawn from the coronary sinus. In some dogs, the antioxidant enzymes superoxide dismutase (15,000 U/kg) and catalase (55,000 U/kg) (SOD/Cat) were administered before shocks.
Ascorbate free radicals were generated by DC shocks. A peak AFR increase of 14 +/- 2% (mean +/- SEM) was seen 5 to 6 min after 100-J epicardial shocks. A peak AFR increase of 7 +/- 5% occurred after transthoracic shocks. There was a significant linear relation between the shock energy and peak percent AFR increase: %AFR increase = 0.18 (Shock energy) + 2.9 (r = 0.73, p < 0.0001). Shocks delivered to hearts in ventricular fibrillation (30 s) resulted in generation of AFR equal to but not greater than that observed during similar shocks delivered to beating hearts in sinus rhythm. Multiple successive shocks (100 J delivered twice or five times) did not result in a greater AFR increase than single 100-J shocks, indicating that peak, not cumulative, energy is the principal determinant of AFR increase. Animals receiving SOD/Cat before shock administration showed significant attenuation of the AFR increase.
Direct current epicardial and transthoracic shocks generate free radicals; antioxidant enzymes reduce the free radical generation by shocks.
我们试图证明心脏的直流电（DC）电击会产生自由基。
尽管除颤是一种挽救生命的操作，但已知其具有心肌毒性。这种毒性的机制尚不清楚。如果直流电电击产生自由基，那么自由基可能是心肌损伤的一种机制。
在犬模型中，对跳动和颤动心脏的心外膜施加10至100焦耳的直流电电击，并对跳动心脏的犬进行200焦耳的经胸电击。测量动脉血和从冠状窦持续抽取的血液中的抗坏血酸自由基（AFR）浓度。在一些犬中，在电击前给予抗氧化酶超氧化物歧化酶（15,000 U/kg）和过氧化氢酶（55,000 U/kg）（SOD/Cat）。
直流电电击产生抗坏血酸自由基。100焦耳心外膜电击后5至6分钟，AFR峰值增加14±2%（平均值±标准误）。经胸电击后AFR峰值增加7±5%。电击能量与AFR峰值增加百分比之间存在显著的线性关系：AFR增加百分比 = 0.18（电击能量）+ 2.9（r = 0.73，p < 0.0001）。对心室颤动（30秒）的心脏进行电击产生的AFR与对窦性心律的跳动心脏进行类似电击时观察到的AFR相等但不更大。多次连续电击（100焦耳电击两次或五次）导致的AFR增加并不比单次100焦耳电击更大，表明峰值能量而非累积能量是AFR增加的主要决定因素。在电击前接受SOD/Cat的动物，其AFR增加显著减弱。
心外膜和经胸直流电电击会产生自由基；抗氧化酶可减少电击产生的自由基。
