Establishment of a nonshockable rhythm cardiac arrest model caused by asphyxia

ObjectiveCardiac arrest (CA) is caused by a nonshockable rhythm with a low success rate of return of spontaneous circulation (ROSC) and a poor prognosis. This study intended to establish a nonshockable rhythm CA model caused by asphyxia. Materials and methodsHealthy adult male Wistar rats were injected with vecuronium bromide to induce CA. After the CA duration reached the target time point, cardiopulmonary resuscitation was performed. The survival status and neurological and cardiac function were evaluated after ROSC. Brain histopathology, including hematoxylin staining, Nissl staining and Terminal dUTP nick-end labeling (TUNEL) staining, was performed to evaluate the surviving cells and apoptotic cells. Apoptosis-related proteins after ROSC for 72 h were analyzed by western blot. ResultsCA was successfully induced in all animals. The time for the three groups of animals to PEA was 320 & PLUSMN; 22 s in the CA-8 group, 322 & PLUSMN; 28 s in the CA-12 group and 320 & PLUSMN; 18 s in the CA-15 group. The time to asystole was 436 & PLUSMN; 54 s in the CA-8 group, 438 & PLUSMN; 62 s in the CA-12 group and 433 & PLUSMN; 56 s in the CA-15 group. The NDS of rats in the CA group was significantly decreased after ROSC for 24 h. The NDS in the CA-15 group was 5-16 points, while it was 58-67 points and 15-43 points in the CA-8 and CA-12 groups, respectively. The cardiac function of animals in the CA group was impaired after ROSC, and the ejection fraction, fractional shortening, stroke volume and cardiac output, were all significantly decreased. Brain histopathology showed that the number of surviving neurons was decreased, and the number of apoptotic cells was increased in CA group, the longer the CA duration, the more apoptotic cells increased. The expression of the proapoptotic protein Bax and the apoptotic executive protein caspase3 in the hippocampus of CA rats was significantly increased, while the expression of the antiapoptotic protein Bcl-2 was significantly reduced. Conclusions The use of vecuronium can successfully induce CA caused by nonshockable rhythm in rats, which will help to further study the pathophysiological changes after CA by nonshockable rhythm.

Automated summary

This study established a model of cardiac arrest caused by asphyxia induced by nonshockable rhythm. The longer the duration of cardiac arrest, the fewer surviving neurons and the more apoptotic cells there were. The study demonstrated that vecuronium bromide can successfully induce a model of cardiac arrest caused by nonshockable rhythm.