Preliminary observation on the effects of myocardial energy metabolism-promoted resuscitation strategy on hemorrhagic induced cardiac arrest in rabbits

Abstract

Objective To observe the effects of myocardial energy metabolism-promoted resuscitation strategy on hemorrhagic induced cardiac arrest (HiTCA) in rabbits. Methods Twenty 9-month-old rabbits were randomly divided into 2 groups(n=10), and HiTCA model was prepared by controlled hemorrhage. Then the rabbits received whole blood infusion and whole blood infusion+adenosine triphosphate + polarization liquid, respectively. Mean arterial pressure was detected by common carotid artery intubation; Blood routine was examined by automatic blood cell count analyzer; Coagulogram was detected by automatic coagulation analyzer; Blood biochemical indexes was detected by automatic dry biochemical analyzer; Arterial blood gas was determined by arterial blood gas analyzer; S100β, C-reactive protein and Syndecan-1 were detected by ELISA. Results The rates of restoration of spontaneous circulation (ROSC) were 100% in both groups, and the 24 h survival rate of each group was 80% and 100%. After HiTCA blood glucose and blood potassium in group B were significantly lower than that of group A(P < 0.05); INR values were significantly increased in both groups(P < 0.05);Compared with group A, group B showed a lower level in lactic acid, creatinine, urea nitrogen, glutamic-pyruvic transaminase, glutamic-oxalacetic transaminase, creative kinase isoenzyme-MB, CRP and Syndecan-1(P < 0.05)in every time point after 4 h of HiTCA. In the 2 time pointa (8 and 24 h after HiTCA), group B displayed a lower concentration level of S100β, compared with group A(P < 0.05). Conclusion Resuscitation strategy based on promoting energy metabolism could improve organs function with hemorrhage induced cardiac arrest through improving energy metabolism of viscera and coagulation function.

Keywords

• traumatic cardiac arrest
• hemorrhage-induced cardiac arrest
• return of spontaneous circulation
• adenosine triphosphate
• glucose-insulin-potassium therapy