Organ damage evaluation in a temperature-controlled circulatory arrest rat model

Abstract

Background: Deep hypothermic circulatory arrest (DHCA) is commonly used in adult aortic surgery and pediatric complex congenital heart disease, and is associated with pathophysiological changes and postoperative complications. Here, a temperature-controlled circulatory arrest model in rats was established to study the suitable temperature of circulatory arrest by investigating the damage to body organs under different temperatures. Methods: Thirty Sprague‒Dawley rats were randomly divided into 5 equal groups for DHCA experiments: I (15–20 °C), II (20–25 °C), III (25–30 °C), IV (normothermic cardiopulmonary bypass), and V (sham operation group). Blood gas analysis, homodynamic parameters, and intervals of cardiac recovery were measured at different time points in all groups. Morphological changes in intestinal tissue were observed under light and electron microscopes. Oxidative stress was measured by MPO activity, MDA, and SOD content. Tissue damage was confirmed by serum detection of ALT, AST, BUN, Cr, and LDH. To examine the inflammatory response, cytokines, including IL-1, IL-4, IL-10, IFN-γ, and TNF-α, were detected. Results: The extracorporeal circulation technique caused damage to the body; the degree of the damage caused by the circulatory arrest technique may be related to circulating temperature, with the least amount of damage occurring at 20–25 °C compared to 15–20 °C and 25–30 °C. Ischemia and hypoxia can cause intestinal tissue damage, which manifests primarily as a loss of the intestinal mucosal barrier. Ischemic intestinal damage caused by DHCA was not associated with inflammation. Conclusion: The study provides new insights into the pathophysiologic mechanisms of DHCA.