To test the hypothesis that the controlled reperfusion of warm blood cardioplegiacontaining mannitol would result in more effectively improved recovery of myocardial function by prevent-ing or reducing a potentially harmful component of reperfusion. Methods: Thirty-two cats were divided in-to four groups. Group Ⅰwas not subjected to ischemia or reperfusion injury. Group Ⅱ was subjected to60 min hypothermic ischemia. Group Ⅲwas subjected to 60 min hypothermic ischemia and 60 min reperfu-sion. Group Ⅳ was controlled reperfusion with warm blood cardioplegia containing mannitol. Results:Myocardial functlon was significantly depressed after 60 min reperfusion- Increased myocardial water con-tent and low ATP c0ntent were observed also. Controlled reperfusion with warm bl0od cardioplegia con-taining mannitol was helpful to improve the recovery of myocardial function and ATP content, and to re-duce the myocardial water content. Conclusion: These results indicate that controlled reperfusion after is-chemia provides benefit in avoiding myocardium from reperfusion injury.

The negative effects of low temperature can readily induce a variety of diseases. We sought to understand the reasons why cold stress induces disease by studying the mechanisms of fine-tuning in macrophages following cold exposure. We found that cold stress triggers increased macrophage activation accompanied by metabolic reprogramming of aerobic glycolysis. The discovery, by genome-wide RNA sequencing, of defective mitochondria in mice macrophages following cold exposure indicated that mitochondrial defects may contribute to this process. In addition, changes in metabolism drive the differentiation of macrophages by affecting histone modifications. Finally, we showed that histone acetylation and lactylation are modulators of macrophage differentiation following cold exposure. Collectively, metabolism-related epigenetic modifications are essential for the differentiation of macrophages in cold-stressed mice, and the regulation of metabolism may be crucial for alleviating the harm induced by cold stress.
Acetylation ; Animals ; Cold-Shock Response ; Epigenesis, Genetic ; Macrophages/metabolism* ; Mice ; Mitochondria/metabolism*