论文部分内容阅读
本研究利用鼠的正常心肌细胞在正常或感染性休克家兔血浆中进行培养,研究感染性休克时心肌的生化和形态学改变,并进一步证实体内存在着损害细胞的内源性中毒因子的释放和蓄积,这些因子的作用与pH、氧、CO_2、电解质或营养等异常无关。经与5%的感染性休克兔血浆培养后,培养液中释放的乳酸脱氢酶(LDH)显著高于与正常兔血浆培养者;经与10%感染休克血浆培养后释放的LDH更多。全部经正常血浆处理的培养基中均不能测出肌酸激酶活性,只有与10%感染血浆培养4或5小时者才可测出肌酸激酶活性。
In this study, normal rat cardiomyocytes were cultured in normal or septic rabbit plasma to study the biochemical and morphological changes of myocardium during septic shock and to further confirm the release of endogenous toxicants that impair cells in vivo And accumulation, the role of these factors and pH, oxygen, CO 2, electrolyte or nutrition and other abnormalities unrelated. After cultured in sera with 5% of septic shock rabbits, the lactate dehydrogenase (LDH) released from the culture medium was significantly higher than that of the normal rabbit plasma culture; more LDH was released after being incubated with 10% septic shock plasma. Creatine kinase activity was undetectable in all normal plasma-treated media, and creatine kinase activity was measured only in 4 or 5 hours of culture with 10% of infected plasma.