研究磷酸肌酸对失血性休克家兔心肌缺血再灌注损伤的保护作用。

新西兰大耳白兔20只，随机分为磷酸肌酸注射液治疗组（CP组）和生理盐水对照组（N组），各10只。制作家兔失血性休克模型，监测血流动力学指标（MAP）；分别于休克前（T₀）、休克60 min（T₁）、复苏30 min（T₂）、60 min（T₃）、120 min（T₄）5个时间点抽血检测心肌肌钙蛋白I（cTnI）和肌酸激酶（CK），实验终点取心脏组织观察其病理学及超微结构的改变，检测心肌线粒体Na⁺-K⁺-ATP酶和Ca²⁺-ATP酶活性，并用TUNEL法检测心肌细胞的凋亡。

与N组比较，CP组心肌病理组织学改变程度较轻；CP组在复苏期各个时间点的CK值和cTnI值均明显减低（P<0.05）；CP组家兔心肌线粒体中的Na⁺-K⁺-ATP酶和Ca²⁺-ATP酶活力均明显升高；CP组心肌TUNEL阳性细胞明显减少（P<0.05）。

磷酸肌酸具有抗失血性休克所致的心肌再灌注损伤作用。

To observe protective effects of exogenous phosphocreatine on myocardial damage induced by hemorrhagic shock and its mechanisms.

Twenty healthy white rabbits were randomly divided into Control group (Group N) and Exogenous Phosphocreatine group (Group CP). Acute hemorrhagic shock animal model was established according to Wigger’s method. The changes of mean arterial pressure (MAP), serum creatine phosphokinase(CK) and cardiac Troponin I (cTn-I), myocardial mitochondrial ATPase, apoptosis and myocardial morphological structure were observed.

There were excessive myocardial injuries in Group N, while in Group CP the myocardial myofilament disarray and the pathological finding were not as severe as in Group N. Compared with the group N, the level of CK and cTnI significantly decreased during reperfusion, the activity of mitochondrial Na⁺-K⁺-ATPase and Ca²⁺-ATPase significantly increase and the total number of staining myocytes of CP group were lower(P<0.05).

CP can protect markedly the myocardial damage induced by hemorrhagic shock.