体外循环术中心肌缺血-再灌注损伤后肌浆网Ca2+调节蛋白mRNA表达

目的 研究体外循环术中心肌缺血－再灌注（Ｉ－Ｒ）损伤后肌浆网Ｃａ２＋调节蛋白ｍＲＮＡ表达。方法 实验用犬１２只，主动脉阻断缺血６０ｍｉｎ、继之开放后再灌注６０ｍｉｎ，建立体外循环术中全心缺血－再灌注心肌损伤模型。于主动脉阻断期间，分组以冷晶体液停跳液间断灌注（ＩＣＣＣ）或温血停跳液持续灌注（ＣＷＢＣ）做心肌保护。采用ＲＴＰＣＲ技术，测定 ＳＲ Ｃａ２＋－ＡＴＰ酶、钙螯合蛋白的ｍＲＮＡ水平，观察心输出量（ＣＯ）／左室收缩末期压（ＬＶＥＳＰ）两项心功能指标和心肌细胞超微结构的变化。结果 与缺血前比较，再灌注６０ｍｉｎ后：①ＩＣＣＣ组两种蛋白ｍＲＮＡ均显著上升（Ｐ＜０．０１），ＣＷＢＣ组无显著变化（Ｐ＞０．０５）；②两组ＣＯ／ ＬＶＥＳＰ均显著下降（Ｐ＜０．０１），但组间比较，ＩＣＣＣ组下降更为明显（Ｐ＜０．０１）；③ＩＣＣＣ组心肌细胞出现超微结构破坏性改变，ＣＷＢＣ组超微结构保持良好。结论 体外循环术中心肌Ｉ－Ｒ损伤后早期，心肌细胞肌浆网Ｃａ２＋调节蛋白发生了损伤后的分子修复；这种修复可能与心肌损伤程度呈相关。

mRNA expression of sarcoplasmic reticulum calcium regulatory proteins in myocardium from ischemia-reperfusion injury during cardiopulmonary bypass

Objective To investigate mRNA ex-pression of sarcoplasmic reticulum (SR) calcium regulatolt proteins in myocardium from ischemia-reperfusion (I-R) injury during cardiopulmonary bypass (CPB). Method In 12 anaesthetized canines, animal model was established by aortic crossclamping (AXC) for 60 min, subsequently decrossclamping and reperfusing for 60 min. During the period of AXC, 6 canines received continuous warm blood cardioplegia (CWBC n = 6), 6 canines re-ceived intermittent cold crystal cardioplegia (ICCC n =6). Levels of mRNA encoding SR Ca2 -ATPase and calsequenstrin were measured by using reverse transcrip-tion-polymerase chain reaction (RT-PCR), cardiac function (cardiac output. CO and left ventricular end systolic pressure. LVESP) assessments were made, and ultra-structure changes of myocardium were observed at two time points: before AXC at baseline, at 60 mm of reper-fusion alter decrossclamping. Results Compared with be-fore AXC at baseline, it was fund that at 60 mm of reperfusion: (1) SR Ca -ATPase and calsequenstrin mBNA levels significantly increased in ICCC group (P <0.01). All the corresponding mRNA was unchanged in CWBC group (P>0.05).(2)CO and LVESP were markedly de-pressed in both groups (P <0.01), but compared with CWBC group far more depressed in ICCC group (P < 0.01). (3)Cellular ultrastructure injury were observed in ICCC group, while it was generally well preserved in CW-BC group. Conclusion During CPB, a molecular repair-ing of SR calcium regulatory proteins occurs in the early time of reperfusion alter ischemia, and this molecular re-pairing might be assoiated with the severity of myocardial I-R injury.