糖酵解对缺血后心肌钙离子平衡及心功能恢复的作用

Effects of glycolysis on calcium homeostasis and functional recoveryof postischemic myocardium

目的和方法：作者在麻醉狗顿抑心肌模型上观察用碘乙酸盐（ＩＡＡ）抑制糖酵解对缺血后心肌钙镁离子平衡恢复及心功能的影响．心肌钙镁离子用原子吸收分光光度计测定．心脏血液动力学指标用多导生理记录仪测定．结果：在非缺血对照组心脏，用ＩＡＡ抑制糖酵解并不改变钙镁离于水平及心功能状态．缺血１５ｍｉｎ后，心肌钙水平（μｍｏｌ／ｇ）增高（未缺血区１．４０±０．２０，缺血区１．８０±０．１７，Ｐ＜０．０５），镁离子降低，再灌注３０ｍｉｎ后钙水平继续增高（未缺血区１．５０±０．２７，异常区２．２６±０．０９，Ｐ＜０．０１），再灌注６０ｍｉｎ后有所恢复（未缺血区１．５４±０．１６，异常区２．２１±０．２０）．而糖酵解抑制组在再灌注３０ｍｉｎ时钙水平显著增高（未缺血区１．５７±０．０７，异常区２．９０±０．２５，Ｐ＜０．０１）与未用ＩＡＡ组相比有显著差异．镁离子则持续较低水平．糖酵解抑制后降低更为明显，与未用ＩＡＡ组相比Ｐ＜０．０１．说明抑制了糖酵解会导致细胞内持久而严重的钙超载．糖酵解抑制还可导致较明显的心功能损害，左心室舒张压增高，舒张常数值增加，±ｄｐ／ｄｔ＿ｍａｘ下降．结论：在体情况下，抑制糖酵解会引起更为严重的钙超载和血液?

Objective:To observe the effects of inhibition of glycolysis with iodoacetate(IAA) on calciumhomeostasis and functional recovery of stunned myocardium in anesthetized dogs. Metbods:Atomic absorp-tion spectrophotometry was employed to measure myocyte calcium and magnesium contents.Hemodynamicswere monitored with a multichannel electrophysiologic recorder. Results :In nonischemic canine hearts(con-trol),IAA’s inhibition of glycolysis failed to change the[Ca￣(2+)] and [Mg￣(2+)] levels and cardiac functional con-ditions,whereas in hearts subjected to 15-minute ischemia, [Ca￣(2+)] was increased from nonischemic 1.40±0.20 μ mol/g to ischemic 1.80±0.17 μmol/g(P<0. 05)while [Mg￣(2+)] was decreased. After 30 minutes ofreperfusion, [Ca￣(2+)] continued to increase from 1.50±0.21 μmol/g(nonischemic area)to 2.26±0. 09 μmol/g(abnormal area) and 60 minutes of reperfusion saw a slight restoration(1. 54±0.16 μmol/g in nonischemicarea and 2. 21±0. 20 μmol/g in abnormal area).In glycolysis-inhibiting group the calcium level registered asignificant rise after 30 minutes of reperfusion :1.57±0.07 μmol/g in nonischemic area and 2.90±0.25μmol/g in abnormal area(P<0.01).There was a significant difference between glycolysis-inhibiting groupand the group to which IAA was not applied.[Mg￣(2+)]maintained a relatively low level and registered a moreremarkable drop during inhibition of glycolysis,P<0.01 in comparison with the non IAA-administeringgroup, suggesting inhibition of glycolysis causes sustained severe calcium overload in addition to an obviousharm to cardiac function. Left ventricular end-diastolic pressure and diastolic factor T was augmented and ±dp/dt_(max) declined. Conclusion:The in vivo inhibition of glycolysis led to severe calcium overload and hemody-namic changes,indicating glycolysis plays an important role in restoration of calcium homeostasis in postis-chemic myocardium;ATP derived from glycolysis takes a significant part in myocardial ion transport in thestage of ischemia and the early stage of reperfusion and in cardiac functional recovery.