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目的:评估分析模拟急性缺血-再灌注对糖尿病与正常家兔心室肌细胞L型钙通道电流(ICa,L)的作用。方法:采用四氧嘧啶静脉注射建立6周的糖尿病家兔模型,胶原酶分离家兔左心室肌细胞,以膜片钳全细胞模式记录糖尿病家兔和正常对照家兔心室肌细胞在基线状态,模拟缺血灌流5min和再灌注5min三个时相的ICa,L。结果:糖尿病组和对照组心室肌细胞最大ICa,L密度在基线状态无显著差异;对照组细胞(n=11)最大ICa,L密度在基线、缺血灌流后和再灌注后分别为(-8.36±1.63)pA/pF、(-5.90±1.75)pA/pF和(-4.22±1.02)pA/pF,缺血时ICa,L小于基线(P<0.01),而再灌注后ICa,L较之基线(P<0.01)和缺血时(P<0.05)均显著减小;糖尿病组细胞(n=9)最大ICa,L密度在基线、缺血灌流后和再灌注后分别为(-7.55±1.62)pA/pF、(-6.05±1.58)pA/pF和(-5.12±1.13)pA/pF,仅再灌注后ICa,L明显小于基线(P<0.01),而缺血时ICa,L分别与基线(P>0.05)和再灌注后(P>0.05)相比均无显著差异。结论:糖尿病状态下的心室肌细胞ICa,L对急性缺血损伤呈现“钝化”反应,随缺血进程的衰减较正常细胞缓慢,而缺血后再灌注则对于有无糖尿病的心肌均强力抑制ICa,L。本研究结果可能有助于提示糖尿病条件下的缺血-再灌注心肌损伤机制以及对合并缺血性心脏病的糖尿病患者的治疗方案。
OBJECTIVE: To evaluate the effects of acute ischemia-reperfusion on L-type calcium channel current (ICa, L) in diabetic and normal rabbit ventricular myocytes. Methods: Diabetic rabbits were established by intravenous injection of alloxan for 6 weeks. Collagenase was used to isolate rabbit left ventricular myocytes. Whole-cell patch clamp model was used to record the changes of ventricular myocytes in diabetic rabbits and normal rabbits. ICa, L were simulated at 5 min after ischemia and 5 min after reperfusion. Results: The maximum density of ICa and L in ventricular myocytes in diabetic group and control group were not significantly different at baseline. The maximum density of ICa and L in control group (n = 11) was (-) at baseline, after ischemia and reperfusion PA / pF and (-4.22 ± 1.02) pA / pF were significantly lower than those of baseline (P <0.05) (P <0.01) and ischemia (P <0.05). The maximal density of ICa and L in the cells of diabetic group (n = 9) were significantly lower at baseline, after ischemia and after reperfusion PA / pF and (- 5.12 ± 1.13) pA / pF, respectively. The levels of ICa and L in reperfusion group were significantly lower than those in baseline group (P <0.01) There was no significant difference compared with baseline (P> 0.05) and reperfusion (P> 0.05) respectively. CONCLUSION: The ICa and L of ventricular myocytes in diabetic rats show a “passive” response to acute ischemic injury, with the attenuation of ischemic progression being slower than that of normal cells. However, the ischemic postconditioning of myocardium with or without diabetes Strong inhibition of ICa, L. The results of this study may be helpful to suggest the mechanism of myocardial ischemia-reperfusion injury in diabetic patients and the treatment of diabetic patients with ischemic heart disease.