Keller V A, Toporoff B, Raziano R M, Pigott J D, Mills N L
Department of Surgery, Tulane University Medical Center, New Orleans, Louisiana, USA.
Ann Thorac Surg. 1998 Nov;66(5):1600-3. doi: 10.1016/s0003-4975(98)00997-7.
Nonischemic myocardial dysfunction in patients with diabetes mellitus appears to be attenuated with long-term L-carnitine therapy. The effect of acute L-carnitine supplementation on rat hearts from euglycemic and diabetic animals subjected to ischemia and reperfusion is investigated in this study.
Study rats had diabetes mellitus induced by streptozocin (65 mg/kg intraperitoneally), and control rats had injection of saline solution (n = 12 per group). About 1 month later, the hearts were suspended on a Langendorff apparatus and perfused with either standard buffered Krebs-Henseleit solution or this standard solution supplemented with L-carnitine (5 mmol/L). After stabilization, normothermic, zero-flow ischemia was instituted for 20 minutes followed by 60 minutes of reperfusion. There were four study groups (n = 6 per group): hearts that were from euglycemic rats and that were perfused with standard buffered Krebs-Henseleit solution (E-STD); hearts that were from diabetic animals and that were perfused with the same standard buffered solution (DM-STD); hearts taken from diabetic animals and perfused with L-carnitine-enriched solution (DM-CAR); and hearts taken from euglycemic rats and perfused with the enriched solution (E-CAR).
At 60 minutes of reperfusion, left ventricular developed pressure was significantly better in hearts from both groups (diabetic and euglycemic) with carnitine supplementation (DM-CAR versus DM-STD and E-CAR versus E-STD, p < 0.01 for both, by analysis of variance). Left ventricular end-diastolic pressure was significantly lower in the DM-CAR group compared with all other groups (p < 0.01 by analysis of variance).
These findings suggest that acute L-carnitine supplementation significantly improves the recovery of the ischemic myocardium in diabetic and euglycemic rats.
糖尿病患者的非缺血性心肌功能障碍似乎可通过长期左旋肉碱治疗得到缓解。本研究探讨了急性补充左旋肉碱对正常血糖和糖尿病动物缺血再灌注大鼠心脏的影响。
研究大鼠通过链脲佐菌素(65mg/kg腹腔注射)诱导糖尿病,对照大鼠注射生理盐水(每组n = 12)。约1个月后,将心脏悬挂在Langendorff装置上,用标准缓冲Krebs-Henseleit溶液或补充左旋肉碱(5mmol/L)的该标准溶液进行灌注。稳定后,进行20分钟的常温零流量缺血,随后再灌注60分钟。有四个研究组(每组n = 6):来自正常血糖大鼠且用标准缓冲Krebs-Henseleit溶液灌注的心脏(E-STD);来自糖尿病动物且用相同标准缓冲溶液灌注的心脏(DM-STD);取自糖尿病动物并用富含左旋肉碱溶液灌注的心脏(DM-CAR);取自正常血糖大鼠并用富含左旋肉碱溶液灌注的心脏(E-CAR)。
再灌注60分钟时,补充肉碱的两组(糖尿病组和正常血糖组)心脏的左心室舒张末压均显著改善(DM-CAR与DM-STD以及E-CAR与E-STD相比,方差分析均显示p < 0.01)。与所有其他组相比,DM-CAR组的左心室舒张末压显著更低(方差分析p < 0.01)。
这些发现表明,急性补充左旋肉碱可显著改善糖尿病和正常血糖大鼠缺血心肌的恢复。