摘要
目的:从心肌能量代谢的变化,了解α1受体在缺血心肌中发挥效应的机制。方法:Langendorff灌流模拟心肌缺血。W estern b loting测定心肌GLUT4、GLUT1的表达量。同时观察糖原、ATP、乳酸及线粒体的变化。结果:缺血前使用苯肾上腺素激活α1受体,缺血时测得GLUT4(47.6±12.0)%、GLUT1(27.2±7.1)%、糖原88.9±2.3μmol/g、ATP 3.0±0.3μmol/g、乳酸24±4.2μmol/g。缺血前使用哌唑嗪阻断α1受体,缺血时测得GLUT4(31.1±8.8)%、GLUT1(22.9±5.9)%、糖原28.7±2.3μmol/g、ATP 1.9±0.3μmol/g、乳酸50.7±9.5μmol/g。阻断组和激活组GLUT4、GLUT1均增高,但激活组更显著(P<0.05)。激活组的糖原和ATP比阻断组高(P<0.05或P<0.01),乳酸则相反(P<0.01)。激活组线粒体损害程度小,阻断组线粒体则损伤显著(P<0.05)。结论:α1受体通过改变GLUT4、GLUT1表达,调控葡萄糖转运,影响糖酵解和高能磷酸物合成。
AIM： To study the mechanism of α1-adrenoceptor exerting biological effects on energy metabolism in ischemia myocardium. METHODS： Ischemia model was established according to Langendorff method. The expressions of GLUT4 and GLUT1 were dectected by Western blotting. In the mean time. The changes of glycogen, lactic acid, ATP and mitochondria were measured. RESULTS： GLUT4, GLUT1 ,glycogen,ATP and lactic acid were （27.2 ±7.1 ） % , 88.9 ±2.3 μ mol/g, 3.0 ±0.3 μ mol/g, （47.6 ± 12） % , 24 ±4.2 μ mol/g respectively when phenylenphrine was used to activate α1- adrenoceptors before ischemia. However, GLUT4, GLUT1, lactic acid, glycogen and ATP was （31. 1 ± 8.8）% , （22.9 ±5.9% ）, 50.7 ±9.5 μ mol/g, 28.7 ±2.3 μ mol/g and 1.9 ±0.3 μ mol/g respectively when prazosin was given to block α1 - adrenoceptors during pre-ischemia. GLUT1 and GLUT4 increased in activated and blocked groups, and significant increases were found in the activated group（P 〈0.05 ）. Glycogen and ATP in the activated group were higher than those in the blocked group（P 〈 0.05 or P 〈 0.01 ）. However, lactic acid was lower in the actived group than in the blocked group（P 〈0.01 ）. The mitochondria injury in the activated group wasnot serious . In contrast, the mitochondria in the blocked group was not seriously （P 〈 0.05 ）. CONCLUSION： By changing the expressions of GLUT4 and GLUT1, adjustting transporting of glucose, α1- adrenoceptors influence glycolysis and synthesis of energy-rich phosphate, thus controlling energy metabolism in cardiac muscle cells .
出处
《心脏杂志》
CAS
2005年第6期546-548,共3页
Chinese Heart Journal
关键词
Α1受体
能量代谢
缺血
机制
α1-adrenoceptors
energy metabolism
ischemia
mechanism
