Heathers G P, Brunt R V
J Mol Cell Cardiol. 1985 Sep;17(9):907-16. doi: 10.1016/s0022-2828(85)80104-8.
Glycerol 3-phosphate acyltransferase (GPAT) and Triglyceride lipase (TGL) were measured in homogenates from non-ischaemic and ischaemic tissue from the isolated perfused rat heart. Ischaemia was produced by occlusion of the left descending coronary artery for 10 min. Compared to activities measured in tissue from normally perfused hearts, GPAT activity measured in tissue from the ischaemic area was considerably reduced. TGL activity in the ischaemic area was markedly increased compared to activity measured in normally perfused hearts. No change was seen in GPAT or TGL activity measured in tissue from the non-ischaemic area. The change in activities produced by ischaemia were prevented by pre-perfusion with the cardio-selective beta-antagonist Atenolol. Reperfusion of the ischaemic area resulted in TGL activity returning to the value measured in tissue from normally perfused hearts. However, GPAT activity, after 1 min of reperfusion, fell to a value lower than after 10 min ischaemia. The reperfusion-induced fall in GPAT activity was prevented by pre-perfusion with the alpha 1 antagonist Doxasozin. Pre-perfusion of the alpha 2 antagonist Yohimbine resulted in a prolongation of the increased TGL activity in the ischaemic area during reperfusion. All changes in enzyme activities were prevented by injection of 6 OH-dopamine 24 h before hearts were removed. These changes in enzyme activities show that during ischaemia there is an increased beta-adrenergic drive. On reperfusion the beta-adrenergic drive is removed but an alpha 1 adrenergic drive becomes apparent.
在分离灌注的大鼠心脏的非缺血组织和缺血组织匀浆中测量了3-磷酸甘油酰基转移酶(GPAT)和甘油三酯脂肪酶(TGL)。通过闭塞左冠状动脉降支10分钟来产生缺血。与正常灌注心脏组织中测得的活性相比,缺血区域组织中测得的GPAT活性显著降低。与正常灌注心脏中测得的活性相比,缺血区域的TGL活性明显增加。在非缺血区域组织中测得的GPAT或TGL活性未见变化。缺血引起的活性变化可通过用心脏选择性β受体拮抗剂阿替洛尔预灌注来预防。缺血区域再灌注导致TGL活性恢复到正常灌注心脏组织中测得的值。然而,再灌注1分钟后,GPAT活性降至低于缺血10分钟后的水平。再灌注诱导的GPAT活性下降可通过用α1拮抗剂多沙唑嗪预灌注来预防。α2拮抗剂育亨宾预灌注导致再灌注期间缺血区域TGL活性增加的时间延长。在取出心脏前24小时注射6-羟基多巴胺可预防酶活性的所有变化。这些酶活性的变化表明,在缺血期间β肾上腺素能驱动增加。再灌注时,β肾上腺素能驱动被消除,但α1肾上腺素能驱动变得明显。