Basic Fibroblast growth factor improves high energy phosphate metabolism in the ischemic myocardium in rabbits

碱性成纤维细胞生长因子（basic fibroblast growth factor，bFGF）已被证明在治疗慢性缺血性心肌和急性心肌梗死中有效。已经提出，限制突然冠状动脉闭塞后的梗死面积的有益作用不能仅仅归因于血管生成和独立于血管生成或bFGF的心脏保护作用的心肌挽救。我们推测bFGF可能通过改变缺血心肌的高能磷酸盐代谢来延长细胞存活和心肌存活。在17只日本白色家兔的心脏内灌注Langendorff制剂，在基础状态10 min、全脑缺血20 min和缺血后再灌注60 min期间，每5 min用~ 1H-NMR测定三磷酸腺苷（ATP）、磷酸肌酸（CrP）和无机磷（Pi）<31>。其中8例于缺血前1 min在灌流液中注入bFGF 100 μg。bFGF处理的心脏在缺血后再灌注期间ATP较高。总之，bFGF有效地维持缺血后心肌中较高的ATP。这种作用可能有助于限制急性心肌梗死的梗死范围。

Basic fibroblast growth factor (bFGF) has been shown effective in the treatment of chronic iscnemic myocardium as well as in acute myocardial infarction. The beneficial role to limit infarct size following abrupt coronary occlusion can not be attributable solely to angiogenesis and myocardial salvage independent of angiogenesis or cardioprotective effect of bFGF has been proposed. We hypothesized that bFGF may modify high energy phosphate metabolism in the ischemic myocardium to extend cell survival and prolong myocardial survival. In 17 Japanese white rabbits, the heart was perfused with Langendorff preparation and adenosine triphosphate (ATP), creatine phosphate (CrP) and inorganic phosphate (Pi) were measured every 5 min using ^<31>P-NMR during 10 min basal state, 20 min global ischemia following by 60 min postischemic reperfusion. In 8 of these, bFGF 100 μg was injected in the perfusate 1 min prior to the global ischemia. ATP was higher during postischemic reperfusion in bFGF-treated heart.In conclusion, bFGF was effective to maintain ATP higher in the postischemic myocardium. This effect may contribute to limit infarct size in the acute myocardial infarction.