Linke A M, Heinle H
Arch Int Physiol Biochim. 1981 Nov;89(4):313-22. doi: 10.3109/13813458109069481.
Parallel with the spontaneous mechanical activity, changes in steady-state levels of reduced pyridine nucleotides (PN) of rat portal veins were recorded by continuous monitoring of surface fluorescence. These data were correlated with changes in tissue concentrations of glucose, lactate and ATP when subjected to long-term anoxia and/or glucose depletion. In response to anoxia and addition of glucose the fluorescence intensity excited at 366 nm increased, representing a reduction of PN. This was accompanied by a higher tissue lactate content. Spontaneous contraction force decreased independently of accelerated glycolysis, which did not compensate for eliminated oxidative metabolism. The frequency of spontaneous contractions changed time-dependent. When O2 was added after more than 3 h of anoxia the spontaneous activity was restituted and PN were re-oxidized. Contraction relaxation cycles of spontaneous activity were accompanied by phasic changes of PN fluorescence clearly detectable in vessels supplied with glucose only. Suppressive effects of O2 and/or glucose depletion upon spontaneous contractile activity seem to be mediated more by alterations of cell membrane properties than by changes in energy metabolism.
与自发性机械活动同时,通过连续监测表面荧光记录大鼠门静脉中还原型吡啶核苷酸(PN)稳态水平的变化。当长期缺氧和/或葡萄糖耗尽时,这些数据与组织中葡萄糖、乳酸和三磷酸腺苷(ATP)浓度的变化相关。响应缺氧和添加葡萄糖,在366nm激发的荧光强度增加,表明PN减少。这伴随着组织中乳酸含量升高。自发性收缩力下降,与加速糖酵解无关,糖酵解无法补偿被消除的氧化代谢。自发性收缩的频率随时间变化。缺氧超过3小时后添加氧气,自发性活动恢复,PN被重新氧化。自发性活动的收缩舒张周期伴随着仅供应葡萄糖的血管中PN荧光的明显阶段性变化。氧气和/或葡萄糖耗尽对自发性收缩活动的抑制作用似乎更多地是由细胞膜特性的改变介导的,而不是由能量代谢的变化介导的。