Blum H
Department of Medicine and Biochemistry, University of Pennsylvania School of Medicine, Philadelphia 19104.
Circ Shock. 1989 Dec;29(4):291-300.
Rats were bled to a mean arterial pressure of 40 mm Hg until the onset of decompensatory shock (marked by the need to return some blood in order to maintain the blood pressure) at which time all the shed blood was returned. 31P-nuclear magnetic resonance (NMR) spectra of their livers were collected during the shock and a subsequent 60 min recovery period. Adenosine triphosphate (ATP) levels fell linearly with time, in some instances to zero during shock. ATP recovery was very rapid after return of shed blood but did not return to its preshock values. Levels of ATP remained stable during the 60 min of recovery. From the rapid recovery after total depletion of ATP in this study and in other NMR studies on perfused ischemic livers, as well as the discrepancy in residual levels of ATP during shock and ischemia as measured by in vivo NMR or by extraction techniques, we argue in favor of metabolically inaccessible pools of adenine nucleotides during these hepatic stresses.
将大鼠放血至平均动脉压为40毫米汞柱，直至失代偿性休克开始（以需要回输一些血液以维持血压为标志），此时将所有流出的血液回输。在休克期间以及随后60分钟的恢复期收集大鼠肝脏的31P-核磁共振（NMR）光谱。三磷酸腺苷（ATP）水平随时间呈线性下降，在某些情况下，休克期间降至零。回输流出的血液后，ATP恢复非常迅速，但未恢复到休克前的值。在60分钟的恢复期内，ATP水平保持稳定。基于本研究以及其他关于灌注缺血肝脏的核磁共振研究中ATP完全耗尽后的快速恢复，以及通过体内核磁共振或提取技术测量的休克和缺血期间ATP残留水平的差异，我们认为在这些肝脏应激期间存在代谢上无法接近的腺嘌呤核苷酸池。
