Sayeed M M, Chaudry I H, Baue A E
Surgery. 1975 Mar;77(3):395-402.
This study was undertaken to determine the effects of hemorrhagic shock on cellular energy production and utilization in the lung. Energy-dependent Na+ minus K+ transport was measured by quantitating tissue cation changes during a cold (0.5 degrees C.) and a subsequent warm (37 degrees C.) incubation of lung slices from rats in late hemorrhagic shock and from unbled control rats. Active Na+ extrusion and K+ reaccumulation by the tissue were observed upon rewarming of lung slices from shock animals. Whereas K+ reaccumulation was not altered with shock, the rate of Na+ extrusion was approximately 40 percent higher. The measurement of the intracellular water content with cold and warm incubations showed no alterations with shock. Extracellular water increased with chilling in shock tissue but not in normal tissue. Lung tissue contents of adenosine triphosphate, adenosine disphosphate, or adenosine monophosphate were likewise unaltered. Thus cellular energy utilization or production in the lung was not damaged by hemorrhagic shock but a tendency toward increased interstitial water seemed to be present.
本研究旨在确定失血性休克对肺细胞能量产生和利用的影响。通过对晚期失血性休克大鼠和未失血对照大鼠的肺切片在低温(0.5℃)及随后的温育(37℃)过程中组织阳离子变化进行定量,来测定能量依赖性钠钾转运。休克动物的肺切片复温后,观察到组织有主动的钠排出和钾再蓄积。虽然休克对钾再蓄积没有影响,但钠排出速率约高40%。低温和温育时细胞内含水量的测定显示休克对此无影响。休克组织在冷却时细胞外液增加,而正常组织则不然。三磷酸腺苷、二磷酸腺苷或一磷酸腺苷的肺组织含量同样未改变。因此,失血性休克并未损害肺细胞的能量利用或产生,但似乎存在间质水增加的趋势。