Bredenberg C E, Nomoto S, Webb W R
Ann Surg. 1980 Jul;192(1):86-94. doi: 10.1097/00000658-198007000-00015.
The pulmonary and systemic hemodynamic response to four hours of hemorrhagic shock and resuscitation has been studied in 17 baboons using both open and closed chest models. No pulmonary artery (PA) hypertension occurred during shock or resuscitation except for an increase in lft ventricular end diastolic pressure (LVEDP) secondary to intravascular volumee overload with Dextran. Pulmonary vascular resistance (PVR) increased during shock but returned to control levels with reinfusion of shed blood and correction of acidosis. PVR was moderately elevated following reinfusion of shed blood if acidosis was not corrected or if volum resuscitation was inadequate. No increase in gradients occurred between PA pressure and left atrial (LA) pressure or LVEDP and there was no gradients between small pulmonary vein and LA pressure. Arterial PO2 uniformly increased during shock and remained at or above control levels of reinfusion. Gross or histologic evidence of "congestive atelectasis" or "shock lung" was not observed. These observations suggest that in the subhuman primate, hemorrhage alone does not produce significant injury to the lung during shock or the immediate postresuscitation interval. Hemorrhage alone did not produce changes in the lung which would result in increased pulmonary microvascular hydrostatic pressure following appropriate resuscitation.
利用开胸和闭胸模型，在17只狒狒身上研究了四小时失血性休克及复苏过程中的肺循环和体循环血流动力学反应。除了因右旋糖酐导致血管内容量过载继发左心室舒张末期压力（LVEDP）升高外，休克或复苏期间未发生肺动脉（PA）高压。休克期间肺血管阻力（PVR）增加，但随着回输失血和纠正酸中毒，其恢复至对照水平。如果未纠正酸中毒或容量复苏不足，回输失血后PVR会适度升高。PA压力与左心房（LA）压力之间或LVEDP与LA压力之间均未出现梯度增加，小肺静脉与LA压力之间也没有梯度。休克期间动脉血氧分压（PO2）持续升高，并在回输时维持在对照水平或高于对照水平。未观察到“充血性肺不张”或“休克肺”的大体或组织学证据。这些观察结果表明，在非人灵长类动物中，单纯出血在休克期间或复苏后即刻不会对肺造成显著损伤。单纯出血不会导致肺发生变化，而这种变化会在适当复苏后导致肺微血管静水压升高。
