Schumacker P R, Saba T M
Ann Surg. 1980 Jul;192(1):95-102. doi: 10.1097/00000658-198007000-00016.
The influence of reticuloendothelial (RE) blockade on the pulmonary hemodynamic and gas exchange response to thrombin induced low-grade intravascular coagulation was studied in dogs during fibrinolytic inhibition. Neither saline infusion nor experimentally induced RE blockade significantly increased pulmonary vascular resistance, physiologic dead space, or pulmonary venous admixture. Intravascular coagulation in the absence of RE blockade resulted in a significant (p less than 0.05) elevation in pulmonary vascular resistance which was transient and returned to prechallenge levels over a two to four hour period. This response was not associated with any significant change in physiological dead space. In contrast, intravascular coagulation in the presence of RE blockade resulted in significant (p less than 0.05) hemodynamic and gas exchange abnormalities. These included an acute elevation in pulmonary vascular resistance, a decrease in arterial oxygenation, an increase in pulmonary venous admixture, and a sustained elevation in physiologic dead space. These events were associated with an elevation in the lung wet-to-dry weight ratios. Gas exchange and hemodynamic alterations afterthrombin infusion during RE blockade suggest a functional role for the reticuloendothelial system in the prevention of pulmonary injury during intravascular coagulation. Thus, this study suggests a possible role of the RES in minimizing pulmonary injury during states of increased microaggregate formation.
在纤维蛋白溶解抑制期间，对犬进行研究，以探讨网状内皮系统（RE）阻断对凝血酶诱导的轻度血管内凝血所致肺血流动力学和气体交换反应的影响。输注生理盐水或实验性诱导的RE阻断均未显著增加肺血管阻力、生理死腔或肺静脉混合血。在无RE阻断的情况下发生血管内凝血，会导致肺血管阻力显著（p<0.05）升高，该升高是短暂的，并在2至4小时内恢复到激发前水平。这种反应与生理死腔的任何显著变化均无关。相比之下，在存在RE阻断的情况下发生血管内凝血，会导致显著（p<0.05）的血流动力学和气体交换异常。这些异常包括肺血管阻力急剧升高、动脉氧合降低、肺静脉混合血增加以及生理死腔持续升高。这些情况与肺湿重与干重比值升高有关。在RE阻断期间输注凝血酶后出现的气体交换和血流动力学改变表明，网状内皮系统在预防血管内凝血期间的肺损伤中具有功能性作用。因此，本研究提示网状内皮系统在减少微聚集体形成增加状态下的肺损伤方面可能发挥作用。
