[Acute respiratory failure based on liver dysfunction in canine liver ischemia model].
From the analysis of 182 consecutive surgical patients who underwent hepatectomy and/or were associated with liver cirrhosis during 1963-1982, acute respiratory failure was proved to be so much often in those patients. The case rate of this complication tends to increase according to resected size of liver tissue and severity of liver cirrhosis. Those cases showed clinical signs of pulmonary interstitial edema and were often associated with coagulopathy and endotoxemia. In order to clarify the pathophysiological mechanism of the acute respiratory failure based on liver dysfunction, a canine experimental model in which blood inflow into the liver was completely blocked was newly devised, and respiratory state in this model was analysed. The following results were obtained. The increase of EVLW (extravascular lung water) measured by modified double indicator dilution method was linear to the increase of PWP (pulmonary wedge pressure) in both liver failure group and control group. But the coefficient of the regression line was three times larger in the former group than in the latter. It suggests that permeability of pulmonary capillary was highly increased in liver failure group. All dogs with liver failure showed typical symptomes of lung edema at maximal PWP. Disseminated intravascular coagulation, consumption of neutrophils, decrease of CH50 and serum opsonin were thought to be mediators of the increase of lung vascular permeability. Steroid and PGI2 blocked the increase of the lung vascular permeability completely but not the increase of lung vascular resistance in this experimental model.
D000208:Acute Disease; D000818:Animals; D002199:Capillary Permeability; D004211:Disseminated Intravascular Coagulation / Q000209:etiology; D004285:Dogs; D007511:Ischemia; D008099:Liver / Q000098:blood supply*; D008107:Liver Diseases / Q000150:complications; D011654:Pulmonary Edema / Q000209:etiology / Q000503:physiopathology; D012131:Respiratory Insufficiency / Q000209:etiology / Q000503:physiopathology*