[Acute @entity1576 based on XXXX in @entity235 @entity409 model].

@entity1 @entity5694 @entity3126 @entity235 @entity4 @entity409 @entity1003 @entity4770 @entity1578 @entity5642 @entity1576 @entity1575 @entity479
From the analysis of 182 consecutive surgical @entity1 who underwent hepatectomy and/or were associated with @entity1575 during 1963-1982, @entity1576 was proved to be so much often in those @entity1 . The case rate of this complication tends to increase according to resected size of liver tissue and severity of @entity1575 . Those cases showed clinical signs of @entity3126 and were often associated with @entity1003 and @entity5694 . In order to clarify the pathophysiological mechanism of the @entity1576 based on @entity409 , a @entity235 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 @entity1578 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 @entity1578 group. All @entity235 with @entity1578 showed typical symptomes of @entity4 at maximal PWP. @entity5642 , consumption of neutrophils, decrease of CH50 and serum opsonin were thought to be mediators of the increase of lung vascular permeability. @entity479 and @entity4770 blocked the increase of the lung vascular permeability completely but not the increase of lung vascular resistance in this experimental model.
