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[Acute respiratory failure based on liver dysfunction in canine liver ischemia model]
Nihon Geka Gakkai Zasshi
|November 1, 1985
Summary
Acute respiratory failure is common after liver surgery or in cirrhosis patients. Liver dysfunction increases lung capillary permeability, leading to pulmonary edema, mediated by coagulopathy and endotoxemia.
Area of Science:
- Hepatology
- Pulmonology
- Critical Care Medicine
Context:
- Acute respiratory failure (ARF) is a frequent complication in patients undergoing hepatectomy or with liver cirrhosis.
- The incidence of ARF correlates with the extent of liver resection and cirrhosis severity.
- Clinical manifestations include pulmonary interstitial edema, coagulopathy, and endotoxemia.
Purpose:
- To investigate the pathophysiological mechanisms of ARF associated with liver dysfunction.
- To establish and analyze a canine model of acute liver failure by complete blockade of hepatic blood inflow.
- To assess respiratory changes, specifically extravascular lung water (EVLW) and pulmonary wedge pressure (PWP), in the experimental model.
Summary:
- In a canine model, liver failure significantly increased pulmonary capillary permeability, indicated by a threefold greater EVLW increase relative to PWP compared to controls.
- Dogs with liver failure exhibited pulmonary edema at maximal PWP.
- Mediators such as disseminated intravascular coagulation, neutrophil consumption, decreased CH50, and reduced serum opsonin were implicated in increased lung vascular permeability.
Impact:
- Findings suggest that liver dysfunction directly compromises pulmonary capillary integrity, leading to edema.
- Disseminated intravascular coagulation, neutrophil consumption, and complement system alterations may play key roles in ARF pathogenesis.
- Steroids and prostacyclin (PGI2) effectively mitigated increased lung vascular permeability but not vascular resistance in this model.