Enhanced iNOS gene expression in the steatotic rat liver after normothermic ischemia.

Background: Impaired hepatic microcirculation in the steatotic liver has been identified as a considerable factor for increased vulnerability after ischemia/reperfusion (I/R). Changes in regulation and synthesis of vasoactive mediators, such as nitric oxide (NO) and endothelin (ET-1), may result in functional impairment of postischemic sinusoidal perfusion. The aim of the current study was to assess the impact of I/R injury on postischemic gene expression of NO and ET-1 in steatotic livers.

Intestinal barrier dysfunction in developing liver cirrhosis: An in vivo analysis of bacterial translocation.

Aim: Transmucosal passage of bacteria across the intestine, the essential step for bacterial translocation, has been identified as a key event in the pathogenesis of life-threatening infections in cirrhosis. Existing animal models of liver cirrhosis only provide indirect information about the pathogenesis of such infections. The aim of this study has been to assess transmucosal passage and bacterial translocation directly in vivo using a rat model of developing liver cirrhosis.

ET-1-induced pulmonary vasoconstriction shifts from ET(A)- to ET(B)-receptor-mediated reaction after preconstriction.

Endothelin-1 (ET-1) has been reported to induce pulmonary vasoconstriction via either ET(A) or ET(B) receptors, and vasorelaxation after ET-1 injection has been observed. Our study investigated the effects of ET-1 in isolated rabbit lungs, which were studied at basal tone (part I) and after preconstriction (U-46619; part II). Pulmonary arterial pressure (PAP) and lung weight gain were monitored continuously.