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1 Scetion of Digestive Diseases, Yale University School of Medicine, West Haven, CT, USA
2 Hepatic Hemodynamic Laboratory, VA Medical System, New Haven, CT, USA
3 Hepatic Hemodynamic Laboratory, VA Medical System, New Haven, CT, USA; Scetion of Digestive Diseases, Yale University School of Medicine, West Haven, CT, USA
* To whom correspondence should be addressed. E-mail: roberto.groszmann{at}yale.edu.
The intra-hepatic nitric oxide (NO) production is decreased in cirrhotic livers. Objective. To identify, in cirrhotic rat livers, intra-hepatic vascular segments where the deficit of NO facilitates the effect of vasoconstrictors. Method. Using a modified rat liver perfusion system with measurement of both the perfusion and sinusoidal (wedged hepatic vein) pressures, we studied the effect of the NO synthase blocker N
-nitro-L-arginine (NNA) on the response to methoxamine (
1-adrenoreceptor agonist) in different segments of the intra-hepatic circulation of normal and cirrhotic rat livers. Results: NNA enhanced the pre-sinusoidal, sinusoidal and post-sinusoidal responses to methoxamine in normal livers, as well as the pre-sinusoidal response in cirrhotic livers. However, NNA did not change the already enhanced sinusoidal/post-sinusoidal response to methoxamine in cirrhotic livers. The post-sinusoidal response to methoxamine was higher in cirrhotic rats with ascites than in those without ascites. Conclusions: NO modulates the pre-sinusoidal, sinusoidal, and post-sinusoidal vascular tone in normal rat livers. NO production in cirrhotic rat livers is severely impaired in the sinusoidal and post-sinusoidal areas but is preserved in the pre-sinusoidal area as evidenced by its normal response to NNA. We speculate that an increased post-sinusoidal response to catecholamines may participate in the genesis of ascites in cirrhosis.
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