In vitro evidence for vascular hyporesponsiveness in clinical and experimental cirrhosis.

The mechanisms responsible for vascular hyporesponsiveness in cirrhosis have been investigated extensively using isolated vessel techniques. Increased vasodilator (nitric oxide) production has been implicated in many studies, but there is also evidence of altered receptor/second messenger function and vascular remodelling. Interpretation is hampered by the use of different vessels from a variety of animal models, whilst the relevance of these studies to the condition in humans remains unclear. Additional, more focused investigations, using both human and animal vessels, are required to ascertain the exact cause of the vascular abnormalities associated with hepatic cirrhosis.