Physiopathology of splanchnic vasodilation in portal hypertension

Figure 1 Physiopathology of portal hypertension. In cirrhosis, the initiating factor leading to portal hypertension is an increase in intrahepatic vascular resistance (R), whereas the increase in portal blood flow (F) is a secondary phenomenon that maintains and worsens the increased portal pressure, giving rise to the hyperdynamic circulation syndrome. The different factors implicated in the distinct mechanisms of portal hypertension are shown. AII: angiotensin II; AEA: anandamide; AM: adrenomedullin; CGRP: calcitonine gene related peptide; CO: carbon monoxide; ET: endothelin; H₂S: hydrogen sulfide; LT: leukotrienes; NE: norepinephrine; NO: nitric oxide; PGI₂: prostacyclin; SP: substance P; TXA₂: thromboxane A₂.