THE SPLANCHNIC HYPEREMIA OF PORTAL HYPERTENSION CAN BE ATTENUATED BY INCREASING RED BLOOD CELL VOLUME. A NITRIC OXIDE RELATED MECHANISM

lower GMBF (53±5 vs 70-+5, p<0.05) and SMABF (8.7±0.4 vs 13.5-+0.8, p<0.0Ol), and significantly higher (p<0.05) MAP (112_+3 vs 98_+5), GVR (1.99 _+0.2 vs 1.27_+0.1), and MVR (11.7_+0.7 vs 6.3_+0.3). PP was not significantly modified by EPO. Despite a similar increase in hematocrit, blood cell volume, and viscosity, mild and not significant increments in GVR (2.8_+0.3 vs 2.6-+0.4) and MVR (19.8_+1.8 vs 14.1_+2.7) were observed in SO rats treated with EPO. These minor changes in vascular resistance in SO rats were fully related to the increments in viscosity, since gastric or mesenteric hindrances were not modified by EPO. in contrast, gastric (0.18_+0.04 vs 0.13+0.01) and mesenteric (1.02_+0.12 vs 0.68-+0.04) hindrances were significantly increased (p<0.05) in EPO treated PH rats reflecting actual vasoconstriction. direcf vascular effect of EPO was ruled out by the lack of changes on MAP or SMABF following EPO (100 or 200 U/kg, i.v.) (n=4). The reduction in GMBF (-21_+ 7 vs -7-+2) and in SMABF (-7 • vs -3.8_+0.7) induced by L-NAME was significantly greater in vehicle than in EPO treated PH rats. (~oncluslon: Gastrointestinal vasodilation associated with portal hypertension can be attenuated by increasing red blood cell volume. Inactivation of overproduced NO by hemoglobin may account for this effect.