Abstract
We determined the roles of liver and splanchnic vascular bed in anaphylactic hypotension using in vivo and isolated perfused BALB/c mouse liver preparations. An intravenous injection of ovalbumin antigen into the Intact-sensitized mice caused a decrease in systemic arterial pressure (Psa) from 92±2 (SE) to 39±3 mmHg but caused only a slight increase in portal venous pressure (Ppv) from 6.4±0.1 cmH2O to the peak of 9.9±0.5 cmH2O at 3.5 min after antigen. The elimination of the splanchnic vascular beds by ligation of the celiac and mesenteric arteries, combined with total hepatectomy attenuated anaphylactic hypotension. The ligation of these arteries alone, but not partial hepatectomy (70%), also attenuated anaphylactic hypotension similarly. In contrast, sensitized mouse liver perfused portally at constant flow did not show anaphylactic venoconstriction, but showed substantial constriction in response to the anaphylaxis-associated substance of platelet-activating factor, indicating that venoconstriction observed in in vivo mice may be induced by mediators released from extrahepatic tissues. These results suggest that splanchnic vascular beds are involved in BALB/c mouse anaphylactic hypotension: They presumably act as sources of chemical mediators to cause the anaphylaxis-induced portal hypertension, which induced splanchnic congestion resulting in a decrease in circulating blood volume and thus systemic arterial hypotension. Mouse hepatic anaphylactic venoconstriction may be induced by factors outside the liver, but not by anaphylactic reaction within the liver. [J Physiol Sci. 2007;57 Suppl:S81]
