Portal venular constriction during anaphylactic shock in anesthetized rats

Abstract

Hepatic venoconstriction occurs in rat anaphylactic hypotension. However, the exact venoconstrictive site remains unknown, and we therefore attempted to determine its location by using hepatic venography and histology. Anaphylaxis was induced in anesthetized Sprague-Dawley rats by i.v. administration of ovalbumin antigen. Venography of the portal vein (n = 8) was obtained at baseline and maximal hepatic venoconstriction. We separately examined photomicrographs of the liver sections. Along with systemic hypotension, portal venous pressure increased to a peak of 28 ± 3 cm-H 2 O at 2 min after antigen injection. Post-antigen portal venography revealed that 40% of portal venules (76 vessels/total 188 vessels) with diameters from 160 to 300 μm were not visualized, suggesting that stenosis or obliteration occurred distally. The corresponding upstream portal vessels exhibited markedly bulging. Stenosis was also observed in some portal branches with diameters from 180 to 420 μm (9%; 17 vessels/total 188 vessels). Light microscopically, most portal venules with an estimated baseline diameter less than 110 μm showed stenosis, but statistically significant stenosis was found in those with baseline diameters of 20-70 μm. In conclusion, anaphylactic hepatic venoconstriction occurs over a wide range of portal veins with diameters less than 420 μm, and occurs markedly in portal venules with diameters less than 70 μm in anesthetized rats.Anaphylactic hypotension is in part caused by a decrease in effective circulating blood volume, which could be caused by vasodilation in conjunction with the peripheral blood pooling, as well as by a shift of intravascular fluid to the extravascular space due to increased vascular permeability (2). In canine anaphylactic shock, hepatic venoconstriction, especially selective constriction of the postsinusoidal hepatic veins, induces pooling of blood in the upstream splanchnic organs, as well as in the liver itself (5,6,20). Likewise, in rat anaphylactic hypotension, hepatic venoconstriction occurs, although the liver blood volume decreases rather than increasing (8,16,19). This anaphylactic hepatic venoconstriction plays a significant role in the genesis of blood pressure fall, based on the finding that the elimination of acute portal hypertension by means of surgical perturbations or portacaval shunting attenuates the antigen-induced systemic hypotension in anesthetized rats (10, 16). However, detailed information on the anaphylactic hepatic venoconstriction which causes acute portal hypertension is limited. The anatomical site for anaphylactic venoconstriction of the liver remains unknown. In a previous work using the hepatic vascular occlusion method, we reported that the portal veins are the primary site of anaphylactic hepatic venoconstriction in isolated perfused rat livers (16). Recently this notion was reinforced by measuring the hepatic venular pressure with a servo-null micropipette pressure measurement technique: anaphylactic venoconstriction in the liver venous circulation occ...