Anaphylactic shock is sometimes life-threatening, and it is accompanied by hepatic venoconstriction in animals, which, in part, accounts for anaphylactic
hypotension. Roles of
norepinephrine and α-
adrenoceptor in
anaphylaxis-
induced hypotension and
portal hypertension were investigated in anesthetized
ovalbumin-sensitized Sprague-Dawley rats. The sensitized rats were randomly allocated to the following pretreatment groups (n = 6/group): 1) control (nonpretreatment), 2) α1-
adrenoceptor antagonist
prazosin, 3) nonselective α-
adrenoceptor antagonist
phentolamine, 4)
6-hydroxydopamine-induced
chemical sympathectomy, and 5) surgical hepatic
sympathectomy.
Anaphylactic shock was induced by an
intravenous injection of the
antigen. The systemic arterial pressure (SAP), central venous pressure (CVP), portal venous pressure (PVP), and portal venous blood flow (PBF) were measured, and splanchnic [Rspl: (SAP-PVP)/PBF] and portal venous [Rpv: (PVP-CVP)/PBF] resistances were determined. Separately, we measured efferent hepatic sympathetic nerve activity during
anaphylaxis. In the control group, SAP markedly decreased, followed by a gradual recovery toward baseline. PVP and Rpv increased 3.2- and 23.3-fold, respectively, after
antigen. Rspl decreased immediately, but only transiently, after
antigen, and then increased 1.5-fold later than 10 min. The α-
adrenoceptor antagonist pretreatment or
chemical sympathectomy inhibited the late increase in Rspl and the SAP recovery. Pretreatment with α-
adrenoceptor antagonists, or either chemical or surgical hepatic
sympathectomy, did not affect the
antigen-induced increase in Rpv. Hepatic sympathetic nerve activity did not significantly change after
antigen. In conclusion, α-
adrenoceptor antagonists and
chemical sympathectomy exacerbate
anaphylaxis-
induced hypotension, but not
portal hypertension, in anesthetized rats. Hepatic sympathetic nerves are not involved in anaphylactic
portal hypertension.