HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 293/5/R1947    most recent 00904.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Liu, W. Articles by Kurata, Y. Search for Related Content PubMed PubMed Citation Articles by Liu, W. Articles by Kurata, Y.

NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION

Involvement of splanchnic vascular bed in anaphylactic hypotension in anesthetized BALB/c mice

Department of Physiology II, Kanazawa Medical University, Uchinada Ishikawa, Japan

Submitted 27 December 2006 ; accepted in final form 10 August 2007

Using in vivo and isolated perfused liver preparations of BALB/c mice, we determined the roles of the liver and splanchnic vascular bed in anaphylactic hypotension. Intravenous injection of ovalbumin antigen into intact-sensitized mice decreased systemic arterial pressure (P_sa) from 92 ± 2 to 39 ± 3 (SE) mmHg but only slightly increased portal venous pressure (P_pv) from 6.4 ± 0.1 cmH₂O to the peak of 9.9 ± 0.5 cmH₂O at 3.5 min after antigen. Elimination of the splanchnic vascular beds by ligation of the celiac and mesenteric arteries, combined with total hepatectomy, attenuated anaphylactic hypotension. Ligation of these arteries alone, but not partial hepatectomy (70%), similarly attenuated anaphylactic hypotension. In contrast, isolated sensitized mouse liver perfused portally at constant flow did not show anaphylactic venoconstriction but, rather, substantial constriction in response to the anaphylaxis-associated platelet-activating factor, indicating that venoconstriction in mice in vivo 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.

anaphylactic shock; hepatic circulation; portal hypertension; splanchnic congestion