AJP - Heart Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Heart Circ Physiol 266: H1162-H1168, 1994;
0363-6135/94 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wu, Z. Y.
Right arrow Articles by Benoit, J. N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wu, Z. Y.
Right arrow Articles by Benoit, J. N.

AJP - Heart and Circulatory Physiology, Vol 266, Issue 3 1162-H1168, Copyright © 1994 by American Physiological Society


ARTICLES

Vascular NE responsiveness in portal hypertension: role of portal pressure and portosystemic shunting

Z. Y. Wu and J. N. Benoit
Department of Physiology and Biophysics, Louisiana State University Medical Center, Shreveport 71130.

Previous studies have suggested that the development of portal venous collaterals and subsequent portosystemic shunting is the key event responsible for the reduced vasoconstrictor effectiveness in chronic portal hypertension. The purpose of the present study was to test this hypothesis. Thirty-nine male Sprague-Dawley rats were divided into four groups: end-to-side portacaval shunt (PCS, n = 11), chronic prehepatic portal hypertension (CPH, n = 10), acute prehepatic portal hypertension (APH, n = 8), and sham-operated controls (Sham, n = 10). The small intestine was prepared for microcirculatory studies. First-order arteriolar diameter and erythrocyte velocity were measured on-line, and blood flow was subsequently calculated. Once steady-state values were obtained the preparation was topically exposed to incremental doses of norepinephrine. The half-maximal effective dosage (ED50) for maximal vasoconstriction (diameter response) was significantly increased in PCS (4.5 microM) and CPH (1.5 microM) compared with Sham (0.8 microM). However, the ED50 was significantly lower in APH (0.17 microM) than in Sham. Similarly the ED50 for maximal blood flow reduction was higher in PCS (2.4 microM) and CPH (1.2 microM) compared with Sham (0.2 microM). The results demonstrate that vascular norepinephrine responsiveness is reduced in both portacaval shunted and chronic portal hypertensive rats, but not in acute portal hypertension. These data indicate that portosystemic shunting, not portal pressure elevation, is the key event leading to the reduced vascular norepinephrine responsiveness observed in CPH conditions.


This article has been cited by other articles:


Home page
Am. J. Physiol. Gastrointest. Liver Physiol.Home page
H.-Y. Zhang, Y. Shirasawa, X. Chen, H. Yu, and J. N. Benoit
Impaired agonist-dependent myosin phosphorylation and decreased RhoA in rat portal hypertensive mesenteric vasculature
Am J Physiol Gastrointest Liver Physiol, April 1, 2005; 288(4): G603 - G608.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
M. C. Payne, H.-Y. Zhang, Y. Shirasawa, Y. Koga, M. Ikebe, J. N. Benoit, and S. A. Fisher
Dynamic changes in expression of myosin phosphatase in a model of portal hypertension
Am J Physiol Heart Circ Physiol, May 1, 2004; 286(5): H1801 - H1810.
[Abstract] [Full Text] [PDF]


Home page
HeartHome page
S Moller and J H Henriksen
Cirrhotic cardiomyopathy: a pathophysiological review of circulatory dysfunction in liver disease
Heart, January 1, 2002; 87(1): 9 - 15.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online