Downregulation of hepatic [beta]-adrenergic receptors following
hemorrhagic shock.
Tait, Stephen M., Ping Wang, Zheng F. Ba, and Irshad H. Chaudry.
Shock and Trauma Research Institute, Departments of Physiology and
Surgery, Michigan State University, East Lansing, Michigan 48824
APStracts 2:0014G, 1995.
Although it is well known that sympathoadrenal activity increases
under various adverse circulatory conditions, it is not known whether
there are any alterations in hepatic plasma membrane [beta]-adrenergic
receptors following trauma-hemorrhage and crystalloid resuscitation.
To study this, rats underwent a 5 cm midline laparotomy (i.e., trauma
induced) and were bled to and maintained at a mean arterial pressure
of 40 mmHg until 40% of the maximal bleedout (MB) volume was returned
in the form of Ringer's lactate (RL). The animals were then
resuscitated with four times the volume of MB in the form of RL over
60 minutes. Hepatic plasma membranes were isolated using
discontinuous Percoll gradient centrifugation. The maximum binding
capacity (Bmax) and the dissociation constant (Kd, i.e., 1/affinity)
of [125I]-Iodopindolol binding to [beta]-adrenergic receptors was
determined using a membrane filtration assay and Scatchard analysis.
The results indicate that there was a significant decrease in the
Bmax at the time of maximal bleedout, which persisted despite
crystalloid resuscitation following hemorrhage. However, there were
no significant changes in the Kd at any time points during this
study. The downregulation of [beta]-adrenergic receptor binding capacity
may be responsible for metabolic abnormalities observed following
hemorrhagic shock.
Received 6 June 1994; accepted in final form 3 January 1995.
APS Manuscript Number G217-4.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 February 1995.