Hypoxia does not directly stimulate ischemically sensitive
abdominal visceral afferents during ischemia.
Fu, Liang-Wu, Hui-Lin Pan, Koullis F. Pitsillides, John C. Longhurst.
Division of Cardiovascular Medicine, Departments of Internal
Medicine and Human Physiology, University of California, Davis,
Davis, CA 95616
APStracts 2:0538H, 1995.
Abdominal ischemia activates ischemically sensitive sympathetic
visceral afferents and evokes reflex excitation of the cardiovascular
system. These afferents respond to ischemic metabolites including
lactic acid, bradykinin, prostaglandins and reactive oxygen species.
Severe hypoxemia also has been shown to activate these afferents. It
is not known, however, if the regional tissue hypoxia induced by
abdominal ischemia directly or indirectly activates ischemically
sensitive visceral afferents. To determine the role of tissue hypoxia
in activation of ischemically sensitive abdominal afferents,
continuous single-unit activity of ischemically sensitive abdominal
sympathetic C-fiber afferents (CV = 0.51-1.48 m/s) and regional
tissue PO2, measured by a polarographic oxygen electrode in porta
hepatis, duodenum and pancreas, were recorded simultaneously in
anesthetized cats before and during 10-15 min of ischemia. Abdominal
ischemia rapidly decreased regional tissue PO2 from 161+/-10 to 8+/-2
mmHg (p<0.01) within an interval of 136+/-12 s. By contrast,
after longer latency (399+/-24 s, p<0.01 vs PO2 interval), the
activity of these afferents increased from 0.06+/-0.01 to 0.33+/-0.07
imp/s (p<0.01). Furthermore, the activity of ischemically
sensitive afferents gradually increased throughout ischemia with peak
activity (0.68+/-0.14 imp/s) occurring at 600+/-39 s, although tissue
PO2 remained constant. There was no correlation between the changes
of tissue PO2 and discharge activity of these afferents (r = -0.428,
p = 0.144). These data suggest that tissue hypoxia induced by
abdominal ischemia is not directly responsible for activation of
ischemically sensitive sympathetic visceral afferents, but likely
acts in an indirect fashion by promoting formation of other metabolic
products capable of activating these nerve endings.
Received 17 July 1995; accepted in final form 17 November 1995.
APS Manuscript Number H667-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 8 December 95