Renal sympathetic nerve activity during cardiac ischemia and
reperfusion in rats.
Ustinova, E. E., and H. D. Schultz.
Department of Physiology and Biophysics, University of Nebraska
College of Medicine, Omaha, Nebraska 68198
APStracts 3:0248R, 1996.
We studied the role played by prostaglandins and oxygen-derived free
radicals in mediating reflex changes in renal sympathetic nerve
activity (RSNA) during myocardial ischemia and reperfusion. Ligation
of the left coronary artery for 20 min, and reperfusion for 10 min
were performed in anesthetized rats with sinoaortic denervation and
with intact cardiac afferent nerves (control, n=7), with cardiac
sympathetic denervation (SD, n=7), with vagal denervation (VD, n=6),
and with combined SD+VD (n=6). In control rats, RSNA decreased by
10+3% from baseline (p<0.05) during the first minute of ischemia
and increased above baseline after 5 min of ischemia with the maximum
increase at the first minute of reperfusion. In rats with SD, RSNA
decreased by 19+4% from baseline (p<0.05) at the first minute of
ischemia and remained depressed during the entire ischemic and
reperfusion periods. In rats with VD, RSNA increased by 26+5% from
baseline (p<0.05) at the first minute of ischemia, and the
increase in RSNA at the end of the ischemic period and at reperfusion
was greater than in control rats. No changes in RSNA during ischemia
and reperfusion were observed with combined SD+VD. Reflex changes in
RSNA that occurred at the onset of ischemia in both VD (n=7) and SD
(n=7) rats were abolished by indomethacin (5 mg/kg. i.v., 20 min
before ischemia). Reflex changes in RSNA after prolonged ischemia
(>10 min) and during reperfusion in both VD (n=7) and SD (n=7)
were abolished by the antioxidant, deferoxamine (20 mg/kg. i.v., 20
min before ischemia). Deferoxamine also diminished the increase of
RSNA at the onset of ischemia in VD rats. Thus, in rats, the vagal
afferent reflex predominates during early ischemia and the
sympathetic afferent reflex predominates during prolonged ischemia
and reperfusion. Reflex changes in RSNA that occur at the onset of
ischemia are mediated by activation of vagal and sympathetic afferent
endings by prostaglandins. Reflex changes in RSNA after prolonged
ischemia and during reperfusion are mediated by activation of vagal
and sympathetic afferent endings by oxygen-derived free radicals.
Received 31 January 1996; accepted in final form 3 April 1996.
APS Manuscript Number R66-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 4 July 96