Ischemia- and reperfusion-sensitive cardiac sympathetic afferents: influence of hydrogen peroxide and hydroxyl radicals. Huang, Hsiang-Shang, Hui-Lin Pan, Gregory L. Stahl, and John C. Longhurst. Department of Internal Medicine, Division of Cardiovascular Medicine and Department of Human Physiology, University of California, Davis, Davis, California 95616
APStracts 2:0120H, 1995.
Activation of cardiac sympathetic affferents leads to excitatory cardiovascular reflexes and pain during myocardial ischemia. We hypothesized that cardiac sympathetic afferents are activated by reactive oxygen species produced during ischemia and reperfusion. Single-unit nerve activity of 55 afferents was recorded from the left paravertebral sympathetic chain (T1-T4) in cats anesthetized with [alpha]-chloralose. Receptive fields of all afferents were located on the right or left ventricle. Mechanical and chemical sensitivities of each afferent ending were evaluated by von Frey hairs, cardiac distension and local application of bradykinin (BK, 142 pmol) or H2O2 (7.5-15 [mu]mol) to the receptive field. Thirty one afferents (56%) were responsive to bradykinin, H2O2 and ischemia (2 or 10 min). Deferoxamine (DEF, 10-100 mg/kg), dimethylthiourea (DMTU, 10-100 mg/kg) or iron-loaded DEF (10 mg/kg) were employed to evaluate the role of H2O2 and hydroxyl radicals ( OH) in activating these afferents (10A[delta], 21C) during ischemia and reperfusion. Treatment with the nonspecific scavenger, DMTU (n = 10), significantly diminished the increase in discharge activity evoked by ischemia and reperfusion. Treatment with DEF also significantly attenuated the responses during ischemia and reperfusion. Thus, reactive oxygen species, particularly OH, activate a group of cardiac sympathetic A[delta]- and C-fiber afferents during myocardial ischemia and reperfusion and may play an important role in mediating cardiovascular sympathetic reflex responses and/or pain transmission.

Received 11 October 1994; accepted in final form 15 March 1995.
APS Manuscript Number H911-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on  4 April 1995.