Zhang Y, Richardson D, McCray A
Department of Physiology and Biophysics, Sanders-Brown Center on Aging, University of Kentucky, College of Medicine, Lexington 40536-0230.
Microvasc Res. 1994 Mar;47(2):177-87. doi: 10.1006/mvre.1994.1014.
This study tested whether or not nitric oxide (NO) is involved in mediating the response of cutaneous capillary blood flow to an indirect heat stress. Blood cell velocity (BCV) in capillaries within the subepidermal plexus of the tail of anesthetized Sprague-Dawley rats was measured by videomicroscopy while the animals' trunk was exposed to a 35 degrees environment. Vascular conductance, estimated as the ratio of BCV to mean arterial pressure (MAP), increased by 259% in saline (placebo)-treated rats. Intravenous administration of 32 mg/Kg of the NO synthesis inhibitor NG-nitro-L-arginine (NNA) attenuated the response of vascular conductance (BCV/MAP) to body heating regardless of whether NNA was given before or during the heat stress procedure. In a subset of NNA-treated animals, infusion of the NO substrate L-arginine restored the BCV/MAP response to heat stress. In summary, the results of this study support the hypothesis that NO is involved in the response of cutaneous capillary blood flow to heat stress. Possible mechanisms mediating the local release of NO are discussed.