Effects of histamine receptor blockade on cardiovascular changes induced by 35 GHz radio frequency radiation heating
Source: Autonomic & Autacoid Pharmacology, Volume 24, Number 1, January 2004 , pp. 17-28(12)
Abstract:Summary 1 The role of histamine in heat-induced cardiovascular changes is uncertain. The purpose of this study was to examine effects of histamine H-1- and H-2-antagonism on heart rate, mean arterial blood pressure (MAP), localized body temperature changes, survival times, and lethal body temperatures that occur during the exposure of anaesthetized rats to 35 GHz radio frequency radiation (RFR). 2 Forty-eight ketamine-anaesthetized Sprague-Dawley rats were exposed, in several different treatment groups (n = 8 in each), to 35 GHz RFR at a level that resulted in significant body heating and subsequent death. During irradiation, a continuous increase in heart rate and a biphasic response in blood pressure (initial increase followed by a decrease) were observed in all groups of animals. 3 An H-1-antagonist, diphenhydramine (1 mg kg−1 body wt) and an H-2-antagonist, cimetidine (5 mg kg−1), administered after sustained RFR exposure, failed to reverse the RFR-induced hypotension. High doses of the drugs (5 and 10 mg kg−1, respectively) also did not alter the response. Post-RFR survival time was significantly decreased in the high-dose drug-treated group, compared with vehicle-treated (0.9% NaCl, 50% ethanol and 50% D5W) controls. 4 In experiments in which the two drugs were administered prior to RFR exposure, MAP in animals receiving high-dose antihistamines was significantly depressed compared with that of vehicle-treated animals during the first 35 min of RFR exposure. Antihistamine pretreatment, however, did not alter the total RFR exposure time required for death to occur. 5 In summary, pharmacological blockade of H-1 and H-2 receptors is not beneficial in anaesthetized rats made hypotensive by RFR exposure. This indicates that activation of H-1 and H-2 receptors by histamine does not occur to any significant extent and does not mediate the hypotensive response developed in this model of hyperthermia.
Document Type: Research article
Affiliations: 1: Air Force Research Laboratory, Directed Energy Bio-Effects Division, Radio Frequency Radiation Branch, Brooks City-Base, TX 78235-5147 2: Department of Biology, Trinity University, San Antonio, TX 78212, USA
Publication date: 2004-01-01