RESPONSES OF RAT MESENTERIC-ARTERIES TO NOREPINEPHRINE DURING EXPOSURE TO HEAT-STRESS AND ACIDOSIS

Both cardiovascular abnormalities and metabolic acidosis can be prominent in heat stroke and may contribute to morbidity and mortality in heat stroke victims. Thus the effects of heat stress and/or low pH on the responses of rat mesenteric arteries (similar to 300 mu m) to norepinephrine (NE; 10(-8)-10(-5) M) and acetylcholine (ACh; 10(-5) M) were examined. Arteries (5-7/ group) were isolated, cannulated with micro-pippettes, placed under constant intraluminal pressure (50 mmHg), and then examined during 60-min exposures to either 1) 37, 42, or 43 degrees C or 2) 37 or 42 degrees C under conditions of low pH (pH = 7.0 by addition of 1 N HCl). Contractile responses to NE remained unaltered during exposure to 42 and 43 degrees C. When arteries were returned from that elevated temperature back to 37 degrees C for 30 min, enhanced (P < 0.05) contractile responses to NE were observed. Exposure to low pH depressed contractile responses to NE to a similar extent in arteries tested at 37 or 42 degrees C. Dilations to ACh were not altered by exposure to 42 degrees C, regardless of pH conditions, but were progressively reduced during the 43 degrees C (P = 0.09) exposure. Arteries exposed to NE demonstrated vasomotion. The NE-induced vasomotion, while maintained at 37 degrees C, was reduced (P < 0.05) by exposure to 43 degrees C. In conclusion, the contractile response to NE in mesenteric arteries was not altered by heat stress per se (up to 43 degrees C) but was depressed by low pH. The latter response was not potentiated by heat stress. Also, in mesenteric arteries, vasomotion induced by NE can be reduced by heat stress.