The systemic and regional hemodynamic responses to vasoconstrictor agents are blunted during hyperthermia. This hyporesponsiveness is not observed in vitro, suggesting that adrenergic receptor function is not altered with increasing temperature. Therefore, the purpose of this study was to determine whether the baroreflex-mediated hemodynamic and sympathetic neural responses to vasoactive agents are altered during heating. The responses to bolus injections of phenylephrine (0.1-20 μg/kg i.v.) and sodium nitroprusside (SNP, 0.1-40 μg/kg i.v.) were examined in conscious, unrestrained male Sprague-Dawley rats (n = 8) at body core temperatures of 37 and 41.5°C. Heating increased mean arterial blood pressure (+40±2 mmHg), heart rate (+68±8 bpm), mesenteric resistance (+35±11 mmHg/kHz), and splanchnic sympathetic nerve activity (SpNA, +19±7 μV). The hemodynamic responses to phenylephrine and SNP were blunted with heating, whereas the SpNA responses to both agents were augmented or unchanged. At 41.5°C, the baroreflex curves relating heart rate and SpNA to mean arterial blood pressure were shifted to the right. The operating range (Δ = -117±27 bpm) and gain (Δ = 1.8±0.4 bpm/mmHg) of the blood pressure-heart rate reflex were also significantly reduced during heating. These results indicate that heating alters the cardiovascular and sympathetic neural responses to vasoactive agents in vivo. Furthermore, the data suggest that the arterial baroreflexes are reset toward higher blood pressure values and baroreflex control of heart rate is attenuated during hyperthermia.
|State||Published - Mar 20 1998|