Baroreflex control of heart rate during heating in subjects with low orthostatic tolerance.

BACKGROUND: Heat stress induces a reduction of orthostatic tolerance. The cardiovascular responses, including the cardiac baroreflex response to heat stress, were examined to test the hypothesis that subjects with orthostatically low tolerance demonstrate an impaired baroreflex control of heart rate (HR) during heat stress. METHODS: There were 44 healthy young volunteers who underwent whole body heat stress produced by a hot-water-perfused suit during supine rest for 45 min and 75 degrees head-up tilt (HUT) for 6 min. Esophageal temperature, HR, arterial pressure, and skin blood flow in the forearm and palm were measured continuously throughout the experiment. The sensitivity of the arterial baroreflex control of HR was calculated from the spontaneous changes in beat-to-beat arterial pressure and HR. RESULTS: The HUT was uneventful for 22 volunteers (higher tolerance group), but 22 volunteers (lower tolerance group) reached presyncope after 195 +/- 19 s. Esophageal temperature, HR, arterial pressure, and skin blood flow changed similarly in the two groups during heating. In the preheating condition, the sensitivity of the baroreflex control of HR did not differ significantly between the two groups. Heating did not alter the sensitivity of baroreflex control of HR in the higher tolerance group, but decreased it significantly in the lower tolerance group. Heating increased the number of heartbeats used for analysis of the baroreflex sensitivity in the higher tolerance group, but did not change it in the lower tolerance group. CONCLUSIONS: These results suggest that the impairment of vagal baroreflex control of HR during heat exposure aggravates the orthostatic intolerance in heat-stressed humans.

Heat acclimation increases skin vasodilation and sweating but not cardiac baroreflex responses in heat-stressed humans.

In the present study, to test the hypothesis that exercise-heat acclimation increases orthostatic tolerance via the improvement of cardiac baroreflex control in heated humans, we examined cardiac baroreflex and thermoregulatory responses, including cutaneous vasomotor and sudomotor responses, during whole body heating before and after a 6-day exercise-heat acclimation program [4 bouts of 20-min exercise at 50% peak rate of oxygen uptake separated by 10-min rest in the heat (36 degrees C; 50% relative humidity)]. Ten healthy young volunteers participated in the study. On the test days before and after the heat acclimation program, subjects underwent whole body heat stress produced by a hot water-perfused suit during supine rest for 45 min and 75 degrees head-up tilt (HUT) for 6 min. The sensitivity of the arterial baroreflex control of heart rate (HR) was calculated from the spontaneous changes in beat-to-beat arterial pressure and HR. The HUT induced a presyncopal sign in seven subjects in the preacclimation test and in six subjects in the postacclimation test, and the tilting time did not differ significantly between the pre- (241 +/- 33 s) and postacclimation (283 +/- 24 s) tests. Heat acclimation did not change the slope in the HR-esophageal temperature (Tes) relation and the cardiac baroreflex sensitivity during heating. Heat acclimation decreased (P < 0.05) the Tes thresholds for cutaneous vasodilation in the forearm and dorsal hand and for sweating in the forearm and chest. These findings suggest that short-term heat acclimation does not alter the spontaneous baroreflex control of HR during heat stress, although it induces adaptive change of the heat dissipation response in nonglabrous skin.

Enhancement of immunoreactivity for endothelin-1 and endothelin-converting enzyme-1 in the cadmium-treated rat thoracic aorta.

Male rats received daily intraperitoneal injections of cadmium sulfate (2.0 mg/kg) for 3, 6, and 8 days (cadmium-treated groups) or physiological saline for 8 days (control group). The thoracic aortae from both groups were used for electron microscopy and immunocytochemistry for big endothelin (ET)-1, ET-1 and ET-converting enzyme (ECE)-1, and the blood plasma and homogenized thoracic aortae were prepared for assays of big ET-1 and ET-1 concentrations. A remarkable increase in the number of Weibel-Palade (WP) bodies, enhanced immunoreactivities for ET-1 and ECE-1 along the endothelium, and elevated concentrations of ET-1 in the blood plasma as well as in homogenized thoracic aortae were observed in the cadmium-treated groups. However, immunoreactivity for big ET-1 and the plasma and aortic tissue concentrations of big ET-1 did not show any significant changes between the control and cadmium-treated groups. By immunoelectron microscopy, immunoreactivities for ET-1 and ECE-1 were much more pronounced in the increased WP bodies. Since WP bodies are involved in the extracellular release of ET-1 in the manner of a regulated pathway, these findings indicate that cadmium administration induces the enhanced release of ET-1, which is actively processed by ECE-1 in the WP bodies.