Whether the vascular responses to noepinephrine (NE), an adrenergic vasoconstrictor, and acetylchorine (ACh), an endothelium-vasodilator, could be altered after the cessation of the chronic exposure to hypoxia still remain unclear in endothelium-intact rat pulmonary artery. The purpose of this study was to determine whether NE- and phenylephrine (PE)-induced pulmonary vasoconstrictions, and ACh-induced pulmonary vasodilation responses were altered just after, 1 week after and 2 weeks after the cessation of the chronic exposure to normobaric hypoxia (15%O₂) for 3 weeks in rat pulmonary artery. The vascular responses in NE- and PE-induced vasoconstrictions, and ACh-induced vasodilation were determined on pulmonary arterial rings using in vitro microvessel techniques, and the pulmonary vascular tension was measured with a force transducer. Concentration-dependent response relationships were determined by cumulative addition of 10⁻⁹–10⁻⁶ M NE, 10⁻⁸–10⁻⁵ M PE and 10⁻⁸–10⁻⁵ M ACh. The sensitivities of NE- and PE-induced vasoconstrictive responses, indicated as EC₅₀, were significantly increased just and 1 week after the cessation of the chronic exposure to hypoxia for 3 weeks. The sensitivities of NE- and PE-induced vasoconstrictive responses 2 weeks after the cessation of the chronic exposure to hypoxia did not differ from those of the controls. But the sensitivity of ACh-induced vasodilation responses, indicated as IC₅₀, was significantly decreased only just after the cessation of the chronic exposure to hypoxia. Our data demonstrate that chronic exposure to hypoxia could enhance sympathetic vasoconstriction and reduce endothelium-dependent vasodilation in pulmonary artery.

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The purpose of this study was to clarify influences of non-uniformed cooling stimuli on thermoregulation, and thermal and comfort votings during trunk and extremity cooling conditions by using a water-perfused suit (WPS). Eight women subjects were kept in the supine posture in a climatic chamber at an ambient temperature of 30.0±0.5°C, 50±3% of relative humidity and 0.2 m/sec air velocity. Water temperature (Tw) of WPS were maintained thermal neutrality at 33°C for 30 min constantly. Then the Tw lowered to 30°C, 27°C, 24°C for every 30 min under trunk cooling (TC) (Tw of extremity was maintained at 33°C constant) and extremity cooling (EC) conditions (TW of trunk was maintained at 33°C constant). The skin temperature (T_sk) of distal end of extremities significantly decreased and the chest skin blood flow (chest SBF) significantly increased in both cooling conditions (p<0.05). Chest T_sk rose significantly in EC, but it significantly lowered in TC for direct cooling. There were not observed significant positive correlations between mean body temperature and chest SBF, and chest T_sk under both cooling conditions. Therefore, it is not considered that increasing chest SBF induced by the mechanism for thermophysiological regulations during both cooling conditions. As showing the significant correlations between mean body temperature and thermal, and comfort sensations in EC, it was suggested that thermal and discomfort sensations were attenuated by increasing chest T_sk.

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