Thornton R M, Proppe D W
Department of Physiology, University of Texas Health Science Center, San Antonio.
Am J Physiol. 1988 Aug;255(2 Pt 2):H266-71. doi: 10.1152/ajpheart.1988.255.2.H266.
Previous studies indicate that the heat stress-induced cutaneous vasodilation in baboons is attenuated during dehydration by mechanisms other than the well-known neurohumoral vasoconstrictor mechanisms. Therefore, this study sought to determine whether dehydration also attenuates locally mediated maximum hindlimb blood flow and vascular conductance in baboons. Five baboons were chronically instrumented to measure arterial blood pressure and mean external iliac artery blood flow (MIBF). Hindlimb vasodilation was induced by occlusions of the external iliac artery for 2.5, 5.0, 7.5, and 10.0 min and by close-arterial injections of acetylcholine (ACh) and sodium nitroprusside (NP) in graded doses. These vasodilatory stimuli were applied in euhydrated and dehydrated states, the latter being produced by water deprivation for 64-68 h. Maximum MIBF and iliac vascular conductance (IVC) after arterial occlusion were reduced by 67-70% during dehydration. Also, maximum MIBF and IVC produced by ACh in the dehydrated state were 46-52% lower than in the euhydrated state. A similar reduction in the responses to NP occurred during dehydration. It is concluded that the maximum hindlimb blood flow and vascular conductance produced by local, nonneurohumoral mechanisms are attenuated in the baboon during dehydration.
先前的研究表明，在狒狒中，热应激诱导的皮肤血管舒张在脱水期间会通过除了众所周知的神经体液血管收缩机制之外的其他机制而减弱。因此，本研究旨在确定脱水是否也会减弱狒狒局部介导的最大后肢血流量和血管传导率。对五只狒狒进行长期仪器植入，以测量动脉血压和平均髂外动脉血流量（MIBF）。通过阻断髂外动脉2.5、5.0、7.5和10.0分钟以及通过分级剂量的动脉内注射乙酰胆碱（ACh）和硝普钠（NP）来诱导后肢血管舒张。这些血管舒张刺激在正常水合状态和脱水状态下施加，后者是通过剥夺水分64 - 68小时产生的。在脱水期间，动脉阻断后的最大MIBF和髂血管传导率（IVC）降低了67 - 70%。此外，在脱水状态下，ACh产生的最大MIBF和IVC比正常水合状态下低46 - 52%。在脱水期间，对NP的反应也出现了类似的降低。得出的结论是，在脱水期间，狒狒中由局部非神经体液机制产生的最大后肢血流量和血管传导率会减弱。
