Simmons Grant H, Minson Christopher T, Cracowski Jean-Luc, Halliwill John R
Department of Human Physiology, University of Oregon, Eugene, OR 97403-1240, USA.
J Appl Physiol (1985). 2007 Aug;103(2):608-15. doi: 10.1152/japplphysiol.01443.2006. Epub 2007 May 17.
Hypoxia and hypercapnia represent special challenges to homeostasis because of their effects on sympathetic outflow and vascular smooth muscle. In the cutaneous vasculature, even small changes in perfusion can shift considerable blood volume to the periphery and thereby impact both blood pressure regulation and thermoregulation. However, little is known about the influence of hypoxia and hypercapnia on this circulation. In the present study, 35 healthy subjects were instrumented with two microdialysis fibers in the ventral forearm. Each site was continuously perfused with saline (control) or bretylium tosylate (10 mM) to prevent sympathetically mediated vasoconstriction. Skin blood flow was assessed at each site (laser-Doppler flowmetry), and cutaneous vascular conductance (CVC) was calculated as red blood cell flux/mean arterial pressure and normalized to baseline. In 13 subjects, isocapnic hypoxia (85 and 80% O(2) saturation) increased CVC to 120 +/- 10 and 126 +/- 7% baseline in the control site (both P < 0.05) and 113 +/- 3 (P = 0.087) and 121 +/- 4% baseline (P < 0.05) in the bretylium site. Adrenergic blockade did not affect the magnitude of this response (P > 0.05). In nine subjects, hyperpnea (matching hypoxic increases in tidal volume) caused no change in CVC in either site (both P > 0.05). In 13 subjects, hypercapnia (+5 and +9 Torr) increased CVC to 111 +/- 4 and 111 +/- 4% baseline, respectively, in the control site (both P < 0.05), whereas the bretylium site remained unchanged (both P > 0.05). Thus both hypoxia and hypercapnia cause modest vasodilation in nonacral skin. Adrenergic vasoconstriction of neural origin does not restrain hypoxic vasodilation, but may be important in hypercapnic vasodilation.
缺氧和高碳酸血症因其对交感神经输出和血管平滑肌的影响而对体内平衡构成特殊挑战。在皮肤血管系统中，即使灌注的微小变化也会使相当大的血量转移到外周，从而影响血压调节和体温调节。然而，关于缺氧和高碳酸血症对这种循环的影响知之甚少。在本研究中，35名健康受试者在前臂腹侧植入了两根微透析纤维。每个部位持续用生理盐水（对照）或溴苄铵（10 mM）灌注，以防止交感神经介导的血管收缩。在每个部位评估皮肤血流量（激光多普勒血流仪），并将皮肤血管传导率（CVC）计算为红细胞通量/平均动脉压，并将其标准化为基线值。在13名受试者中，等容性缺氧（氧饱和度为85%和80%）使对照部位的CVC分别增加至基线值的120±10%和126±7%（均P<0.05），在溴苄铵部位增加至基线值的113±3%（P = 0.087）和121±4%（P<0.05）。肾上腺素能阻断不影响这种反应的幅度（P>0.05）。在9名受试者中，呼吸急促（潮气量与缺氧时增加相匹配）在两个部位均未引起CVC变化（均P>0.05）。在13名受试者中，高碳酸血症（+5和+9 Torr）使对照部位的CVC分别增加至基线值的111±4%和111±4%（均P<0.05），而溴苄铵部位保持不变（均P>0.05）。因此，缺氧和高碳酸血症均可导致非手足部皮肤适度血管舒张。神经源性肾上腺素能血管收缩并不抑制缺氧性血管舒张，但可能在高碳酸血症性血管舒张中起重要作用。
