McCord Gregg R, Cracowski Jean-Luc, Minson Christopher T
Department of Human Physiology, University of Oregon, Eugene, Oregon 97406-1240, USA.
Am J Physiol Regul Integr Comp Physiol. 2006 Sep;291(3):R596-602. doi: 10.1152/ajpregu.00710.2005.
The specific mechanisms by which skin blood flow increases in response to a rise in core body temperature via cutaneous active vasodilation are poorly understood. The primary purpose of this study was to determine whether the cyclooxygenase (COX) pathway contributes to active vasodilation during whole body heat stress (protocol 1; n = 9). A secondary goal was to verify that the COX pathway does not contribute to the cutaneous hyperemic response during local heating (protocol 2; n = 4). For both protocols, four microdialysis fibers were placed in forearm skin. Sites were randomly assigned and perfused with 1) Ringer solution (control site); 2) ketorolac (KETO), a COX-1/COX-2 pathway inhibitor; 3) NG-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor; and 4) a combination of KETO and L-NAME. During the first protocol, active vasodilation was induced using whole body heating with water-perfused suits. The second protocol used local heaters to induce a local hyperemic response. Red blood cell flux (RBC flux) was indexed at all sites using laser-Doppler flowmetry, and cutaneous vascular conductance (CVC; RBC flux/mean arterial pressure) was normalized to maximal vasodilation at each site. During whole body heating, CVC values at sites perfused with KETO (43 +/- 9% CVCmax), L-NAME (35 +/- 9% CVCmax), and combined KETO/L-NAME (22 +/- 8% CVCmax) were significantly decreased with respect to the control site (59 +/- 7% CVCmax) (P < 0.05). Additionally, CVC at the combined KETO/L-NAME site was significantly decreased compared with sites infused with KETO or L-NAME alone (P < 0.05). In the second protocol, the hyperemic response to local heating did not differ between the control site and KETO site or between the L-NAME and KETO/L-NAME site. These data suggest that prostanoids contribute to active vasodilation, but do not play a role during local thermal hyperemia.
皮肤血流量通过皮肤主动血管舒张对核心体温升高做出反应的具体机制尚不清楚。本研究的主要目的是确定环氧化酶（COX）途径是否在全身热应激期间（方案1；n = 9）对主动血管舒张有贡献。第二个目标是验证COX途径在局部加热期间（方案2；n = 4）对皮肤充血反应没有贡献。对于这两个方案，将四根微透析纤维置于前臂皮肤中。部位随机分配并用以下溶液灌注：1）林格溶液（对照部位）；2）酮咯酸（KETO），一种COX-1/COX-2途径抑制剂；3）NG-硝基-L-精氨酸甲酯（L-NAME），一种一氧化氮合酶抑制剂；4）KETO和L-NAME的组合。在第一个方案中，使用水灌注套装进行全身加热诱导主动血管舒张。第二个方案使用局部加热器诱导局部充血反应。使用激光多普勒血流仪在所有部位测量红细胞通量（RBC通量），并将皮肤血管传导率（CVC；RBC通量/平均动脉压）标准化为每个部位的最大血管舒张。在全身加热期间，与对照部位（59±7% CVCmax）相比，灌注KETO（43±9% CVCmax）、L-NAME（35±9% CVCmax）和KETO/L-NAME组合（22±8% CVCmax）部位的CVC值显著降低（P < 0.05）。此外，与单独灌注KETO或L-NAME的部位相比，KETO/L-NAME组合部位的CVC显著降低（P < 0.05）。在第二个方案中，对照部位与KETO部位之间或L-NAME与KETO/L-NAME部位之间对局部加热的充血反应没有差异。这些数据表明，前列腺素有助于主动血管舒张，但在局部热充血期间不起作用。
