Faculty of Health and Sport Sciences, University of Tsukuba, Tsukuba City, Japan.
Human and Environmental Physiology Research Unit, University of Ottawa, Ottawa, ON, Canada.
Microcirculation. 2020 Jan;27(1):e12586. doi: 10.1111/micc.12586. Epub 2019 Sep 12.
Post-occlusive reactive hyperemia (PORH) following arterial occlusion is widely used to assess cutaneous microvascular function, though the underlying mechanisms remain to be fully elucidated. We evaluated the hypothesis that Ca -activated, ATP-sensitive, and voltage-gated K channels (K , K , and K channels, respectively) contribute to PORH while nitric oxide synthase (NOS) and cyclooxygenase (COX) do not.
On separate occasions, cutaneous blood flow (laser Doppler flowmetry) was monitored before and following 5-min arterial occlusion at forearm skin sites treated via microdialysis with the following: Experiment 1 (n = 11): (a) lactated Ringer solution (Control), (b) 10 mM N -nitro- -arginine (NOS inhibitor), (c) 10 mM ketorolac (COX inhibitor), and (d) combined NOS+COX inhibition; Experiment 2 (n = 14): (a) lactated Ringer solution (Control), (b) 50 mM tetraethylammonium (non-selective K channel blocker), (c) 5 mM glibenclamide (non-specific K channel blocker), and (d) 10 mM 4-aminopyridine (non-selective K channel blocker).
Separate and combined NOS and COX inhibition did not influence PORH. Conversely, tetraethylammonium and glibenclamide attenuated, whereas 4-aminopyridine augmented PORH.
We showed that tetraethylammonium, glibenclamide, and 4-aminopyridine modulate PORH with no roles of NOS and COX in human non-glabrous forearm skin in vivo. Thus, cutaneous PORH changes could reflect altered K channel function.
动脉闭塞后再充血（PORH）广泛用于评估皮肤微血管功能，尽管其潜在机制仍有待充分阐明。我们评估了以下假设：钙激活、ATP 敏感和电压门控钾通道（分别为 K ATP 、K V 和 K Ca 通道）有助于 PORH，而一氧化氮合酶（NOS）和环氧化酶（COX）则没有。
在不同的情况下，通过激光多普勒流量测量法在前臂皮肤部位监测动脉闭塞前和闭塞后 5 分钟的皮肤血流，通过微透析进行以下处理：实验 1（n=11）：（a）乳酸林格溶液（对照），（b）10mM N -硝基- -精氨酸（NOS 抑制剂），（c）10mM 酮咯酸（COX 抑制剂），以及（d）NOS+COX 联合抑制；实验 2（n=14）：（a）乳酸林格溶液（对照），（b）50mM 四乙铵（非选择性 K 通道阻滞剂），（c）5mM 格列本脲（非特异性 K 通道阻滞剂），以及（d）10mM 4-氨基吡啶（非选择性 K 通道阻滞剂）。
NOS 和 COX 的单独和联合抑制均不影响 PORH。相反，四乙铵和格列本脲减弱，而 4-氨基吡啶增强 PORH。
我们表明，在体内，非诺贝特、格列本脲和 4-氨基吡啶调节 PORH，NOS 和 COX 在人体非无毛前臂皮肤中不起作用。因此，皮肤 PORH 的变化可能反映了 K 通道功能的改变。
