Calcium-activated potassium channels contribute to human skeletal muscle microvascular endothelial dysfunction related to cardiopulmonary bypass.
Calcium-activated potassium channels contribute to human skeletal muscle microvascular endothelial dysfunction related to cardiopulmonary bypass.
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DOI：
10.1016/j.surg.2008.03.032
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发表时间：
2008-08
期刊：
影响因子：
3.8
通讯作者：
Sellke, Frank W.
中科院分区：
文献类型：
--
作者：
Liu, Yuhong;Sellke, Eric W.;Feng, Jun;Clements, Richard T.;Sodha, Neel R.;Khabbaz, Kamal R.;Senthilnathan, Venkatachalam;Alper, Seth L.;Sellke, Frank W.
我们研究了体外循环（CPB）中钙激活钾（KCa）通道活性在人骨骼肌微血管功能中的作用。从CPB前后采集的组织中解剖人骨骼肌小动脉（直径80- 180 μm）。在体外舒张反应的预收缩的小动脉在加压无流动状态下进行了检查，在存在的KCa通道激活剂/阻断剂和其他几种血管扩张剂。与CPB前相比，CPB后对中间（IKCa）和小电导（SKCa）KCa通道激活剂NS 309、内皮依赖性血管舒张剂5′-二磷酸腺苷（ADP）和P物质的反应降低（P < .05），而对大电导（BKCa）KCa通道激活剂NS 1619和内皮非依赖性血管舒张剂，硝普钠（SNP）无变化。内皮剥脱减少NS 309引起的舒张反应，并消除ADP或P物质引起的舒张反应（P<0.05），但对NS 1619或SNP引起的舒张反应无影响。CPB后BKCa、IKCa和SK 3Ca的多肽水平未发生变化。IK/SK介导的舒张主要是内皮依赖性的，而BK介导的舒张似乎在很大程度上独立于人骨骼肌微血管系统的内皮功能。CPB相关的微血管功能障碍可能部分源于外周微血管中内皮SK和IK通道的功能受损。
We investigated the role of calcium-activated potassium (KCa) channel activity in human skeletal muscle microvascular function in the setting of cardiopulmonary bypass (CPB). Human skeletal muscle arterioles (80- to 180 μm in diameter) were dissected from tissue harvested before and after CPB. In vitro relaxation responses of precontracted arterioles in a pressurized no-flow state were examined in the presence of KCa channel activators/blockers and several other vasodilators. Post-CPB responses to the activator of intermediate (IKCa) and small conductance (SKCa) KCa channels, NS309, to the endothelium-dependent vasodilator adenosine 5′-diphosphate (ADP), and to substance P were reduced compared with pre-CPB responses (P < .05), respectively, whereas responses to the activator of large conductance (BKCa) KCa channels, NS1619, and to the endothelium-independent vasodilator, sodium nitroprusside (SNP) were unchanged. Endothelial denudation decreased NS309-induced relaxation and abolished that induced by ADP or substance P (P< .05), but had no effect on relaxation induced by either NS1619 or SNP. Polypeptide levels of BKCa, IKCa, and SK3Ca were not altered post-CPB. IK/SK-mediated relaxation is predominantly endothelium dependent, whereas BK-mediated relaxation seems to be largely independent of endothelial function in human skeletal muscle microvasculature. CPB-associated microvascular dysfunction likely arises in part from impaired function of endothelial SK and IK channels in the peripheral microvasculature.
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影响因子：
4.6
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