首页> 外文期刊>American Journal of Physiology >Chronic intermittent hypoxia impairs endothelium-dependent dilation in rat cerebral and skeletal muscle resistance arteries.
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Chronic intermittent hypoxia impairs endothelium-dependent dilation in rat cerebral and skeletal muscle resistance arteries.

机译:慢性间歇性缺氧会损害大鼠脑和骨骼肌阻力动脉的内皮依赖性舒张功能。

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The goal of the present study was to evaluate the effects of relatively short-term chronic intermittent hypoxia (CIH) on endothelial function of resistance vessels in the skeletal muscle and cerebral circulations. Sprague-Dawley rats were exposed to 14 days of CIH (10% fraction of inspired oxygen for 1 min at 4-min intervals, 12 h/day, n = 6). Control rats (n = 6) were housed under normoxic conditions. After 14 days, resistance arteries of the gracilis muscle (GA) and middle cerebral arteries (MCA) were isolated and cannulated with micropipettes, perfused and superfused with physiological salt solution, and equilibrated with 21% O2-5% CO2 in a heated chamber. The arteries were pressurized to 90 mmHg, and vessel diameters were measured via a video micrometer before and after exposure to ACh (10-7-10-4 M), sodium nitroprusside (10-6 M), and acute reduction of Po2 in the perfusate/superfusate (from 140 to 40 mmHg). ACh-induced dilations of GA and MCA from animals exposed to CIH were greatly attenuated, whereas responses to nitroprusside were similar to controls. Dilations of both GA and MCA in response to acute reductions in Po2 were virtually abolished in animals exposed to CIH compared with controls. These findings suggest that exposure to CIH reduces the bioavailability of nitric oxide in the cerebral and skeletal muscle circulations and severely blunts vasodilator responsiveness to acute hypoxia.
机译:本研究的目的是评估相对短期的慢性间歇性缺氧(CIH)对骨骼肌和脑循环阻力血管内皮功能的影响。将Sprague-Dawley大鼠暴露于14天的CIH中(10%的吸入氧气,每隔4分钟间隔1分钟,每天12小时,n = 6)。对照组(n = 6)置于常氧条件下。 14天后,分离并用微量移液管插管并擦拭细纹肌(GA)和大脑中部动脉(MCA)的阻力动脉,并用生理盐溶液灌注和灌注,并在加热室中用21%O2-5%CO2进行平衡。将动脉加压至90 mmHg,并在暴露于ACh(10-7-10-4 M),硝普钠(10-6 M)和急性减少Po2中的Po2之前和之后通过视频测微计测量血管直径。灌注液/过熔融液(140至40 mmHg)。 ACh诱导的暴露于CIH的动物的GA和MCA的扩增大大减弱,而对硝普钠的响应与对照组相似。与对照组相比,在暴露于CIH的动物中,GA和MCA对Po2急性减少的反应的扩张实际上被消除了。这些发现表明,暴露于CIH会降低一氧化氮在大脑和骨骼肌循环中的生物利用度,并严重钝化血管扩张剂对急性缺氧的反应能力。

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