Brain injury impairs ATP-sensitive K+ channel function in piglet cerebral arteries
Brain injury impairs ATP-sensitive K+ channel function in piglet cerebral arteries
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DOI：
10.1161/01.str.28.11.2273
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发表时间：
1997-11-01
期刊：
影响因子：
8.3
通讯作者：
Armstead, WM
中科院分区：
文献类型：
--
作者：
Armstead, WM
背景和目的创伤是婴幼儿死亡的主要原因，颅脑损伤的死亡率增加。以往的研究表明，软膜动脉收缩，并对几个一氧化氮（NO）依赖性扩张刺激的反应钝化后，流体冲击损伤（FPI）的新生猪。血管肌肉的膜电位是血管张力的主要决定因素，而K+通道的活性是膜电位的主要调节者。最近的数据表明，NO释放剂硝普钠（SNP）和S-亚硝基-N-乙酰青霉胺（SNAP）和8-溴-cGMP通过ATP敏感性K+通道（K-ATP）激活引起舒张。本研究旨在探讨FPI对K-ATP通道功能的影响。方法氯醛糖麻醉的新生猪，配备一个封闭的颅窗连接到一个由一个充满盐水的圆柱形水库和一个金属摆锤组成的打击装置。通过使摆锤撞击气缸上的活塞，产生中度脑损伤（1.9至2.1 atm）。用视频显微测量仪测量软膜动脉直径。数据采用重复测量方差分析。一个阿尔法水平的P
Background and Purpose Traumatic injury is the leading cause of death for infants and children, and mortality is increased with head injury. Previous studies have shown that pial arteries constricted and that responses to several nitric oxide (NO)-dependent dilator stimuli were blunted after fluid percussion injury (FPI) in newborn pigs. Membrane potential of vascular muscle is a major determinant of vascular tone, and activity of K+ channels is a major regulator of membrane potential. Recent data show that the NO releasers sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine (SNAP) and 8-bromo-cGMP elicit dilation via ATP-sensitive K+ channel (K-ATP) activation. The present study was designed to investigate the effect of FPI on K-ATP channel function.Methods Chloralose-anesthetized newborn pigs equipped with a closed cranial window were connected to a percussion device that consisted of a saline-filled cylindrical reservoir and a metal pendulum. Brain injury of moderate severity (1.9 to 2.1 atm) was produced by allowing the pendulum to strike a piston on the cylinder. Pial artery diameter was measured with a video microscaler. Data were analyzed by repeated measures ANOVA. An alpha level of P