Lack of direct endotoxin-induced vasoactive effects on isolated skeletal muscle arterioles.
Lack of direct endotoxin-induced vasoactive effects on isolated skeletal muscle arterioles.
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对分离的骨骼肌小动脉缺乏直接内毒素诱导的血管活性作用。
DOI：
10.1097/00024382-199503000-00010
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Hill,MA
中科院分区：
文献类型：
--
作者：
Glembot,TM;Britt,LD;Hill,MA
感染性休克仍然是重症监护病房死亡的主要原因。本研究旨在确定内毒素是否对周围血管阻力的主要决定因素——骨骼肌小动脉产生直接影响。从雄性Sprague-Dawley大鼠中分离出一级细动脉，用玻璃微移液管插管，在生理盐水溶液中灌注，使其在没有腔内流动的情况下实现自发的基底张力。在暴露于2.5 [mu] g/mL肠炎沙门氏菌内毒素（ET） 1-2小时前后评估苯肾上腺素反应性。基底直径（ET前为91+/-5 [mu] m， ET后为98+/-5 [mu] m）和苯肾上腺素反应性均无变化。体内暴露于ET (15 mg/kg) 1小时后基底张力没有变化，但在全身ET 4小时后收获的小动脉张力增加(无ET时为43+/-4%，有ET时为57+/-3%，p<。05)。为了确定上游导管血管是否释放了导致骨骼肌小动脉血管扩张的因子，我们将分离的血管化小动脉串联到1厘米的主动脉段，并在没有和2.5 [mu] g/mL ET的情况下进行灌注。观察到小动脉基底直径从ET前的94+/-14 [mu] m增加到ET后的120+/-17 [mu] m （p< 0.05）。05)。这些研究表明，ET对孤立的血管化骨骼肌小动脉没有直接影响，并且从上游动脉床释放出与一氧化氮不一致的血管舒张物质。
Septic shock continues to be a major cause of mortality in the intensive care unit. This study was conducted to determine if endotoxin exerts a direct effect on the major determinant of peripheral vascular resistance, skeletal muscle arterioles. First order cremasteric arterioles were isolated from male Sprague-Dawley rats, cannulated with glass micropipettes, superfused in physiologic saline solution, and allowed to achieve spontaneous basal tone in the absence of intraluminal flow. Phenylephrine responsiveness was assessed before and after exposure to 2.5 [mu] g/mL Salmonella enteritidis endotoxin (ET) for 1-2 h. There was no change in either basal diameter (91+/-5 [mu] m before ET and 98+/-5 [mu] m after ET) or phenylephrine responsiveness. In vivo exposure to ET (15 mg/kg) resulted in no change in basal tone at 1 h, however increased tone was observed in arterioles harvested after 4 h of systemic ET (43+/-4% without ET and 57+/-3% with, p<. 05). To determine if upstream conduit vessels released factors responsible for the vasodilation of skeletal muscle arterioles, isolated cannulated cremasteric arterioles were connected in series to a 1 cm segment of aorta and superfused without and with 2.5 [mu] g/mL ET. An increase in basal diameter was observed in arterioles from 94+/-14 [mu] m before ET to 120+/-17 [mu] m after ET (p<. 05). These studies demonstrate that ET has no direct effect on isolated cannulated skeletal muscle arterioles, and that a vasodilating substance not consistent with nitric oxide is released from the upstream arterial bed.