Vascular smooth muscle contractile function is impaired during early and late stages of sepsis.
Vascular smooth muscle contractile function is impaired during early and late stages of sepsis.
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DOI：
10.1006/jsre.1994.1089
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发表时间：
1994-06
期刊：
影响因子：
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通讯作者：
S. H. Wurster;P. Wang;R. Dean;I. Chaudry
中科院分区：
文献类型：
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作者：
S. H. Wurster;P. Wang;R. Dean;I. Chaudry
虽然血管平滑肌收缩力受损发生在多微生物脓毒症的晚期，但尚不清楚这是否也发生在脓毒症的早期，如果是这样，是否有不同的机制负责这种平滑肌功能障碍。为了确定这一点，通过盲肠结扎和穿孔（CLP）使大鼠经受脓毒症。CLP或假手术后，所有动物立即接受3 ml/100 g体重生理盐水。然后在CLP后5、10或35小时（CLP后5-10小时，早期脓毒症; CLP后35小时，晚期脓毒症）处死脓毒症和假手术大鼠，并制备主动脉环用于使用器官室技术的收缩研究。在有或没有完整内皮的环中测定去甲肾上腺素（NE，10（-9）至10（-5）M;受体介导过程）和KCl（7.5至90 mM;非受体介导）的剂量反应收缩。内皮细胞的去除通过对内皮依赖性血管扩张剂乙酰胆碱的反应没有松弛来证实。结果表明，NE和KCl诱导的血管收缩在CLP后5小时没有改变。然而，在CLP后10小时，血管收缩力显着下降，在内皮完整的环。CLP后10小时去除内皮素可使NE和KCl引起的收缩恢复到假手术水平。与此相反，平滑肌收缩功能障碍，观察到在晚期脓毒症（35小时后CLP），没有恢复内皮细胞的去除。因此，在早期脓毒症中观察到的平滑肌损伤是由于脓毒症内皮释放的介质所致。（250字处删节）
Although impairment of vascular smooth muscle contractility occurs during the late stages of polymicrobial sepsis, it is not known whether this also occurs in early stages of sepsis and, if so, whether different mechanisms are responsible for such smooth muscle dysfunction. To determine this, rats were subjected to sepsis by cecal ligation and puncture (CLP). Immediately following CLP or sham operation, all animals received 3 ml/100 g body wt normal saline. Septic and sham rats were then sacrificed at 5, 10, or 35 hr after CLP (5-10 hr post-CLP, early sepsis; 35 hr post-CLP, late sepsis), and aortic rings were prepared for contraction studies using organ chamber technique. Dose-response contractions to norepinephrine (NE, 10(-9) to 10(-5) M; receptor-mediated process) and KCl (7.5 to 90 mM; non-receptor mediated) were determined in rings with or without intact endothelium. Endothelial cell removal was confirmed by the absence of relaxation in response to an endothelium-dependent vasodilator, acetylcholine. The results indicate that NE- and KCl-induced vascular contractions were not altered at 5 hr after CLP. At 10 hr post-CLP, however, vascular contractility decreased markedly in the endothelium intact rings. Endothelium removal at 10 hr after CLP restored the contraction induced by NE and KCl to sham levels. In contrast, the smooth muscle contractile dysfunction, observed during late sepsis (35 hr post-CLP), was not restored by the removal of endothelium. Thus, the smooth muscle impairment, observed in early sepsis, is due to mediators released from septic endothelium.(ABSTRACT TRUNCATED AT 250 WORDS)