Endothelium-dependent relaxation is depressed at the macro- and microcirculatory levels during sepsis.

Endothelium-dependent relaxation is depressed at the macro- and microcirculatory levels during sepsis.
复制标题

脓毒症期间,宏观和微循环水平上的内皮依赖性舒张受到抑制。

DOI:
10.1152/ajpregu.1995.269.5.r988
复制
发表时间:
1995
期刊:
The American journal of physiology.
影响因子:
--
通讯作者:
Chaudry,IH
Chaudry,IH
中科院分区:
--
文献类型:
--
作者:
Wang,P;Ba,ZF;Chaudry,IH

文献摘要

被引文献

相似文献

本研究的目的是确定是否内皮源性一氧化氮(NO)的生产减少在大循环和微循环水平在败血症。为了检验这一点,通过盲肠结扎和穿孔(CLP)使大鼠经受脓毒症。CLP后5 h(即,高动力败血症中点)或假手术时,分离主动脉和上级肠系膜动脉。对内皮依赖性血管扩张剂乙酰胆碱(ACh)和内皮非依赖性血管扩张剂硝酸甘油(NTG)的反应进行了测定。在其他研究中,在CLP后5或20小时(低动力性脓毒症)分离小肠。在离体肠中测定对ACh和NTG的反应。结果表明,CLP后5小时,主动脉和上级肠系膜动脉的内皮依赖性舒张功能均受到抑制。与此相反,NTG引起的舒张作用无显著差异。此外,乙酰胆碱诱导的血管舒张在离体小肠CLP后5和20小时下降,而没有任何显着改变NTG诱导的松弛。由于研究表明,ACh诱导的舒张主动脉在CLP后20小时减少,可以得出结论,内皮源性NO释放在脓毒症的高动力和低动力阶段受到抑制,不仅在大动脉,而且在微循环水平。
The objective of this study was to determine whether endothelium-derived nitric oxide (NO) production is reduced at the macrocirculatory and microcirculatory levels during sepsis. To examine this, rats were subjected to sepsis by cecal ligation and puncture (CLP). At 5 h after CLP (i.e., midpoint of hyperdynamic sepsis) or sham operation, the aorta and superior mesenteric artery were isolated. Responses to an endothelium-dependent vasodilator, acetylcholine (ACh), and an endothelium-independent vasodilator, nitroglycerin (NTG), were determined. In additional studies, the small intestine was isolated 5 or 20 h (hypodynamic sepsis) after CLP. Responses to ACh and NTG were determined in the isolated intestine. The results indicate that endothelium-dependent relaxation in both the aorta and superior mesenteric artery was depressed at 5 h after CLP. In contrast, there was no significant difference in the relaxation induced by NTG. Moreover, ACh-induced vascular relaxation in the isolated small intestine decreased at 5 and 20 h post-CLP without any significant alterations in NTG-induced relaxation. Since studies have shown that ACh-induced relaxation in the aorta is reduced at 20 h after CLP, it could be concluded that endothelium-derived NO release is depressed during hyperdynamic and hypodynamic stages of sepsis, not only in large arteries, but also at the microcirculatory level.