EDRF as a possible mediator of sepsis-induced arteriolar dilation in skeletal muscle.
EDRF as a possible mediator of sepsis-induced arteriolar dilation in skeletal muscle.
复制标题
EDRF 作为脓毒症引起的骨骼肌小动脉扩张的可能介质。
DOI：
10.1152/ajpheart.1992.262.3.h880
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Harris,PD
中科院分区：
文献类型：
--
作者：
Lübbe,AS;Garrison,RN;Cryer,HM;Alsip,NL;Harris,PD
血管内皮细胞在体内和体外影响微血管直径，并参与脓毒症的宿主防御机制。我们研究了高心排菌血症（HOB）和低心排活大肠杆菌败血症（LOS）时骨骼肌小动脉扩张是否由内皮源性舒张因子（EDRF）介导。对苯二酚（HQ）对EDRF的局部化学阻断显著减弱了乙酰胆碱诱导的小动脉扩张。HQ还防止HOB期间大鼠提睾肌中的大微动脉（55-135微米）收缩和小微动脉（6-22微米）扩张。在LOS中，HQ也可预防小动脉扩张，但仅在血压与基线相比无变化的早期。HQ在LOS期间不改变大微动脉收缩。我们的结论是，菌血症期间骨骼肌中的小微动脉血管扩张至少部分由EDRF介导。由于EDRF不能介导大的小动脉收缩，并且由于HQ在HOB期间使大的小动脉收缩钝化，我们现在怀疑HQ也至少部分地干扰一些大的小动脉血管收缩机制，可能是白三烯或内皮衍生的收缩因子，其介导HOB期间的大的小动脉收缩。我们的数据还表明，LOS期间大的小动脉收缩部分是由HQ不受影响的因素介导的。内皮细胞在骨骼肌对活大肠杆菌的微循环反应中起重要作用。大肠杆菌败血症通过一种以上的机制。
Vascular endothelial cells influence microvessel diameters in vivo and in vitro and participate in host-defense mechanisms during sepsis. We examined whether small arteriole dilation in skeletal muscle during high cardiac output bacteremia (HOB) and low cardiac output live Escherichia coli sepsis (LOS) is mediated by an endothelium-derived relaxing factor (EDRF). Local chemical blockade of EDRF by hydroquinone (HQ) substantially blunted acetylcholine-induced dilation of small arterioles. HQ also prevented large arteriole (55-135 microns) constriction and small arteriole (6-22 microns) dilation in the cremaster muscle of rats during HOB. In LOS, small arteriole dilation was also prevented by HQ but only during the early period when blood pressure was unchanged from baseline. HQ did not alter large arteriole constriction during LOS. We conclude that small arteriole vasodilation in skeletal muscle is mediated at least in part by EDRF during bacteremia. Because EDRF cannot mediate large arteriole constriction and because HQ blunted large arteriole constriction during HOB, we now suspect that HQ also interferes at least in part with some large arteriole vasoconstrictor mechanism, possibly leukotrienes or an endothelium-derived constricting factor, which mediates large arteriole constriction during HOB. Our data also suggest that large arteriole constriction during LOS is partly mediated by factors that are unaffected by HQ. The endothelium appears to play an important role in the microcirculatory responses of skeletal muscle to live E. coli sepsis through more than one mechanism.