ENDOTOXIN INVIVO IMPAIRS ENDOTHELIUM-DEPENDENT RELAXATION OF CANINE ARTERIES INVITRO

被引:96
作者
WYLAM, ME [1 ]
SAMSEL, RW [1 ]
UMANS, JG [1 ]
MITCHELL, RW [1 ]
LEFF, AR [1 ]
SCHUMACKER, PT [1 ]
机构
[1] UNIV CHICAGO, NEPHROL SECT, CHICAGO, IL 60637 USA
来源
AMERICAN REVIEW OF RESPIRATORY DISEASE | 1990年 / 142卷 / 06期
关键词
D O I
10.1164/ajrccm/142.6_Pt_1.1263
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
We studied the effect of endotoxin administration in vivo on arterial smooth muscle responses in vitro, testing the hypotheses that endotoxin augments adrenergic vasoconstriction and impairs endothelium-dependent vascular relaxation. Ten mongrel dogs were anesthetized and mechanically ventilated. Five received a bolus infusion of Escherichia coli endotoxin (5 mg/kg), and the remainder received a sham infusion. After 4 to 5 h, the anesthetized dogs were rapidly exsanguinated, and femoral, renal, and superior mesenteric arteries were removed. Arterial rings were mounted on force transducers in organ baths; contraction to phenylephrine or potassium-substituted Krebs-Henseleit solution (KCl), and relaxation to nitroprusside or acetylcholine were studied. Smooth muscle contractions to phenylephrine or KCl were similar between sham and endotoxin for each agonist. Also, nitroprusside-elicited relaxation from half-maximal phenylephrine-elicited contraction was similar. However, relaxation elicited by acetylcholine was markedly impaired in vessels from endotoxin-treated dogs. The negative log molar concentration of acetylcholine producing 50% relaxation for femoral arteries was 7.38 ± 0.11 (endotoxin) versus 8.09 ± 0.12 (control, p = 0.002), for renal arteries it was 6.71 ± 0.33 (endotoxin) versus 7.81 ± 0.18 (control, p = 0.019), and for mesenteric arteries it was 7.27 ± 0.03 (endotoxin) versus 7.95 ± 0.15 (control, p = 0.002). These results demonstrate that endotoxin treatment impairs endothelium-dependent relaxation of canine arteries in vitro. The data suggest that vascular changes in endotoxemia are accompanied by alteration in endothelial cell function, perhaps through altered endothelial production of vasodilatory mediators.
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页码:1263 / 1267
页数:5
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