TY - JOUR
T1 - Endotoxin in vivo impairs endothelium-dependent relaxation of canine arteries in vitro
AU - Wylam, M. E.
AU - Samsel, R. W.
AU - Umans, J. G.
AU - Mitchell, R. W.
AU - Leff, A. R.
AU - Schumacker, P. T.
N1 - Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 1990
Y1 - 1990
N2 - 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.
AB - 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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U2 - 10.1164/ajrccm/142.6_Pt_1.1263
DO - 10.1164/ajrccm/142.6_Pt_1.1263
M3 - Article
C2 - 2252242
AN - SCOPUS:0025633686
SN - 0003-0805
VL - 142
SP - 1263
EP - 1267
JO - American Review of Respiratory Disease
JF - American Review of Respiratory Disease
IS - 6
ER -