Key result
In vivo endotoxin administration significantly decreased aortic contractile responses and markedly impaired endothelium-dependent relaxation in rats and rabbits.
Why the study?
Does in vivo endotoxin administration impair vascular contraction and endothelium-dependent relaxation in rat and rabbit aorta?
Does in vivo endotoxin administration impair vascular contraction and endothelium-dependent relaxation in rat and rabbit aorta?
Endotoxemia induces basal, nonendothelial nitric oxide synthesis and impairs agonist-stimulated release of endothelium-derived relaxing factor, contributing to hemodynamic derangements.
Answers are grounded in this paper and cite their sources.
Endotoxin impairs vascular reactivity in animal sepsis models; hypothesis-generating for human septic shock mechanisms.
In order to determine whether endotoxemia induced generalized defects in vascular contraction and endothelium-dependent relaxation, we studied the effect of in vivo endotoxin administration in Sprague-Dawley rats and New Zealand White rabbits on endothelial and arterial smooth-muscle responses of isolated thoracic aorta in vitro. Endotoxin treatment significantly decreased contractile responses to phenylephrine (PE), angiotensin II (AII), serotonin (5-HT), and potassium chloride. This effect was not altered by indomethacin or endothelial denudation. Treatment of vessels with NG-nitro-L-arginine (NNLA), an inhibitor of arginine-dependent nitric oxide biosynthesis, or with methylene blue, an inhibitor of soluble guanylate cyclase, resulted in significant improvement of the contractile defect in endotoxin-treated vessels. The restorative effect of NNLA on contractile responses in endotoxin-treated aortic rings was similar in the presence or absence of an intact endothelium. Endothelium-dependent relaxation in response to acetylcholine, substance P, or the calcium ionophore A23187 was markedly impaired in vessels from endotoxin-treated rabbits, while endothelium-independent relaxation in response to nitroprusside was similar in both groups. These results suggest that endotoxemia both induces basal, nonendothelial nitric oxide synthesis and impairs the agonist-stimulated release of endothelium-derived relaxing factor (EDRF). These findings may have mechanistic importance in the hemodynamic derangements of endotoxemia.
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Umans et al. (1993) studied Endotoxemia. In vivo endotoxin administration vs. Control was evaluated on Endothelial and arterial smooth-muscle responses of isolated thoracic aorta in vitro. In vivo endotoxin administration significantly decreased aortic contractile responses and markedly impaired endothelium-dependent relaxation in rats and rabbits.
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