Vascular α-adrenoceptor blockade by E. coli endotoxin in the rat

Auclair, Marie-Claude; Svinareff, Pascal; Schmitt, Henri

doi:10.1016/0014-2999(86)90212-8

Cited by 23 publications

(6 citation statements)

References 5 publications

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“…One of the consequences of the administration of bacterial lipopolysaccharide (endotoxin) to experimental animals, or its release from Gram negative organisms in patients with sepsis, is impaired responsiveness to vasoconstrictor agents such as noradrenaline (Parratt 1973;Fink et al, 1985;Auclair et al, 1986;Evequoz et al, 1987) and to sympathetic nerve stimulation (Gray et al, 1990a;Guc et al, 1991;Tomikawa & Okabe, 1992). This reduced responsiveness, which also occurs in pithed animals (Guc et al, 1990;1992) and in blood vessels isolated from animals given endotoxin (Pomerantz et al, 1982;Wakabayashi et al, 1987;Bigaud et al, 1990) has been shown to be due mainly to the induction of nitric oxide synthase (NOS) and to a subsequent elevation of guanosine 3': 5'-cyclic monophosphate (cyclic GMP) Gray et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

The effect of endotoxin on sympathetic responses in the rat isolated perfused mesenteric bed; involvement of nitric oxide and cyclo‐oxygenase products

Fatehi‐Hassanabad

Furman

Parratt

1995

British J Pharmacology

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1 The effects of endotoxin on the vasoconstrictor responses to sympathetic nerve stimulation (SNS) were investigated in the rat isolated perfused mesenteric bed. 2 Rats received either saline (0.1 ml h-') or endotoxin (2.5 mg kg-' h-') intravenously for 4 h; the mesenteric beds were then isolated, perfused with Krebs and prepared for SNS (50 V, 3 ms,. 3 SNS caused a frequency-dependent vasoconstrictor response which was abolished by either tetrodotoxin (10-7 M), prazosin (2.4 x 10-7M) or guanethidine (2.4 x 10-7 M). 7 Both L-NAME (10-3 M) and indomethacin (10-5 M) restored responses to SNS in preparations from endotoxin-treated rats without modifying these responses in control preparations. However, coadministration of L-NAME and indomethacin markedly augmented responses in both control and endotoxin-treated preparations.8 The effects of L-NAME were reversed by addition of L-arginine (10-3 M). 9 The data suggest that endotoxin impairs the release of noradrenaline and that this effect is secondary to increased production of nitric oxide and prostanoids, possibly by the endothelium.

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Section: Introductionmentioning

confidence: 99%

The effect of endotoxin on sympathetic responses in the rat isolated perfused mesenteric bed; involvement of nitric oxide and cyclo‐oxygenase products

Fatehi‐Hassanabad

Furman

Parratt

1995

British J Pharmacology

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“…Plasma concentrations of angiotensin I1 are increased in endotoxemia and have been proposed as a cause of increased peripheral resistance in hypodynamic Nephrectomy and administration of angiotensin I1 antagonists do not affect the hemodynamic pattern of canine e n d o t~x e m i a ,~~ but inhibition of converting enzyme function has resulted in improved hepatosplanchnic flow in endotoxic pigs8' Catecholamines and increased sympathetic nervous system activity have also been proposed as causes of vasoconstriction," despite evidence that adrenergic responsiveness is markedly depressed in endotoxic shock. 82 Responsiveness is depressed to a more marked degree on the arterial side than the venous side, thus catecholamines may contribute to venous pooling." Hypercatab~lism'~ and pulmonary may also be exacerbated by increased activity of the sympathetic nervous system.…”

Section: Other Mdiatorsmentioning

confidence: 99%

Endotoxic Shock Part II: A Review of Treatment

Hardie¹,

Kruse-Elliott

1990

Veterinary Internal Medicne

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THE CLINICIAN faced with treating a patient with endotoxemia or gram-negative sepsis is currently limited primarily to the provision of supportive care. In part I of this review, we presented the cell types and mediators currently thought to be involved in the pathogenesis of endotoxic injury. Part I1 will review the numerous treatment methods under investigation and will indicate methods that are likely to become available in the future.A few cautions are in order when reviewing possible treatments for any shock condition, especially one as complex as endotoxemia. First, a vast number of treatments result in increased survival time, because they block one small part of the shock response, but do not prevent death. Most studies that report increased "survival" use the survival rate at one to three days as their end point. This end point is not really valid, because delayed deaths can occur up to at least seven days after the induction of shock.' Finally, many studies use small numbers of animals because of constraints on survival studies. Before a treatment can truly be declared effective, it should result in a statistically significant increased survival rate at seven days (termed "increased long-term survival").Second, the majority of treatments for endotoxemia involve modification of body defense systems in some From the

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“…Loss of responsiveness to vasoconstrictors is a hallmark of endotoxic shock in humans. Decreased responsiveness to o-adrenoceptor agonists has been documented in vivo during endotoxic shock in rats (Parratt, 1973;Fink et al, 1985;Auclair et al, 1986) and in vitro in blood vessels isolated from rats during endotoxininduced shock (Pomerantz et al, 1982;Wakabayashi et al, 1987). Desensitization of x-adrenoceptors has been suggested as a possible mechanism (Zhou & Jones, 1990).…”

Section: Introductionmentioning

confidence: 99%

“…Although this might be explained by a decreased sensitivity of postjunctional oc,-adrenoceptors (Auclair et al, 1986;Carcillo et al, 1988;Bigaud et al, 1990), an inhibition of neurotransmitter, i.e. noradrenaline (NA), re-' Author for correspondence.…”

Section: Introductionmentioning

confidence: 99%

Endotoxin impairs the response of rabbit mesenteric artery to electrical stimulation via a prejunctional mechanism

Tomikawa¹,

Okabe²

1992

British J Pharmacology

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1 The effect of E. coli lipopolysaccharide (LPS) on sympathetic neuro-effector transmission was studied in the rabbit mesenteric artery. The experiments were performed on artery rings isolated 5 or 20 h after intravenous treatment with LPS or saline as well as on artery rings isolated from non-treated rabbits (for assessment of the effect of in vitro preincubation with LPS). In most experiments, neural elements in the arteries were stimulated electrically (10 V, 2 ms, 1-32 Hz). 2 Preincubation with LPS (10 fg ml-') for 5 or 20 h had no effect on the contraction responses of endothelium-intact artery rings to electrical stimulation. In contrast, in vivo intravenous pretreatment with LPS (10 Sg) led to an inhibition of the contraction; LPS elicited this effect when injected 20 h, but not 5 h, before the experiment. The effect of LPS was eliminated in artery rings isolated from animals receiving an inhibitor of protein synthesis (actinomycin D or cycloheximide) before treatment with LPS. LPS (injected 20 h before the experiment) had no effect on the concentration-response curves for exogenous noradrenaline and tyramine in endothelium-intact artery rings. 3 The inhibition of electrically induced contractions produced by LPS treatment in endothelium-intact artery rings was attenuated by atropine and yohimbine, but not by phentolamine. Yohimbine plus atropine restored the depressed contraction to the normal level. Clonidine and acetylcholine mimicked the effect of LPS in endothelium-intact artery rings isolated from saline-treated animals. 4 When steady-state contractions were induced by 5 min of stimulation at 16 Hz, acetylcholine or clonidine reduced the contraction in endothelium-denuded artery rings from both saline-treated rabbits and animals receiving LPS 20 h before the experiment. The reduction produced by acetylcholine or clonidine of the contraction in artery rings from LPS-treated rabbits was significantly greater than in artery rings from saline-treated animals. 5 These results suggest that treatment of rabbits with LPS inhibits noradrenaline release from sympathetic nerve endings via increased sensitivity of both prejunctional inhibitory muscarinic receptors and x2-adrenoceptors in mesenteric arteries. They also suggest that the effect of LPS is independent of endothelial cells but linked to protein synthesis.

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Vascular α-adrenoceptor blockade by E. coli endotoxin in the rat

Cited by 23 publications

References 5 publications

The effect of endotoxin on sympathetic responses in the rat isolated perfused mesenteric bed; involvement of nitric oxide and cyclo‐oxygenase products

The effect of endotoxin on sympathetic responses in the rat isolated perfused mesenteric bed; involvement of nitric oxide and cyclo‐oxygenase products

Endotoxic Shock Part II: A Review of Treatment

Endotoxin impairs the response of rabbit mesenteric artery to electrical stimulation via a prejunctional mechanism

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