Alterations in Vascular Reactivity in Sepsis and Endotoxemia

Parratt, J. R.

doi:10.1007/978-3-642-83737-1_36

Cited by 15 publications

(9 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Impaired responsiveness to vasoconstrictor catecholamines may contribute importantly to the unrelenting hypotension of septic shock (Parratt, 1989). Attenuation of pressor responses to catecholamines has been demonstrated in animal models of sepsis (Fink et al, 1985) and endotoxaemia (Parratt, 1973;Auclair & Schmitt, 1987).…”

Section: Introductionmentioning

confidence: 99%

Endotoxin‐induced impairment of vasopressor and vasodepressor responses in the pithed rat

Güç

Furman

Parratt

1990

British J Pharmacology

View full text Add to dashboard Cite

1 Effects of E. coli endotoxin on vascular responsiveness to a variety of agents were compared with those of the calcium channel blocking drug nicardipine in pithed rats. 2 Infusion of endotoxin (250pgkg -h-') produced a fall in mean arterial blood pressure (8 mmHg). A similar fall (11 mmHg) was seen in rats receiving nicardipine (1.0 mg kg-'). 3 Endotoxin impaired responsiveness to vasopressin, phenylephrine and cirazoline, producing a shift to the right in the dose-response curves without any change in the maximum response. Responsiveness to 5-hydroxytryptamine (5-HT) and to the a2-adrenoceptor agonists clonidine and BHT 933, was also impaired with a marked reduction in their maximum responses. The dose-response curve to the pressor effects of endothelin was not significantly modified. 4 Nicardipine produced a similar pattern of impairment of responsiveness to these agents to that produced by endotoxin. However, nicardipine also shifted the pressor dose-response curve to endothelin to the right with no significant alteration in its maximum response. 5 The pressor responses to endothelin and to 5-HT were, respectively, preceded and followed by dosedependent depressor responses, which were markedly reduced by endotoxin and nicardipine. 6 The concomitant infusion of arginine vasopressin (0.64iukg-'h-1) prevented endotoxin-induced hypotension and also prevented the impairment in responsiveness to cirazoline and to BHT 933. 7 The similarity of the pattern of impaired pressor responsiveness (except in relation to endothelin) and depressor responsiveness produced by endotoxin and nicardipine may be consistent with a common mechanism of action.

show abstract

Section: Introductionmentioning

confidence: 99%

Endotoxin‐induced impairment of vasopressor and vasodepressor responses in the pithed rat

Güç

Furman

Parratt

1990

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…Administration of LPS produces many of the cardiovascular features characteristic of septic shock, fsr example systemic vasodilatation, a diminished response to vasoconstrictors and hypotension and association with a high mortality rate (Parratt 1989). The first evidence indicating that an extraendothelial production of NO was involved in LPS-induced vascular hyporeactivity to norepinephrine (NE) arose from studies performed in aortae taken from endotoxin treated rats (Bigaud et al 1990;Julou-Schaeffer et al 1990).…”

Section: Introductionmentioning

confidence: 99%

COMPARISON OF RESPONSES TO AMINOGUANIDINE AND N^ω‐NITRO‐L‐ARGININE METHYL ESTER IN THE RAT AORTA

Yen

Chen

1995

Clin Exp Pharma Physio

View full text Add to dashboard Cite

1. We have compared the effect of aminoguanidine with that of N omega-nitro-L-arginine methyl ester on isolated thoracic aortic rings obtained either from endotoxin (lipopolysaccharide, 10 mg/kg, i.v. for 3 h) or vehicle (saline) treated rats. 2. Administration of endotoxin for 3 h resulted in a hypotension and a significant reduction of pressor responses to norepinephrine (1 micrograms/kg, i.v.) in the anaesthetized rat. 3. In intact rings obtained from vehicle treated rats, aminoguanidine (0.3 and 1 mmol/L) had no significant effect on acetylcholine-induced relaxation (10(-9)-10(-5) mol/L), whereas N omega-nitro-L-arginine methyl ester (0.3 mmol/L and 1 mmol/L) abolished that response, suggesting that aminoguanidine does not inhibit the activity of constitutive nitric oxide synthase. 4. Relaxation induced by L-arginine (10(-6)-10(-2) mol/L) was competitively inhibited by both aminoguanidine (0.3 mmol/L) and N omega-nitro-L-arginine methyl ester (0.3 mmol/L) in endothelium-denuded aortic rings obtained from endotoxin treated rats. 5. Three hours of endotoxaemia was associated with an impairment of contraction to norepinephrine (10(-9)-10(-6) mol/L) in the endothelium-denuded aorta ex vivo. This hyporeactivity to norepinephrine was partially restored by treatment of the vessels either with aminoguanidine (0.3 mmol/L) or with N omega-nitro-L-arginine methyl ester (0.3 mmol/L) in vitro. 6. These results in isolated thoracic aortae of the rat reinforce that aminoguanidine is a selective inhibitor of the inducible nitric oxide synthase, whereas N omega-nitro-L-arginine methyl ester is a non-selective inhibitor of both the inducible and constitutive nitric oxide synthase.

show abstract

“…The expression of inducible NO synthase (iNOS) and the production of large quantities of NO (1) contribute to circulatory failure (hypotension and vascular hyporeactivity to vasopressor agents) (2,3) and multiple organ dysfunction syndrome (4).…”

Section: Introductionmentioning

confidence: 99%

CD14 Glycoprotein Expressed in Vascular Smooth Muscle Cells

Choi

Lee

2004

J Pharmacol Sci

View full text Add to dashboard Cite

Abstract. The inducible nitric oxide synthase (iNOS) expression in vascular smooth muscle cells is an important factor for pathogenesis of septic shock or multiple organ dysfunction syndrome. The mechanisms of iNOS expression in such conditions are partly known. This study tried to clarify the signal transduction of lipopolysaccharide (LPS) single stimulation that induces iNOS mRNA and protein in vascular smooth muscle cells (VSMC). VSMC were primarily cultured from rat aorta. The concentrations of nitrite in culture media were measured by the Griess reaction. Western blottings and immunoreaction for iNOS, nuclear factor kB (NFkB) p65, and CD14 protein were performed. mRNAs of iNOS and tumor necrosis factor (TNF) a were analyzed by RT-PCR. Genistein inhibited LPS induced early phase nitrite production, while pyrrolidine dithiocarbamate (PDTC) inhibited nitrite production at a late phase. PDTC significantly reduced NFk B p65 and iNOS protein expression by LPS. TNFa mRNA expression by LPS was not detected in VSMC. Membranous CD14 glycoprotein was detected in VSMC and soluble CD14 glycoprotein was not detected in fetal bovine serum added in culture media. These results suggest that CD14 glycoprotein is present on the cell membranes of VSMC, a nonmyelomonocyte lineage, acting as an LPS receptor. Activations of tyrosine kinase and NFkB p65 are essential for iNOS expression by LPS single stimulation, while TNFa is not a concern to iNOS expression in VSMC.

show abstract

Alterations in Vascular Reactivity in Sepsis and Endotoxemia

Cited by 15 publications

References 29 publications

Endotoxin‐induced impairment of vasopressor and vasodepressor responses in the pithed rat

Endotoxin‐induced impairment of vasopressor and vasodepressor responses in the pithed rat

COMPARISON OF RESPONSES TO AMINOGUANIDINE AND N^ω‐NITRO‐L‐ARGININE METHYL ESTER IN THE RAT AORTA

CD14 Glycoprotein Expressed in Vascular Smooth Muscle Cells

Contact Info

Product

Resources

About

Alterations in Vascular Reactivity in Sepsis and Endotoxemia

Cited by 15 publications

References 29 publications

Endotoxin‐induced impairment of vasopressor and vasodepressor responses in the pithed rat

Endotoxin‐induced impairment of vasopressor and vasodepressor responses in the pithed rat

COMPARISON OF RESPONSES TO AMINOGUANIDINE AND Nω‐NITRO‐L‐ARGININE METHYL ESTER IN THE RAT AORTA

CD14 Glycoprotein Expressed in Vascular Smooth Muscle Cells

Contact Info

Product

Resources

About

COMPARISON OF RESPONSES TO AMINOGUANIDINE AND N^ω‐NITRO‐L‐ARGININE METHYL ESTER IN THE RAT AORTA