The mechanism of vascular leakage induced by leukotriene E4. Endothelial contraction.

Paper

The mechanism of vascular leakage induced by leukotriene E4. Endothelial contraction.

Published 1987 · I. Joris, G. Majno, E. Corey

The American journal of pathology

Q1 SJR score

185

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2

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Abstract

This study identifies the microvascular target of leukotriene E4 (LTE4) by vascular labeling with carbon black and establishes the mechanism of its action at the cellular level by electron microscopy. LTE4 and its tripeptide precursor, leukotriene C4 (LTC4) were injected subcutaneously in guinea pigs. With LTE4, venular labeling was intense at 1000 and 100 ng and slight at 10 ng, with extinction at 1 ng. LTC4 induced a ring of labeled venules around a blank central area, suggestive of vasospasm. The nonpeptidyl leukotriene LTB4 induced no labeling. Histamine (1000 ng) induced an area of vascular labeling about equal to that by 1000 ng LTE4, but the labeling of individual venules was more intense. By electron microscopy, LTE4 was found to induce gaps in the endothelium of the venules; the endothelial cells adjacent to the gaps bulged into the lumen and showed wrinkled nuclei, consistent with cellular contraction. This ultrastructural evidence suggests that LTE4 increases vascular permeability by contraction of endothelial cells selectively, in the postcapillary venules, as was previously demonstrated for other inflammatory mediators, including histamine, serotonin, and bradykinin.

Non-RCT

Animal Study

Highly Cited

Study Snapshot

Leukotriene E4 increases vascular permeability by selectively contracting endothelial cells in postcapillary venules, similar to other inflammatory mediators like histamine, serotonin, and bradykinin.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

The mechanism of vascular leakage induced by leukotriene E4. Endothelial contraction.

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References

Evidence that prolonged histamine suffusions produce transient increases in vascular permeability subsequent to the formation of venular macromolecular leakage sites. Proof of the Majno-Palade hypothesis.

Prolonged histamine suffusions produce transient increases in vascular permeability due to the formation of venular macromolecular leakage sites, supporting the Majno-Palade hypothesis.

In vivo metabolism of leukotriene C4 in man: urinary excretion of leukotriene E4.

Leukotriene C4 is mainly excreted in urine, with 13% of administered radioactivity being excreted as leukotriene E4, in male volunteers.

Microvascular pericytes contain muscle and nonmuscle actins

Pericytes possess both muscle and nonmuscle actins, suggesting they may represent the capillary and venular correlate of smooth muscle cells.

The effect of ethchlorvynol on cultured endothelial cells. A model for the study of the mechanism of increased vascular permeability.

Ethchlorvynol causes pulmonary edema by disrupting the integrity of endothelial cell structures, leading to gaps between cells and causing reversible vascular permeability.

Contractile proteins in pericytes. II. Immunocytochemical evidence for the presence of two isomyosins in graded concentrations

Pericytes contain essential contraction proteins in higher concentration than other cells in the microvasculature, except smooth muscle cells.

Citations

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