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fMLP-stimulated neutrophils increase endothelial [Ca2+](i) and microvessel permeability in the absence of adhesion: role of reactive oxygen species.

Authors
Zhu-LK; Castranova-V; He-PN
Source
Am J Physiol, Heart Circ Physiol 2005 Mar; 288(3):H1331-H1338
NIOSHTIC No.
20026152
Abstract
Our previous study demonstrated that firm attachment of leukocytes to microvessel walls does not necessarily increase microvessel permeability ( Am J Physiol Heart Circ Physiol 283: H2420-H2430, 2002). To further understand the mechanisms of the permeability increase associated with leukocyte accumulation during acute inflammation, we investigated the direct relation of reactive oxygen species (ROS) release during neutrophil respiratory burst to changes in microvessel permeability and endothelial intracellular Ca2+ concentration ([Ca2+](i)) in intact microvessels. ROS release from activated neutrophils was quantified by measuring changes in chemiluminescence. When isolated rat neutrophils (2 x 10(6)/ml) were exposed to formyl-Met-Leu-Phe-OH ( fMLP, 10 muM), chemiluminescence transiently increased from 1.2 +/- 0.2 x 10(4) to a peak value of 6.7 +/- 1.0 x 10(4) cpm/min (n = 12). Correlatively, perfusing individual microvessels with fMLP-stimulated neutrophils in suspension (2 x 10(7)/ml) increased hydraulic conductivity (L-p) to 3.7 +/- 0.4 times the control value (n = 5) and increased endothelial [Ca2+](i) from 84 +/- 7 nM to a mean peak value of 170 +/- 7 nM. In contrast, perfusing vessels with fMLP alone did not affect basal Lp. Application of antioxidant agents, superoxide dismutase, vitamin C, or an iron chelator, deferoxamine mesylate, attenuated ROS release in fMLP-stimulated neutrophils and abolished increases in L-p. These results indicate that release of ROS from fMLP-stimulated neutrophils increases microvessel permeability and endothelial [Ca2+](i) independently from leukocyte adhesion and the migration process.
Keywords
Antioxidants; Antioxidation; Leukocytes; Circulatory-system; Blood-vessels
Contact
P. He, Dept. of Physiology and Pharmacology, School of Medicine, West Virginia Univ., Morgantown, WV 26506-9229
Publication Date
20050301
Document Type
Journal Article
Email Address
phe@hsc.wvu.edu
Fiscal Year
2005
NTIS Accession No.
NTIS Price
Issue of Publication
3
ISSN
0363-6135
NIOSH Division
HELD
Source Name
American Journal of Physiology: Heart and Circulatory Physiology
State
WV
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