ISSN:
1860-1499
Keywords:
Nitric oxide synthase (NOS)
;
Endotoxin
;
Lung
;
Ultrastructure
;
In situ hybridization
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract To evaluate the relationship between pulmonary damage and the induction of nitric oxide synthase (NOS) in endotoxin shock, we injected 10mg/kg ofE. coli endotoxin intraperitoneally to Wistar male rats and observed the changes of the lung during the following 8h by electron microscopy, immunoelectron microscopy, and in situ hybridization. Morphological observation revealed infiltration of macrophages, aggregation of neutrophil in stasis in vascular lumens, and intraalveolar hemorrhage accompanied by epithelial damage. Endothelial constitutive NOS (ecNOS) was immunohistochemically localized in the endoplasmic reticulum of the endothelium of pulmonary arteries and in the cytoplasm of bronchial epithelial cells of control rats. After endotoxin administration, inducible NOS (iNOS) was detected in vascular endothelial cells, vascular smooth muscle cells, bronchial epithelial cells, bronchial smooth muscle cells, alveolar epithelial cells, and macrophages. Reverse transcription polymerase cham reaction (RTPCR) confirmed the expression of ecNOS mRNA and iNOS mRNA in the lung in endotoxin-treated rats and controls. In situ hybridization showed that ecNOS mRNA was expressed in vascular endothelial cells of pulmonary arteries in control rats. After endotoxin administration, iNOS mRNA was expressed in vascular endothelial cells. vascular smooth muscle cells, bronchial epithelial cells, alveolar epithelial cells, and macrophages that had infiltrated the alveolar and perivascular regions. After endotoxin administration, morphological changes and NO overproduction were observed, and it is concluded that NO may play an important role in maintaining the homeostasis of the bloodair barrier in pulmonary structures.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF01545768
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