2004PubMedRequires access

[Function of endothelin-1 in neurogenic pulmonary edema].

Guo-Xian Duan, Zhou Kai-shun, Chunxiu Zhao, You-Ling Jing, Yongqi Hu

Open publisher page 1 citations

Abstract

AIM: To investigate the role of endothelin-1 in the pathogenesis of neurogenetic pulmonary edema. METHODS: The levels of endothelin-1 in plasma and lung were measured in rats which suffered from diffuse brain injury on Marmarous' model. The changes of endothelin-1 in the lungs were also detected using an immunohistochemical method. RESULTS: After heavy diffuse brain injury in rats, the levels of endothelin-1 in plasma and lung began increasing at 1 hour, and peaked at 6 hour. Though a little declining at 24 hour, it maintained a higher level within 48 hours (P < 0.05). Pulmonary pathology showed that after brain injury there were congestion, swelling in pulmonary microvessels with broadened pulmonary interstitial tissue, and leucocyte infiltration was dominated by neutrophils and monocytes from 1 hour on, which peaked at 6 hour. More serious congestion, swelling and protein effusion in pulmonary alveoli were observed at both 24 h and 48 h. Immunohistochemically, endothelin-1 had more significant expression and higher levels of OD in the experimental groups than that in the control's, the most significance of which was at 6 hour. CONCLUSION: The inflammatory injury mechanism caused by endothelin-1 may play an important role in neurogenic pulmonary edema.

About this research paper

What this paper is about

AIM: To investigate the role of endothelin-1 in the pathogenesis of neurogenetic pulmonary edema. METHODS: The levels of endothelin-1 in plasma and lung were measured in rats which suffered from diffuse brain injury on Marmarous' model. The changes of endothelin-1 in the lungs were also detected using an immunohistochemical method. RESULTS: After heavy diffuse brain injury in rats, the levels of endothelin-1 in plasma and lung began increasing at 1 hour, and peaked at 6 hour. Though a little declining at 24 hour, it maintained a higher level within 48 hours (P < 0.05). Pulmonary pathology showed that after brain injury there were congestion, swelling in pulmonary microvessels with broadened pulmonary interstitial tissue, and leucocyte infiltration was dominated by neutrophils and monocytes from 1 hour on, which peaked at 6 hour. More serious congestion, swelling and protein effusion in pulmonary alveoli were observed at both 24 h and 48 h. Immunohistochemically, endothelin-1 had more significant expression and higher levels of OD in the experimental groups than that in the control's, the most significance of which was at 6 hour. CONCLUSION: The inflammatory injury mechanism caused by endothelin-1 may play an important role in neurogenic pulmonary edema.

Why it matters

OpenAlex reports 1 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

AIM: To investigate the role of endothelin-1 in the pathogenesis of neurogenetic pulmonary edema. METHODS: The levels of endothelin-1 in plasma and lung were measured in rats which suffered from diffuse brain injury on Marmarous' model. The changes of endothelin-1 in the lungs were also detected using an immunohistochemical method. RESULTS: After heavy diffuse brain injury in rats, the levels of endothelin-1 in plasma and lung began increasing at 1 hour, and peaked at 6 hour. Though a little declining at 24 hour, it maintained a higher level within 48 hours (P < 0.05). Pulmonary pathology showed that after brain injury there were congestion, swelling in pulmonary microvessels with broadened pulmonary interstitial tissue, and leucocyte infiltration was dominated by neutrophils and monocytes from 1 hour on, which peaked at 6 hour. More serious congestion, swelling and protein effusion in pulmonary alveoli were observed at both 24 h and 48 h. Immunohistochemically, endothelin-1 had more significant expression and higher levels of OD in the experimental groups than that in the control's, the most significance of which was at 6 hour. CONCLUSION: The inflammatory injury mechanism caused by endothelin-1 may play an important role in neurogenic pulmonary edema.

Key concepts: Medicine, Pulmonary edema, Endothelin 1, Edema, Endothelin receptor, Lung, Pathogenesis, Pathology

Related papers

Back to paper searchBrowse research topicsOriginal source
[Function of endothelin-1 in neurogenic pulmonary edema]. — Research Paper | ScholarLens