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Suppression by isoproterenol of endothelial cell morphology and barrier function changes induced by platelet-activating factor

✍ Scribed by Ziqiang Ding; Shaohua Li; Meizheng Jiang; Zhongli Wu


Publisher
Springer
Year
1994
Tongue
English
Weight
560 KB
Volume
18
Category
Article
ISSN
0360-3997

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Excessive nitric oxide (NO) generated by hepatic cells in response to lipopolysaccharide (LPS) and inflammatory substances (e.g., platelet-activating factor [PAF]) is a key contributor to the pathophysiological outcomes observed in the liver during sepsis. In rats subjected to liver-focused endotoxe