Inhibition of P-selectin attenuates neutrophil-mediated myocardial dysfunction in isolated rat heart

The expression of P-selectin on postischemic endothelium after reperfusion has been shown to trigger neutrophil attachment and the subsequent inflammatory responses. Extensive studies have demonstrated that P-selectin is involved in the progression of neutrophil-mediated myocardial infarction and no...

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Bibliographic Details
Published in:European journal of pharmacology 1999-02, Vol.366 (2), p.271-279
Main Authors: Ohnishi, Masako, Yamada, Kazuto, Morooka, Shigeaki, Tojo, Shinichiro J
Format: Article
Language:English
Subjects:
Animals
Antibodies, Monoclonal - immunology
Antibodies, Monoclonal - pharmacology
Biological and medical sciences
Cardiology. Vascular system
Cardiovascular system
Coronary Circulation - drug effects
Heart
Heart - drug effects
Heart - physiopathology
Hemodynamics - drug effects
Humans
In Vitro Techniques
Ischemia and reperfusion injury
Male
Medical sciences
Miscellaneous
Myocardial Reperfusion Injury - physiopathology
Myocarditis. Cardiomyopathies
Neutrophil
Neutrophils - physiology
Oligosaccharides - pharmacology
P-selectin
P-Selectin - drug effects
P-Selectin - immunology
P-Selectin - metabolism
Pharmacology. Drug treatments
Rats
Rats, Wistar
Stunning
Ventricular Dysfunction, Left - physiopathology
Ventricular Function, Left - drug effects
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Summary:The expression of P-selectin on postischemic endothelium after reperfusion has been shown to trigger neutrophil attachment and the subsequent inflammatory responses. Extensive studies have demonstrated that P-selectin is involved in the progression of neutrophil-mediated myocardial infarction and no-reflow phenomenon. In the present study, we examined the effects of selectin inhibitors, sialyl Lewis X-oligosaccharide and anti-P-selectin monoclonal antibody, PB1.3 on neutrophil-dependent left ventricular dysfunction in isolated rat heart. The hearts were subjected to global ischemia for 20 min and then reperfused for 45 min with rat plasma in the presence of human neutrophils during the first 5 min of the reperfusion. Left ventricular developed pressure and other parameters of the left ventricular function deteriorated throughout the reperfusion period in a neutrophil-dependent manner. In contrast, the coronary flow was reduced early on (
ISSN:0014-2999
1879-0712
DOI:10.1016/S0014-2999(98)00923-6