Cardiomyopathy: a role for nitric oxide?
The negative inotropism, myocardial dilatation and cytotoxicity in inflammatory heart disorders may be due to increased generation of nitric oxide (NO) by immunological induction of a high output NO pathway. This short review discusses the initial experiments which lead to this hypothesis, and evaluates data that this pathway exists in animal and human cardiomyopathic disorders. It is proposed that manipulation of this pathway may prove to be beneficial in patients with these disorders.
de Belder
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Department of Cardiology, King's College Hospital, London, UK.
Moncada
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D000208:Acute Disease; D000818:Animals; D009202:Cardiomyopathies / Q000201:enzymology / Q000378:metabolism* / Q000503:physiopathology; D002311:Cardiomyopathy, Dilated / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D004731:Endotoxins / Q000097:blood; D004790:Enzyme Induction; D006084:Graft Rejection / Q000378:metabolism; D006168:Guinea Pigs; D006321:Heart / Q000503:physiopathology; D016027:Heart Transplantation; D006801:Humans; D009205:Myocarditis / Q000378:metabolism; D009206:Myocardium / Q000201:enzymology; D009569:Nitric Oxide / Q000096:biosynthesis / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000096:biosynthesis; D051381:Rats
D016207:Cytokines; D004731:Endotoxins; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase