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Cardiovascular Research 1998 38(1):6-15; doi:10.1016/S0008-6363(98)00022-4
© 1998 by European Society of Cardiology
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Copyright © 1998, European Society of Cardiology

The role of inducible nitric oxide synthase in cardiac allograft rejection

Paul J. Cannona,*, Xiaochun Yanga, Matthias J. Szabolcsc, Stefano Ravallia, Robert R. Sciaccaa and Robert E. Michlerb

aDepartment of Medicine, Columbia University College of Physicians and Surgeons, New York, NY, USA
bDepartment of Surgery, Columbia University College of Physicians and Surgeons, New York, NY, USA
cDepartment of Pathology, Columbia University College of Physicians and Surgeons, New York, NY, USA

* Corresponding author. Department of Medicine, Division of Cardiology, Columbia University, 630 West 168th Street, New York, NY 10032, USA. Tel.: +1 (212) 305-9052; Fax: +1 (212) 305-4648.

Received 16 October 1997; accepted 30 December 1997

The first 150 words of the full text of this article appear below.

Cardiac transplantation is an effective therapy for end-stage heart failure with one and five year survival rates about 80% and 65% respectively [1]. Despite these good results, cardiac allograft rejection remains a problem which produces impaired ventricular performance and death of cardiac myocytes ultimately causing congestive heart failure, low cardiac output, hypotension and reduced pressor responses to catecholamines. Chronic allograft rejection also results in the development of transplant-associated coronary atherosclerosis, a vasculopathy that produces myocardial ischemia, infarction and sudden death and is the leading cause of death in cardiac transplant recipients after the first year [2]. Although there is a large body of evidence concerning the immunological interactions involved in cardiac allograft rejection, knowledge concerning the cellular and biochemical mechanisms responsible for contractile dysfunction and for death of heart muscle cells remains incomplete. Since an inflammatory reaction in the myocardium is an intrinsic component of the pathological changes . . . [Full Text of this Article]


   1 NO synthesis
 

   2 iNOS induction in cardiac allograft rejection
 

   3 iNOS in transplant vasculopathy
 

   4 Relationships of NO, cytokines and cellular immune responses in cardiac allograft rejection
 

   5 iNOS and ventricular contractile function
 

   6 iNOS and cardiac myocyte death
 

   7 Necrosis and apoptosis
 

   8 Apoptosis and iNOS expression in cardiac allograft rejection
 

   9 iNOS expression in myocardial infarction and cardiomyopathy
 

   10 Possible therapeutic implications in allograft rejection and other cardiac disorders
 

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