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Am J Physiol Heart Circ Physiol 284: H10-H16, 2003; doi:10.1152/ajpheart.00401.2002
0363-6135/03 $5.00
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Vol. 284, Issue 1, H10-H16, January 2003

TRANSLATIONAL PHYSIOLOGY
Myocardial fibrosis blunts nitric oxide synthase-related preload reserve in human dilated cardiomyopathy

Jean G. F. Bronzwaer1,2, Christophe Heymes3, Cees A. Visser1,2, and Walter J. Paulus2

1 VU-University Medical Center and 2 Institute for Cardiovascular Research-VU, Vrije Universiteit, 1081 HV Amsterdam, The Netherlands; and 3 Unité 127, Hôpital Lariboisière, Institut National de la Santé et de la Recherche Médicale, F-75475 Paris, France

The purpose of the study was to investigate interactions between myocardial nitric oxide synthase (NOS) and myocardial fibrosis, both of which determine left ventricular (LV) preload reserve in patients with nonischemic dilated cardiomyopathy (DCM). In previous animal experiments, chronic inhibition of NOS induced myocardial fibrosis and limited LV preload reserve. Twenty-eight DCM patients underwent LV catheterization, balloon caval occlusions (BCO; n = 8), intracoronary substance P infusion (n = 8), and procurement of LV endomyocardial biopsies for determinations of collagen volume fraction (CVF), of gene expression of NOS2, NOS3, heme oxygenase (HO)-1, and TNF-alpha , and of NOS2 protein. CVF was unrelated to the intensity of NOS2, NOS3, HO-1, or TNF-alpha gene expression or of NOS2 protein expression. Preload recruitable LV stroke work (PR-LVSW) correlated directly with NOS2 gene expression (P = 0.001) and inversely with CVF (P = 0.04). High CVF (>10%) reduced baseline LVSW and PR-LVSW at each level of NOS2 gene expression. In DCM, myocardial fibrosis is unrelated to the intensity of myocardial gene expression of NOS, antioxidative enzymes (HO-1), or cytokines (TNF-alpha ) and blunts NOS2-related recruitment of LV preload reserve.

collagen; diastole; myocardial contraction


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