Reduced Nitric Oxide Production and Altered Myocardial Metabolism During the Decompensation of Pacing-Induced Heart Failure in the Conscious Dog

The aim of the present study was to determine whether cardiac nitric oxide (NO) production changes during the progression of pacing-induced heart failure and whether this occurs in association with alterations in myocardial metabolism. Dogs (n=8) were instrumented and the heart paced until left vent...

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Bibliographic Details
Published in:Circulation research 1998-11, Vol.83 (10), p.969-979
Main Authors: Recchia, Fabio A, McConnell, Patrick I, Bernstein, Robert D, Vogel, Traci R, Xu, Xiaobin, Hintze, Thomas H
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Blood Pressure - physiology
Carbon Dioxide - metabolism
Cardiology. Vascular system
Consciousness
Diastole - physiology
Dogs
Fatty Acids, Nonesterified - pharmacokinetics
Glucose - pharmacokinetics
Heart
Heart Failure - metabolism
Heart failure, cardiogenic pulmonary edema, cardiac enlargement
Lactic Acid - pharmacokinetics
Male
Medical sciences
Muscle Fibers, Skeletal - enzymology
Myocardium - cytology
Myocardium - metabolism
Nitric Oxide - biosynthesis
Nitric Oxide Synthase - metabolism
Nitric Oxide Synthase Type II
Nitroarginine
Oxygen Consumption - physiology
Pacemaker, Artificial
Respiration
Systole - physiology
Ventricular Dysfunction, Left - metabolism
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Summary:The aim of the present study was to determine whether cardiac nitric oxide (NO) production changes during the progression of pacing-induced heart failure and whether this occurs in association with alterations in myocardial metabolism. Dogs (n=8) were instrumented and the heart paced until left ventricular end-diastolic pressure reached 25 mm Hg and clinical signs of severe failure were evident. Every week, hemodynamic measurements were recorded and blood samples were withdrawn from the aorta and the coronary sinus for measurement of NO metabolites, O2 content, free fatty acids (FFAs), and lactate and glucose concentrations. Cardiac production of NO metabolites or consumption of O2 or utilization of substrates was calculated as coronary sinus-arterial difference times coronary flow. In end-stage failure, occurring at 29 +/- 1.6 days, left ventricular end-diastolic pressure was 25 +/- 1 mm Hg, left ventricular systolic pressure was 92 +/- 3 mm Hg, mean arterial pressure was 75 +/- 2.5 mm Hg, and dP/dtmax was 1219 +/- 73 mm Hg/s (all P
ISSN:0009-7330
1524-4571
DOI:10.1161/01.res.83.10.969