Decreased Basal Production of Nitric Oxide in Patients With Heart Disease

¹ From the Second Department of Internal Medicine, Gunma University School of Medicine, Maebashi, Japan
² From the Department of Laboratory Medicine, Gunma University School of Medicine, Maebashi, Japan

Study objectives: The pathophysiologic role of nitric oxide (NO) released in the lung is not well understood. To determine whether the production of endogenous NO is correlated with any hemodynamic parameters, we measured the amount of NO released from the lung tissue of patients with heart disease.

Methods: Twenty patients (14 with ischemic heart disease, 4 with dilated cardiomyopathy, and 2 with mitral stenosis) and 16 normal control subjects were enrolled in the study. We measured exhaled air samples by using a method developed in our laboratory. The NO release rate from the lungs was calculated from the amount of exhaled NO and the duration of the exhalation.

Results: The rate of NO release was significantly lower in the patients with moderate-to-severe heart failure (New York Heart Association [NYHA] II or III) than in those with mild heart failure (NYHA I) or in normal control subjects. The rate of NO release was positively correlated with the cardiac index (r=0.50, p<0.05), and was negatively correlated with either the systemic (r=0.58, p<0.01) or pulmonary vascular resistance (r=0.45, p<0.05). In the patients with moderate-to-severe heart failure, the amount of NO released and the oxygen tension in the pulmonary artery were significantly lower compared with those parameters in patients with mild heart failure.

Conclusions: Results suggest that the basal production of endogenous NO in the lung tissue of patients with heart failure is impaired, perhaps leading to the elevated pulmonary vascular tone seen in patients with moderate-to-severe heart failure.

Key Words: cardiac index • chemiluminescence analyzer • hypoxic pulmonary vasoconstriction • vascular resistance

Submitted on December 10, 1996
Accepted on August 7, 1997

This article has been cited by other articles:

				A. Kurita, T. Matsui, T. Ishizuka, B. Takase, and K. Satomura Significance of Plasma Nitric Oxide/Endothelial-1 Ratio for Prediction of Coronary Artery Disease Angiology, May 1, 2005; 56(3): 259 - 264. [Abstract] [PDF]

				S. D. Katz, K. Hryniewicz, I. Hriljac, K. Balidemaj, C. Dimayuga, A. Hudaihed, and A. Yasskiy Vascular Endothelial Dysfunction and Mortality Risk in Patients With Chronic Heart Failure Circulation, January 25, 2005; 111(3): 310 - 314. [Abstract] [Full Text] [PDF]

				C. DELCLAUX, B. MAHUT, F. ZERAH-LANCNER, C. DELACOURT, S. LAOUD, D. CHERQUI, C. DUVOUX, A. MALLAT, and A. HARF Increased Nitric Oxide Output from Alveolar Origin during Liver Cirrhosis versus Bronchial Source during Asthma Am. J. Respir. Crit. Care Med., February 1, 2002; 165(3): 332 - 337. [Abstract] [Full Text] [PDF]

				H. Sumino, T. Nakamura, T. Kanda, K. Sato, T. Sakamaki, T. Takahashi, Y. Saito, J. Hoshino, T. Kurashina, and R. Nagai Effect of Enalapril on Exhaled Nitric Oxide in Normotensive and Hypertensive Subjects Hypertension, December 1, 2000; 36(6): 934 - 940. [Abstract] [Full Text] [PDF]

				E. CLINI, G. CREMONA, M. CAMPANA, C. SCOTTI, M. PAGANI, L. BIANCHI, A. GIORDANO, and N. AMBROSINO Production of Endogenous Nitric Oxide in Chronic Obstructive Pulmonary Disease and Patients with Cor Pulmonale . Correlates with Echo-Doppler Assessment Am. J. Respir. Crit. Care Med., August 1, 2000; 162(2): 446 - 450. [Abstract] [Full Text] [PDF]

				E. Clini, L. Bianchi, M. Vitacca, R. Porta, K. Foglio, and N. Ambrosino Exhaled Nitric Oxide and Exercise in Stable COPD Patients Chest, March 1, 2000; 117(3): 702 - 707. [Abstract] [Full Text] [PDF]

				J. D. Symons, C. L. Stebbins, and T. I. Musch Interactions between angiotensin II and nitric oxide during exercise in normal and heart failure rats J Appl Physiol, August 1, 1999; 87(2): 574 - 581. [Abstract] [Full Text] [PDF]