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Ann Thorac Surg 1999;67:1380-1385
© 1999 The Society of Thoracic Surgeons

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Original Articles

Cardiovascular effects of inhaled nitric oxide in a canine model of cardiomyopathy

^a Cardiovascular Division, University of Pennsylvania Health System, Philadelphia, Pennsylvania, USA
^b Cardiothoracic Surgery Division, University of Pennsylvania Health System, Philadelphia, Pennsylvania, USA
^c Departments of Medicine, Surgery and Anesthesiology, University of Pennsylvania Health System, Philadelphia, Pennsylvania, USA

Accepted for publication December 7, 1998.

Address reprint requests to Dr Loh, Cardiovascular Division, Hospital of the University of Pennsylvania, 9 Founders Pavilion, 3400 Spruce St, Philadelphia, PA 19104
e-mail: lohe{at}mail.med.upenn.edu

Background. The inhalation of nitric oxide (NO) in patients with heart failure decreases pulmonary vascular resistance (PVR) and is associated with an increase in pulmonary artery wedge pressure (PAWP). The mechanism for this effect remains unclear.

Methods. In dogs rapid-paced for 8 weeks to induce cardiac dysfunction, we performed left ventricular pressure-volume analysis of unpaced hearts in situ to determine whether during NO inhalation (80 ppm), the mechanism for the rise in PAWP is due to: 1) primary pulmonary vasodilation; 2) a direct negative inotropic effect; or 3) impairment of ventricular relaxation.

Results. Inhalation of NO decreased PVR by 51% ± 3.8% (257 ± 25 vs 127 ± 18 dynes · sec · cm^-5 [NO 80 ppm]; p < 0.001) and increased PAWP (15.4 ± 2.4 vs 18.1 ± 2.6 mm Hg [NO 80 ppm]; p < 0.001). Calculated systemic vascular resistance remained unchanged. Left ventricular (LV) end-diastolic pressure rose (16.4 ± 1.9 vs 19.1 ± 1.8 mm Hg [NO 80 ppm]; p < 0.001), as did LV end-diastolic volume (83.5 ± 4.0 vs 77.0 ± 3.4 mL [NO 80 ppm]; p = 0.006). LV peak +dP/dt was unchanged by NO (1,082 ± 105 vs 1,142 ± 111 mm Hg/sec [NO 80 ppm]; p = NS). There was a trend toward a stroke volume increase (17.4 ± 1.2 vs 18.8 ± 1.3 mL; p = NS), but the relaxation time constant and end-diastolic pressure-volume relation were both unchanged.

Conclusions. In this canine model of cardiomyopathy, inhaled NO decreases pulmonary vascular resistance. The associated increase in left ventricular filling pressure appears to be secondary to a primary pulmonary vasodilator effect of NO without primary effects on the contractile or relaxation properties of the left ventricle.

This article has been cited by other articles:

				B. Gaston Summary: systemic effects of inhaled nitric oxide. Proceedings of the ATS, January 1, 2006; 3(2): 170 - 172. [Abstract] [Full Text] [PDF]

				M. Argenziano and M. L. Dickstein Cardiovascular effects of inhaled nitric oxide in a canine model of cardiomyopathy Ann. Thorac. Surg., May 1, 2000; 69(5): 1644 - 1645. [Full Text] [PDF]