Year: 2000
Type: article
Abstract: In a recent study by Loh and colleagues [1Loh E. Lankford E.B. Polidori D.J. Doering-Lubit E.B. Hanson C.W. Acker M.A. Cardiovascular effects of inhaled nitric oxide in a canine model of cardiomyopathy.Ann Thorac Surg. 1999; 67: 1380-1385Abstract Full Text Full Text PDF PubMed Scopus (5) Google Scholar], administration of inhaled nitric oxide in a canine model of cardiomyopathy resulted in pulmonary vasodilatation and increased left ventricular end-diastolic pressure. Because no appreciable effects on myocardial contractility were demonstrated, the authors concluded that the increase in left ventricular end-diastolic pressure resulted not from myocardial depression by inhaled nitric oxide, but was “probably the result of a small increase in pulmonary flow … and the minimal reserve of the failing left ventricle to increase stroke volume.”We agree with this assessment, and in fact have previously proposed this concept in a theoretical analysis [2Dickstein M.L. Burkhoff D. A theoretic analysis of the effect of pulmonary vasodilation on pulmonary venous pressure implications for inhaled nitric oxide therapy.J Heart Lung Transplant. 1996; 15: 715-721PubMed Google Scholar] and in a study of the effects of inhaled nitric oxide in a porcine model of cardiomyopathy [3Argenziano M. Dean D.A. Moazami N. et al.Inhaled nitric oxide is not a myocardial depressant in a porcine model of heart failure.J Thorac Cardiovasc Surg. 1998; 115: 700-708Abstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar]. In the latter study, we administered inhaled nitric oxide in a porcine model of pacing-induced heart failure, effecting reductions in pulmonary vascular resistance and elevations in left ventricular end-diastolic pressure without influencing myocardial contractility. We concluded that “volume shifts due to pulmonary vasodilatation are responsible for clinically observed elevations in left atrial pressure, and may explain why patients with preexisting ventricular dysfunction are at greatest risk for these pressure elevations.”Unfortunately, in their discussion, Dr Loh and associates incorrectly cited our paper, stating that in our study, “Nitric oxide was administered to open-chest pigs with normal cardiac function.” It appears that they confused our porcine cardiomyopathy study with an earlier report from our laboratory [4Goldstein D.J. Dean D.A. Smerling A. Oz M.C. Burkhoff D. Dickstein M.L. Inhaled nitric oxide is not a negative inotropic agent in a porcine model of pulmonary hypertension.J Thorac Cardiovasc Surg. 1997; 114: 461-466Abstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar], in which inhaled nitric oxide was administered to normal pigs after induction of pulmonary hypertension by a thromboxane analogue.We congratulate Dr Loh and colleagues on their excellent study and are pleased that their results in a canine model of cardiomyopathy have confirmed our findings in a similar porcine model. In a recent study by Loh and colleagues [1Loh E. Lankford E.B. Polidori D.J. Doering-Lubit E.B. Hanson C.W. Acker M.A. Cardiovascular effects of inhaled nitric oxide in a canine model of cardiomyopathy.Ann Thorac Surg. 1999; 67: 1380-1385Abstract Full Text Full Text PDF PubMed Scopus (5) Google Scholar], administration of inhaled nitric oxide in a canine model of cardiomyopathy resulted in pulmonary vasodilatation and increased left ventricular end-diastolic pressure. Because no appreciable effects on myocardial contractility were demonstrated, the authors concluded that the increase in left ventricular end-diastolic pressure resulted not from myocardial depression by inhaled nitric oxide, but was “probably the result of a small increase in pulmonary flow … and the minimal reserve of the failing left ventricle to increase stroke volume.” We agree with this assessment, and in fact have previously proposed this concept in a theoretical analysis [2Dickstein M.L. Burkhoff D. A theoretic analysis of the effect of pulmonary vasodilation on pulmonary venous pressure implications for inhaled nitric oxide therapy.J Heart Lung Transplant. 1996; 15: 715-721PubMed Google Scholar] and in a study of the effects of inhaled nitric oxide in a porcine model of cardiomyopathy [3Argenziano M. Dean D.A. Moazami N. et al.Inhaled nitric oxide is not a myocardial depressant in a porcine model of heart failure.J Thorac Cardiovasc Surg. 1998; 115: 700-708Abstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar]. In the latter study, we administered inhaled nitric oxide in a porcine model of pacing-induced heart failure, effecting reductions in pulmonary vascular resistance and elevations in left ventricular end-diastolic pressure without influencing myocardial contractility. We concluded that “volume shifts due to pulmonary vasodilatation are responsible for clinically observed elevations in left atrial pressure, and may explain why patients with preexisting ventricular dysfunction are at greatest risk for these pressure elevations.” Unfortunately, in their discussion, Dr Loh and associates incorrectly cited our paper, stating that in our study, “Nitric oxide was administered to open-chest pigs with normal cardiac function.” It appears that they confused our porcine cardiomyopathy study with an earlier report from our laboratory [4Goldstein D.J. Dean D.A. Smerling A. Oz M.C. Burkhoff D. Dickstein M.L. Inhaled nitric oxide is not a negative inotropic agent in a porcine model of pulmonary hypertension.J Thorac Cardiovasc Surg. 1997; 114: 461-466Abstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar], in which inhaled nitric oxide was administered to normal pigs after induction of pulmonary hypertension by a thromboxane analogue. We congratulate Dr Loh and colleagues on their excellent study and are pleased that their results in a canine model of cardiomyopathy have confirmed our findings in a similar porcine model.
Source: The Annals of Thoracic Surgery
Authors: Michael Argenziano, Marc L Dickstein
Language: English
Subfield: Pulmonary and Respiratory Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
Estimated APC paid: $3,200
OpenAlex ID: W2020716992