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J Thorac Cardiovasc Surg 1999;117:195
© 1999 Mosby, Inc.

LETTERS TO THE EDITOR

Effect of inhaled nitric oxide on left ventricular and pulmonary vascular function

The conclusions of Argenziano and associates ¹ contradicted their evidence. They concluded: "Inhaled nitric oxide reduced pulmonary vascular resistance but did not alter myocardial contractility or diastolic function." However, their Table I showed the following evidence of increased left heart failure after their 6 experimental pigs inhaled nitric oxide (NO): Cardiac output and ejection fraction decreased while left ventricular end-diastolic volume and pressure increased. The authors cited 3 reports that left atrial pressure increased and pulmonary edema appeared when subjects with left ventricular dysfunction inhaled NO therapeutically. This was further evidence that myocardial contractility and diastolic function deteriorated after inhalation of NO.

The authors' second point was that NO lowered the pulmonary vascular resistance (PVR), which they calculated by the standard formula that is derived from Poiseuille's equation. ² However, "since the experiments from which the equation was derived were performed in straight, rigid tubes with steady, streamlined flow of an ideal, viscous fluid, the relationship cannot be directly applied to the vascular system, in which the vessels are neither straight nor rigid, the blood is not a simple viscous fluid, and the flow is not always streamlined." ²

The common formula for "vascular resistance" is:

PVR = PAP – LAP/Cardiac output

where PAP is mean pulmonary artery pressure and LAP is mean left atrial pressure.This can be misleading, because raising the left atrial pressure, which Argenziano and colleagues ¹ observed in their pigs, decreases the numerator and thereby the calculated PVR. This can happen with no change in pulmonary artery pressure. Raising the left atrial pressure obviously obstructs pulmonary blood flow, but it decreases the calculated PVR. A similarly misleading result occurs when this formula is applied to systemic vascular resistance while phenyleprine (Neo-Synephrine) is administered: The right atrial pressure increases more than the mean arterial pressure increases, thereby decreasing the numerator in the resistance equation. As a result, while vasoconstriction decreases the force of the femoral pulses, the calculated systemic vascular resistance becomes abnormally low, the opposite of the true state.Although the number of pigs was too small to allow adequate statistical evaluation of some measured parameters, the authors did show well that during controlled heart failure inhaled NO decreased pulmonary artery pressure despite elevated left atrial pressure.

Bernard G. Krohn, MD
Department of Cardiology
Good Samaritan Hosiptal
16250 Woodruff Avenue
Bellflower, CA 90706

12/8/93303

References

1. Argenziano M, Dean DA, Moazami N, Goldstein DJ, Rose EA, Spotnitz HM, et al. Inhaled oxide is not a myocardial depressant in a porcine model of heart failure. J Thorac Cardiovasc Surg 1998;115:700-8. [Abstract/Free Full Text]
   
2. Schlant RC, Sonnenblick EH, Katz AM. Normal physiology of the cardiovascular system. In: Alexander RW, Schlant RC, Fuster V, editors. Hurst's The heart. 9th ed. New York: McGraw-Hill Health Professions Division; 1983. p. 103.
   

This Article Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Krohn, B. G. Search for Related Content PubMed PubMed Citation Articles by Krohn, B. G.