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J Thorac Cardiovasc Surg 2001;122:371-377
© 2001 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology (CPS)

Hemodynamic effects of S-nitrosocysteine, an intravenous regional vasodilator

From the Departments of Surgery^a and Physiology and Pharmacology,^b Oregon Health Sciences University, Portland; Heart Institute of the Cascades,^c St Charles Medical Center, Bend; and Academic Center for Cardiac Surgery,^d Providence Health System, Portland, Ore.

Received for publication July 5, 2000. Revisions requested Oct 30, 2000; revisions received Feb 2, 2001. Accepted for publication March 8, 2001. Address for reprints: David C. Stuesse, MD, 2805 SE, 43rd Ave, Portland, OR 97206 (E-mail: stuessed{at}ohsu.edu).

Abstract

Background: S-nitrosocysteine is a carrier form of nitric oxide that can be delivered intravenously. S-nitrosocysteine is rapidly metabolized by plasma (half-life = 2-3 seconds), forming nitric oxide and cysteine. With its short half-life and potent vasodilatory properties, S-nitrosocysteine may be useful as a pulmonary vasodilating agent in cases of postoperative and chronic pulmonary hypertension.
Objective: Our objective was to determine the hemodynamic properties of S-nitrosocysteine on the pulmonary and systemic circulations to assess its potential utility as a pulmonary vasodilatory agent.
Methods: Eleven adult swine were anesthetized. Thermodilution (Swan-Ganz; Baxter International, Inc, Deerfield, Ill) and arterial catheters were inserted. Flow probes were placed around the coronary, renal, superior mesenteric, and iliac arteries. Incremental infusion doses of S-nitrosocysteine (5-80 nmol · kg^–1 · min^–1) were delivered into the right atrium. Cardiac output, right and left heart pressures, heart rate, Pao₂, and iliac, renal, coronary, and mesenteric blood flow rates were recorded at baseline and at each infusion dose of S-nitrosocysteine.
Results: Low-dose S-nitrosocysteine infusion decreased mean pulmonary artery pressure (15%, P = .013) without a significant reduction in mean systemic artery pressure. Higher dose infusions produced further dose-dependent declines in pulmonary vascular resistance and measurable reductions in systemic vascular resistance (P = .01). At an S-nitrosocysteine dosage of 40 nmol · kg^–1 · min^–1, there was a significant reduction in renal (P < .001) and mesenteric (P = .003) blood flow but no change in iliac (P > .2) or coronary (P > .2) blood flow. Cardiac output remained constant up to infusion rates of 40 nmol · kg^–1 · min^–1 (P > .2). Doses higher than 5 nmol · kg^–1 · min^–1 resulted in a substantial dose-dependent reduction in Pao₂ (P < .001), suggesting dilation of atelectatic areas of the lung.
Conclusion: S-nitrosocysteine is a potent vasodilatory agent capable of overcoming the hypoxic vasoconstrictive response of the lung. Our results suggest it may prove useful as a pulmonary vasodilatory agent at low doses. Higher dose infusions reduce mean systemic pressure and lead to compensatory reductions in renal and mesenteric blood flow without a decrease in cardiac output.