Hemodynamic effects of S-nitrosocysteine, an intravenous regional vasodilator

David C. Stuesse, George Giraud, Angelo Vlessis, Albert Starr, Donald Trunkey, Edward Verrier, David Fullerton

Research output: Contribution to journalArticle

7 Citations (Scopus)

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, III) 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.

Original languageEnglish (US)
Pages (from-to)371-377
Number of pages7
JournalJournal of Thoracic and Cardiovascular Surgery
Volume122
Issue number2
DOIs
StatePublished - Aug 1 2001

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Vasodilator Agents
Hemodynamics
Lung
Cardiac Output
Pressure
Kidney
Vascular Resistance
Half-Life
Nitric Oxide
S-nitrosocysteine
Thermodilution
Pulmonary Circulation
Superior Mesenteric Artery
Iliac Artery
Renal Circulation
Heart Atria
Pulmonary Hypertension
Pulmonary Artery
Cysteine
Dilatation

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

Hemodynamic effects of S-nitrosocysteine, an intravenous regional vasodilator. / Stuesse, David C.; Giraud, George; Vlessis, Angelo; Starr, Albert; Trunkey, Donald; Verrier, Edward; Fullerton, David.

In: Journal of Thoracic and Cardiovascular Surgery, Vol. 122, No. 2, 01.08.2001, p. 371-377.

Research output: Contribution to journalArticle

Stuesse, David C. ; Giraud, George ; Vlessis, Angelo ; Starr, Albert ; Trunkey, Donald ; Verrier, Edward ; Fullerton, David. / Hemodynamic effects of S-nitrosocysteine, an intravenous regional vasodilator. In: Journal of Thoracic and Cardiovascular Surgery. 2001 ; Vol. 122, No. 2. pp. 371-377.
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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, III) 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.",
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AU - Giraud, George

AU - Vlessis, Angelo

AU - Starr, Albert

AU - Trunkey, Donald

AU - Verrier, Edward

AU - Fullerton, David

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N2 - 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, III) 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.

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