Inhaled nitric oxide: Selective pulmonary vasodilation in cardiac surgical patients

G. F. Rich, G. D. Murphy, C. M. Roos, Roger A Johns

Research output: Contribution to journalArticle

Abstract

Background: Inhaled nitric oxide (NO), an endothelium-derived relaxing factor, is a selective pulmonary vasodilator. The authors investigated whether the pulmonary vasodilation resulting from 20 ppm inhaled NO is related to the degree of pulmonary hypertension or affected by cardiopulmonary bypass (CPB) or the presence of intravenous nitrates. Methods: In patients undergoing cardiac surgery (n = 20) or in whom the circulation was supported with a ventricular assist device (VAD; n = 5), the lungs were ventilated with 80% O2 and 20% N2 followed by the same gas concentrations containing 20 ppm NO for 6 min. Results: Inhaled NO decreased (P <0.05) the pulmonary artery pressure from 36 ± 3 to 29 ± 2 mmHg and 32 ± 2 to 27 ± 1 mmHg, before and after CPB, respectively, and from 68 ± 12 to 55 ± 9 mmHg in patients with a VAD. Similarly, the pulmonary vascular resistance (PVR) decreased (P <0.05) from 387 ± 44 to 253 ± 26 dyne · cm · s-5 and 260 ± 27 to 182 ± 18 dyne · cm · s-5, before and after CPB, respectively, and from 1,085 ± 229 to 752 ± 130 dyne · cm · s-5 in patients with a VAD. Central venous pressure, cardiac output, systemic hemodynamics, and blood gases did not change after inhalation of NO before or after CPB, whereas arterial oxygen tension, mixed venous hemoglobin saturation, and mean arterial pressure increased (P <0.05) in patients supported with a VAD. All hemodynamic and laboratory data returned to control 6 min after discontinuation of NO. The decrease in PVR was proportional to baseline PVR (ΔPVR = -0.45 PVR(b) + 39.9) before CPB. The pre- and post-CPB slopes were identical despite possible damage to the endothelium resulting from CPB and the post-CPB presence of intravenous nitroglycerin (17 of 20 patients). Conclusions: This study demonstrates that 20 ppm inhaled NO is a selective pulmonary vasodilator in cardiac surgical patients before and after CPB and in patients in whom the circulation is supported with a VAD. Furthermore, NO-induced pulmonary vasodilation is proportional to PVR(b) and does not appear to be altered by CPB, the presence of a VAD, or infusion of nitrates.

Original languageEnglish (US)
Pages (from-to)1028-1035
Number of pages8
JournalAnesthesiology
Volume78
Issue number6
StatePublished - 1993
Externally publishedYes

Fingerprint

Cardiopulmonary Bypass
Vasodilation
Nitric Oxide
Lung
Vascular Resistance
Vasodilator Agents
Nitrates
Arterial Pressure
Gases
Hemodynamics
Endothelium-Dependent Relaxing Factors
Central Venous Pressure
Heart-Assist Devices
Nitroglycerin
Pulmonary Hypertension
Cardiac Output
Inhalation
Pulmonary Artery
Thoracic Surgery
Endothelium

Keywords

  • Endothelium-derived relaxing factor
  • Lungs: pulmonary hypertension; vasodilation
  • Methemoglobin
  • Nitric oxide

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Inhaled nitric oxide : Selective pulmonary vasodilation in cardiac surgical patients. / Rich, G. F.; Murphy, G. D.; Roos, C. M.; Johns, Roger A.

In: Anesthesiology, Vol. 78, No. 6, 1993, p. 1028-1035.

Research output: Contribution to journalArticle

Rich, GF, Murphy, GD, Roos, CM & Johns, RA 1993, 'Inhaled nitric oxide: Selective pulmonary vasodilation in cardiac surgical patients', Anesthesiology, vol. 78, no. 6, pp. 1028-1035.
Rich, G. F. ; Murphy, G. D. ; Roos, C. M. ; Johns, Roger A. / Inhaled nitric oxide : Selective pulmonary vasodilation in cardiac surgical patients. In: Anesthesiology. 1993 ; Vol. 78, No. 6. pp. 1028-1035.
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abstract = "Background: Inhaled nitric oxide (NO), an endothelium-derived relaxing factor, is a selective pulmonary vasodilator. The authors investigated whether the pulmonary vasodilation resulting from 20 ppm inhaled NO is related to the degree of pulmonary hypertension or affected by cardiopulmonary bypass (CPB) or the presence of intravenous nitrates. Methods: In patients undergoing cardiac surgery (n = 20) or in whom the circulation was supported with a ventricular assist device (VAD; n = 5), the lungs were ventilated with 80{\%} O2 and 20{\%} N2 followed by the same gas concentrations containing 20 ppm NO for 6 min. Results: Inhaled NO decreased (P <0.05) the pulmonary artery pressure from 36 ± 3 to 29 ± 2 mmHg and 32 ± 2 to 27 ± 1 mmHg, before and after CPB, respectively, and from 68 ± 12 to 55 ± 9 mmHg in patients with a VAD. Similarly, the pulmonary vascular resistance (PVR) decreased (P <0.05) from 387 ± 44 to 253 ± 26 dyne · cm · s-5 and 260 ± 27 to 182 ± 18 dyne · cm · s-5, before and after CPB, respectively, and from 1,085 ± 229 to 752 ± 130 dyne · cm · s-5 in patients with a VAD. Central venous pressure, cardiac output, systemic hemodynamics, and blood gases did not change after inhalation of NO before or after CPB, whereas arterial oxygen tension, mixed venous hemoglobin saturation, and mean arterial pressure increased (P <0.05) in patients supported with a VAD. All hemodynamic and laboratory data returned to control 6 min after discontinuation of NO. The decrease in PVR was proportional to baseline PVR (ΔPVR = -0.45 PVR(b) + 39.9) before CPB. The pre- and post-CPB slopes were identical despite possible damage to the endothelium resulting from CPB and the post-CPB presence of intravenous nitroglycerin (17 of 20 patients). Conclusions: This study demonstrates that 20 ppm inhaled NO is a selective pulmonary vasodilator in cardiac surgical patients before and after CPB and in patients in whom the circulation is supported with a VAD. Furthermore, NO-induced pulmonary vasodilation is proportional to PVR(b) and does not appear to be altered by CPB, the presence of a VAD, or infusion of nitrates.",
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AU - Murphy, G. D.

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AU - Johns, Roger A

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Y1 - 1993

N2 - Background: Inhaled nitric oxide (NO), an endothelium-derived relaxing factor, is a selective pulmonary vasodilator. The authors investigated whether the pulmonary vasodilation resulting from 20 ppm inhaled NO is related to the degree of pulmonary hypertension or affected by cardiopulmonary bypass (CPB) or the presence of intravenous nitrates. Methods: In patients undergoing cardiac surgery (n = 20) or in whom the circulation was supported with a ventricular assist device (VAD; n = 5), the lungs were ventilated with 80% O2 and 20% N2 followed by the same gas concentrations containing 20 ppm NO for 6 min. Results: Inhaled NO decreased (P <0.05) the pulmonary artery pressure from 36 ± 3 to 29 ± 2 mmHg and 32 ± 2 to 27 ± 1 mmHg, before and after CPB, respectively, and from 68 ± 12 to 55 ± 9 mmHg in patients with a VAD. Similarly, the pulmonary vascular resistance (PVR) decreased (P <0.05) from 387 ± 44 to 253 ± 26 dyne · cm · s-5 and 260 ± 27 to 182 ± 18 dyne · cm · s-5, before and after CPB, respectively, and from 1,085 ± 229 to 752 ± 130 dyne · cm · s-5 in patients with a VAD. Central venous pressure, cardiac output, systemic hemodynamics, and blood gases did not change after inhalation of NO before or after CPB, whereas arterial oxygen tension, mixed venous hemoglobin saturation, and mean arterial pressure increased (P <0.05) in patients supported with a VAD. All hemodynamic and laboratory data returned to control 6 min after discontinuation of NO. The decrease in PVR was proportional to baseline PVR (ΔPVR = -0.45 PVR(b) + 39.9) before CPB. The pre- and post-CPB slopes were identical despite possible damage to the endothelium resulting from CPB and the post-CPB presence of intravenous nitroglycerin (17 of 20 patients). Conclusions: This study demonstrates that 20 ppm inhaled NO is a selective pulmonary vasodilator in cardiac surgical patients before and after CPB and in patients in whom the circulation is supported with a VAD. Furthermore, NO-induced pulmonary vasodilation is proportional to PVR(b) and does not appear to be altered by CPB, the presence of a VAD, or infusion of nitrates.

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KW - Lungs: pulmonary hypertension; vasodilation

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