Inhalation of Nitric Oxide Reduced Pulmonary Hypertension after Cardiac Surgery in a 3.2-kg Infant

Selldén, Hans; Winberg, P.; Gustafsson, Lars E.; Lundell, Bo; Böök, Kim; Frostell, Claes

doi:10.1097/00000542-199303000-00021

Cited by 77 publications

(25 citation statements)

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“…Finally, NO (10 ppm) inhaled for 30 min utes by an infant after cardiac surgery im proved gas exchange permanently while pul monary hypertension was resolved perma nently [21], Furthermore, enhanced resolu 330 Welte/Zwissler/Habazetll/Messmcr PGIj Aerosol versus NO in Pulmonary Hypertension tion of pneumonic infiltrates was observed upon NO inhalation [22], Despite the convincing evidence that in haled NO leads to selective pulmonary vaso dilation and hence may be useful to treat pul monary hypertension, it should be noted that NO itself is a radical with potential cytotoxic effects. Although severe acute lung injury and methemoglobinemia are observed after inha lation of gas mixtures containing high concen trations of NO, there is little evidence for pul monary toxicity at low concentrations (<100 ppm) of NO inhaled for short periods of time in different species [10].…”

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confidence: 99%

PGI<sub>2</sub> Aerosol versus Nitric Oxide for Selective Pulmonary Vasodilation in Hypoxic Pulmonary Vasoconstriction

Welte

Zwißler

Habazettl³

et al. 1993

Eur Surg Res

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Intravenous prostacyclin (PGI2) is a potent pulmonary vasodilator in pulmonary hypertension. However, dose-dependent systemic vasodilation, an increase in intrapulmonary shunt and hypoxemia limit its clinical application. Recently, inhaled nitric oxide (NO) has been reported to elicit selective pulmonary vasodilation, but its clinical use is restricted by its potential toxicity; furthermore, the feasibility of NO application in clinical practice seems difficult. Therefore, we investigated the effects of PGI2 aerosol on pulmonary and systemic circulation and compared the hemodynamic effects to those of inhaled NO. In 6 dogs, ventilation with a hypoxic gas mixture (F102 0.09–0.11) increased pulmonary vascular resistance (PVR) by 196% (HPV). Aerosolization of a PGI₂ solution at a concentration of 430 ng/ml reduced hypoxia-induced increase of pulmonary artery pressure by 48% and PVR by 52% within 6-10 min without systemic vasodilation. The administered dose of PGI2 was 0.87 ± 0.26 ng/kg/min. In 2 dogs, doubling the PGI2 concentration (860 ng/ml) did not enhance the vasodilatory effect. After termination of PGI₂ inhalation, HPV was restored within 10–15 min. Inhaled NO (50 ppm) decreased the HPV-induced increase in PAP by 76% and in PVR by 73% within 5-10 min. Clinically relevant systemic vasodilation was not observed. It is concluded that inhalation of aerosolized PGI₂ leads to selective pulmonary vasodilation in hypoxia-induced pulmonary hypertension. Aerosolized PGI₂ at a concentration of 430 ng/ml was less potent than NO (50 ppm). However, due to the lack of known toxicity and its uncomplicated mode of application, inhaled PGI₂ may be one alternative to inhaled NO in the treatment of acute pulmonary hypertension.

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confidence: 99%

PGI<sub>2</sub> Aerosol versus Nitric Oxide for Selective Pulmonary Vasodilation in Hypoxic Pulmonary Vasoconstriction

Welte

Zwißler

Habazettl³

et al. 1993

Eur Surg Res

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“…In one patient, who had a thermodilution catheter in place, the pulmonary blood flow increased from 1'5 to 1'8 I/min. In the five other children, the arteriovenous difference in oxygen content-decreased from 6x7 (0'9) to 4,8 to from 045 to 0 33. In the two last patients, either Rp/Rs (0-31) or systolic pressure (40 mm Hg) resembled the preoperative value.…”

Section: Introductionmentioning

confidence: 84%

Continuous low dose inhaled nitric oxide for treatment of severe pulmonary hypertension after cardiac surgery in paediatric patients

1996

ACC Current Journal Review

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“…Attention has increasingly been focused on NO inhalation therapies [4][5][6][7][8][9]. Although inhaled NO may be effective in patients with pulmonary hypertension [4,5] and respiratory failure [6][7][8][9], the sudden discontinuation of inhaled NO may produce severe arterial desaturation and pulmonary hypertension [7,8,18].…”

Section: Discussionmentioning

confidence: 99%

“…Nitric oxide (NO) is an endogenous vasodilator mediated by stimulation of the soluble guanylate cyclase [1][2][3], and the addition of low-dose NO to inspired gas has been shown not only potentially to provide selective pulmonary vasodilation in patients with pulmonary hypertension [4,5], but also to improve the ventilation/ perfusion mismatching in patients with respiratory failure [6][7][8][9]. However, NO is a potentially toxic molecule and easily reacts with oxygen (02) to form nitrogen dioxide (NO2).…”

Section: Introductionmentioning

confidence: 99%

Evaluation of Mapleson systems for administration of inhaled nitric oxide

et al. 1996

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To assess the safety of nitric oxide (NO) inhalation during manual-controlled ventilation using Mapleson A, D, and F systems, we examined nitrogen dioxide (NO2) production using a chemiluminescence analyzer. The NO concentration was changed from 0 to 19 parts per million (ppm), and at each level of NO the oxygen (O2) concentration was changed from 21% to 100%. The NO2 concentration was observed to increase when either the O2 or NO concentration was increased. The maximum NO2 concentrations (mean ± standard deviation) of the Mapleson A, D, and F systems were 0.20±0.03, 0.15±0.03, and 0.17±0.02 ppm, respectively, when the concentrations of NO and O2 were 19 ppm and 100%, respectively. The NO2 concentrations of the Mapleson A system were significantly higher than those of either the Mapleson D or F system at 4, 8, and 12 ppm NO and 100% O2, and than that of the Mapleson D system at 19 ppm NO and 100% O2. From the viewpoint of NO2 production, we suggest that the Mapleson D and F systems are safer than the Mapleson A system when manual-controlled ventilation is required.

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Inhalation of Nitric Oxide Reduced Pulmonary Hypertension after Cardiac Surgery in a 3.2-kg Infant

Cited by 77 publications

References 0 publications

PGI<sub>2</sub> Aerosol versus Nitric Oxide for Selective Pulmonary Vasodilation in Hypoxic Pulmonary Vasoconstriction

PGI<sub>2</sub> Aerosol versus Nitric Oxide for Selective Pulmonary Vasodilation in Hypoxic Pulmonary Vasoconstriction

Continuous low dose inhaled nitric oxide for treatment of severe pulmonary hypertension after cardiac surgery in paediatric patients

Evaluation of Mapleson systems for administration of inhaled nitric oxide

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