Comparison of Inhaled Nitric Oxide and Inhaled Aerosolized Prostacyclin in the Evaluation of Heart Transplant Candidates With Elevated Pulmonary Vascular Resistance

Haraldsson, Åsa; Kieler-Jensen, Niels; Nathorst-Westfelt, U.; Bergh, Claes‐Håkan; Ricksten, Sven‐Erik

doi:10.1378/chest.114.3.780

Cited by 132 publications

(88 citation statements)

References 31 publications

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“…4 Inhaled nitric oxide (NO), PGI 2 , and iloprost have been shown to act as selective pulmonary vasodilators without systemic effects, in patients with primary and secondary pulmonary hypertension (PH) as well. [5][6][7][8] Unfortunately, NO is a toxic molecule and requires specialized delivery systems and monitoring due to the production of methemoglobin and higher oxides of nitrogen. 9 Because of its short half-life, NO has to be administered continuously, and even brief interruptions may cause a dangerous rebound of PH.…”

Section: Objectifmentioning

confidence: 99%

“…7,11 On the other hand, Haraldsson et al found no improved effects on hemodynamic variables, comparing inhaled PGI 2 with inhaled NO in the evaluation of heart transplant candidates. 6 Currently, there exists little information regarding the use of milrinone by inhalation. The drug is an adenosine-3',5'-cyclic monophosphate (cAMP)-selective phosphodiesterase enzyme (PDE) inhibitor.…”

Section: Objectifmentioning

confidence: 99%

See 1 more Smart Citation

Selective pulmonary vasodilation with inhaled aerosolized milrinone in heart transplant candidates

Sablotzki¹,

Starzmann²,

Scheubel

et al. 2005

Can J Anesth/J Can Anesth

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Purpose: Selective pulmonary vasodilation is an advantageous method for testing the responsiveness of the pulmonary vasculature of heart transplant candidates. A pilot study was undertaken to test the hypothesis that inhaled aerosolized milrinone may cause selective pulmonary vasodilation.Methods: 18 consecutive male heart transplant candidates with either dilated or ischemic cardiomyopathy were included in this open clinical study. Nine of the patients had significant pulmonary hypertension with a mean pulmonary arterial pressure > 30 mmHg. After baseline measurements, 2 mg of milrinone was administered by ultrasonic nebulization. Pulmonary and systemic hemodynamics were measured ten, 30, and 60 min after inhalation. Results:After inhalation for ten minutes, milrinone induced a significant reduction of mean pulmonary arterial pressure (32.7 ± 9.1 vs 37.7 ± 7.5 mmHg, P = 0.01), pulmonary vascular resistance index (296 ± 150 vs 396 ± 151 dyn·sec -1 ·cm -5 · · m 2 , P = 0.02) and transpulmonary gradient (10.6 ± 5.5 vs 15 ± 4.9, P = 0.01) only in patients with significant pulmonary hypertension. There was no significant effect on mean arterial pressure or systemic vascular resistance at any time after inhalation in either group. Furthermore, there was no influence on extravascular lung water or intrathoracic blood volume. Conclusions:We conclude that inhaled aerosolized milrinone for a short period selectively dilates the pulmonary vasculature in heart transplant candidates with elevated pulmonary arterial pressure, without producing systemic side effects. Further comparative studies are necessary to evaluate possible advantages of milrinone compared to other inhaled vasodilators. Résultats : Après avoir été inhalée pendant 10 min, la milrinone a réduit significativement la tension artérielle pulmonaire moyenne (32,7 ± 9,1 vs 37,7 ± 7,5 mmHg, P = 0,01), l'index de résistance vasculaire pulmonaire (296 ± 15 vs 396 ± 151 dyn·s -1 ·cm -5 ·m 2 , P = 0,02) et le gradient transpulmonaire (10,6 ± 5,5 vs 15 ± 4,9, P = 0,01) Objectif

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Section: Objectifmentioning

confidence: 99%

Section: Objectifmentioning

confidence: 99%

Selective pulmonary vasodilation with inhaled aerosolized milrinone in heart transplant candidates

Sablotzki¹,

Starzmann²,

Scheubel

et al. 2005

Can J Anesth/J Can Anesth

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“…It has been demonstrated that inhaled PGI 2 reduces mPAP and redistributes pulmonary flow without causing significant systemic hypotension. (20,21) The use of inhaled PGI 2 in patients with ARDS has been reported to reduce pulmonary vascular resistance by 30%, improving gas exchange (by redistributing the perfusion to areas that were previously less perfused) without causing systemic hypotension. (22) Experimental studies have shown that the vasodilator properties of IPGI 2 are as effective as are those of nitric oxide.…”

Section: Discussionmentioning

confidence: 99%

Modelo experimental de perfusão pulmonar ex vivo em ratos: avaliação de desempenho de pulmões submetidos à administração de prostaciclina inalada versus parenteral

et al. 2011

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Objective: To present a model of prostaglandin I 2 (PGI 2 ) administration (inhaled vs. parenteral) and to assess the functional performance of the lungs in an ex vivo lung perfusion system. Methods: Forty Wistar rats were anesthetized and placed on mechanical ventilation followed by median sterno-laparotomy and anticoagulation. The main pulmonary artery was cannulated. All animals were maintained on mechanical ventilation and were randomized into four groups (10 rats/group): inhaled saline (IS); parenteral saline (PS); inhaled PGI 2 (IPGI 2 ); and parenteral PGI 2 (PPGI 2 ). The dose of PGI 2 used in the IPGI 2 and PPGI 2 groups was 20 and 10 µg/kg, respectively. The heart-lung blocks were submitted to antegrade perfusion with a low potassium and dextran solution via the pulmonary artery, followed by en bloc extraction and storage at 4°C for 6 h. The heart-lung blocks were then ventilated and perfused in an ex vivo lung perfusion system for 50 min. Respiratory mechanics, hemodynamics, and gas exchange were assessed. Results: Mean pulmonary artery pressure following nebulization decreased in all groups (p < 0.001), with no significant differences among the groups. During the ex vivo perfusion, respiratory mechanics did not differ among the groups, although relative oxygenation capacity decreased significantly in the IS and PS groups (p = 0.04), whereas mean pulmonary artery pressure increased significantly in the IS group. Conclusions: The experimental model of inhaled PGI 2 administration during lung extraction is feasible and reliable. During reperfusion, hemodynamics and gas exchange trended toward better performance with the use of PGI 2 than that with the use of saline.Keywords: Prostaglandins; Lung transplantation; Reperfusion; Models, animal; Rats. ResumoObjetivo: Apresentar um modelo experimental de administração de prostaglandina I 2 (PGI 2 ) por via inalatória vs. parenteral e avaliar o desempenho funcional dos pulmões em um sistema de perfusão pulmonar ex vivo. Métodos: Quarenta ratos Wistar foram anestesiados, ventilados, submetidos a laparotomia com ressecção do esterno e anticoagulados. O tronco da artéria pulmonar foi canulado. Todos os animais foram submetidos a ventilação mecânica. Os animais foram randomizados em quatro grupos (10 ratos/grupo): salina nebulizada (SN); salina parenteral (SP); PGI 2 nebulizada (PGI 2 N); e PGI 2 parenteral (PGI 2 P). A dose de PGI 2 nos grupos PGI 2 N e PGI 2 P foi de 20 e 10 µg/kg, respectivamente. Os blocos cardiopulmonares foram submetidos in situ a perfusão anterógrada com solução de baixo potássio e dextrana a 4°C via artéria pulmonar, extraídos em bloco e armazenados a 4°C por 6 h. Os blocos foram ventilados e perfundidos em um sistema ex vivo por 50 min, sendo obtidas medidas de mecânica ventilatória, hemodinâmica e trocas gasosas. Resultados: Houve redução da pressão arterial pulmonar média após a nebulização em todos os grupos (p < 0,001), sem diferença entre os grupos. Na perfusão ex vivo, a mecânica ventilatória não diferiu entre os grupos. Hou...

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“…Bolus doses between 15 and 30 µg of inhaled prostacyclin have been administered in humans with potent effects on pulmonary pressure and oxygenation. 89,90 Inhaled NO and prostacyclin may have additive actions as both medications act through different vasodilatory pathways. 91 Endothelin-1 is a potent vasoconstrictor released by endothelial cells in the pathophysiology of pulmonary hypertension.…”

Section: Rebound Pulmonary Hypertension and Hypoxemiamentioning

confidence: 99%

Inhaled nitric oxide in 2003: a review of its mechanisms of action

Wang

Kebir

Blaise

2003

Can J Anesth/J Can Anesth

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P Pu ur rp po os se e: : To review the pulmonary and systemic effects of endogenous nitric oxide and inhaled nitric oxide administered to patients.S So ou ur rc ce e: : A systematic search for experimental data, human case reports, and randomized clinical trials since 1980, the year of discovery of endothelium-derived relaxing factor. P Pr ri in nc ci ip pa al l f fi in nd di in ng gs s: : Nitric oxide has pulmonary and systemic effects. Inhaled nitric oxide not only causes selective pulmonary vasodilation but also results in pulmonary vasoconstriction of the vessels perfusing non-ventilated alveolae. The systemic effects of inhaled nitric oxide, which include modulation of the distribution of systemic blood flow, increase in renal output, interaction with coagulation, fibrinolysis and platelet functions, alteration of the inflammatory response, are described and the mechanisms of nitric oxide transport are explained. The possible toxicity of inhaled nitric oxide is also discussed.C Co on nc cl lu us si io on n: : The multiple effects of inhaled nitric oxide support its role as a pulmonary and extra-pulmonary medication.

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Comparison of Inhaled Nitric Oxide and Inhaled Aerosolized Prostacyclin in the Evaluation of Heart Transplant Candidates With Elevated Pulmonary Vascular Resistance

Cited by 132 publications

References 31 publications

Selective pulmonary vasodilation with inhaled aerosolized milrinone in heart transplant candidates

Selective pulmonary vasodilation with inhaled aerosolized milrinone in heart transplant candidates

Modelo experimental de perfusão pulmonar ex vivo em ratos: avaliação de desempenho de pulmões submetidos à administração de prostaciclina inalada versus parenteral

Inhaled nitric oxide in 2003: a review of its mechanisms of action

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