Prostacyclin for the Treatment of Pulmonary Hypertension in the Adult Respiratory Distress Syndrome

Radermacher, Peter; Šantak, B.; Wüst, Hans Joachim; Tarnow, J.; Falke, K. J.

doi:10.1097/00000542-199002000-00005

Cited by 156 publications

(40 citation statements)

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“…It has been successfully used in a variety of experimental conditions and patients with pulmonary hypertension (21)(22)(23)(24)(25). The dosis of i.v.…”

Section: Discussionmentioning

confidence: 99%

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Inhaled Nitric Oxide versus Inhaled Prostacyclin and Intravenous versus Inhaled Prostacyclin in Acute Respiratory Failure with Pulmonary Hypertension in Piglets

et al. 1995

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This study was a prospective, randomized design to compare oxygenation and pulmonary hemodynamics between inhaled nitric oxide (NO) and inhaled prostacylcin (PGI,), and between inhaled and i.v. PGI, in acute respiratory failure with pulmonary hypertension. Acute respiratory failure with pulmonary hypertension was induced in 12 piglets weighing 9-12 kg by repeated lung lavages and a continuous infusion of the stable endoperoxane analogue of thromboxane. Thereafter the animals were randomly assigned either for NO or PGI, application. All animals were treated with different concentrations of NO or different doses of PGI, applied i.v. and inhaled in random order. Continuous monitoring included ECG, central venous pressure (CVP), mean pulmonary artery pressure (MPAP), mean arterial pressure (MAP), artertial oxygen saturation (SaO,), and mixed venous oxygen saturation (SvO,) measurements. NO inhalation of 10 ppm resulted in a significant increase in Pao,/fraction of inspired oxygen (FiO,) from 7.5 2 1.34 kPa to 46.1 2 9.7 kPa. MPAP decreased significantly from 5.1 -t 0.26 kPa to 3.7 i 0.26 kPa during inhaled NO of 40 ppm; i.v. infusion of PGI, slightly increased oxygenation parameters. A significant increase in Pao,/ FiO, up to 32.4 2 3.lkPa was observed during PGI, aerosol delivery (11 < 0.01); i.v. PGI, decreased MAP from 11.5 -+ 0.39 kPa to 9.8 2 0.66 kPa ( p < 0.05) and MPAP from 5.8 -+ 0.53 kPa to 4.5 2 0.66 kPa, respectively ( p < 0.05). PGI, aerosol delivery significantly decreased the MPAP to 3.7 2 0.53 kPa ( p < 0.05) without influencing the MAP. It was concluded that inhaled NO and inhaled PGI, act as selective pulmonary vasodilators in acute respiratory Cdilure with pulmonary hypertension In 1987 N O was reported to be an important endotheliumderived relaxing factor (1, 2). NO is synthesized in the vascular endothelial cell from L-arginine by NO synthase. It rapidly diffuses into the vascular smooth muscle cell and acts by stimulation of guanylate cyclase producing cGMP which me-

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“…It has been successfully used in a variety of experimental conditions and patients with pulmonary hypertension (21)(22)(23)(24)(25). The dosis of i.v.…”

Section: Discussionmentioning

confidence: 99%

“…PGI, has been applied in a variety of clinical and experimental conditions with pulmonary hypertension (21)(22)(23)(24)(25). However, vasodilation occurs in both the pulmonary and systemic vessels which might result in systemic hypotension.…”

Section: Inhaled No Versus Pgi In Respiratory Failure 199mentioning

confidence: 99%

Inhaled Nitric Oxide versus Inhaled Prostacyclin and Intravenous versus Inhaled Prostacyclin in Acute Respiratory Failure with Pulmonary Hypertension in Piglets

et al. 1995

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“…However, a randomized, controlled trial hydralazine, and PGI 2 (prostacyclin), has also not involving 235 patients revealed no beneficial effect of been shown to be beneficial. [88][89][90] Almitrine, a selective lisofylline on the treatment of established ARDS. 80 It pulmonary vasoconstrictor, was shown to increase may be worth trying to use lisofylline for treatment arterial oxygenation via a redistribution of pulmonary of early phase of ARDS.…”

Section: Anti-adhesion Molecule Therapy Antiendotoxin and Anticytokinmentioning

confidence: 99%

Pharmacology of Acute Lung Injury

Tasaka

Hasegawa

Ishizaka

2002

Pulmonary Pharmacology & Therapeutics

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“…Pulmonary artery hypertension might be associated with, or responsible for, the decrease in ejection fraction, cardiac output and oxygen delivery. In addition, an inverse relationship between ejection fraction and pulmonary artery pressure has also been demonstrated in patients with chronic obstructive pulmonary disease and chronic pulmonary artery hypertension [33,34]. Radermacher et al [33] reported improved RV function and cardiac output after prostacyclin administration in eight patients suffering from pulmonary artery hypertension (mean 36 mmHg).…”

Section: Discussionmentioning

confidence: 99%

Right ventricular function and oxygen transport patterns in patients with acute respiratory distress syndrome

et al. 1994

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S-ary We investigated the impact of right ventricular performance on oxygen kinetics in [9], as indicated by decreased right ventricular ejection fraction (RVEF) and RV dilatation (increased RV end-diastolic volume (RVEDV)). However, the reason for this impaired cardiac performance is still under debate. Several authors have speculated about the presence of cardiodepressant substances (e.g. tumour necrosis factor, myocardial depressant factor) resulting in decreased left ventricular ejection fraction despite supranormal cardiac output [l 11. On the other hand, cardiac function may be impaired by increased pulmonary vascular resistance, despite adequate gas exchange [12,13]. These findings are supported by the work of Sibbald et al. [14], who demonstrated the importance of pulmonary artery hypertension in cardiorespiratory failure, resulting in depressed RV ejection fraction. Increasing RV volumes are paralleled by increasing RV wall stress resulting in a mismatch of myocardial O2 delivery and consumption, thus worsening RV performance. Reduced RV stroke volume (SV) is followed by reduced preload of the left ventricle. Additionally, increased RV endsdiastolic volumes may impede left ventricular diastolic performance by shifting the intraventricular septum to the left. This shifting alters the pressure-volume curves of the left ventricle with the net effect of increased filling pressures for a given volume. As a result the decrease in cardiac output (QT) causes an oxygen deficit eventually

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Prostacyclin for the Treatment of Pulmonary Hypertension in the Adult Respiratory Distress Syndrome

Cited by 156 publications

References 0 publications

Inhaled Nitric Oxide versus Inhaled Prostacyclin and Intravenous versus Inhaled Prostacyclin in Acute Respiratory Failure with Pulmonary Hypertension in Piglets

Inhaled Nitric Oxide versus Inhaled Prostacyclin and Intravenous versus Inhaled Prostacyclin in Acute Respiratory Failure with Pulmonary Hypertension in Piglets

Pharmacology of Acute Lung Injury

Right ventricular function and oxygen transport patterns in patients with acute respiratory distress syndrome

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