A Comparative Study of the Vasodilator Effects of Prostaglandin E1 in Patients with Pulmonary Hypertension After Mitral Valve Replacement and with Adult Respiratory Distress Syndrome

Kunimoto, Fumio; Arai, Ken‐ichi; Isa, Yukitaka; Koyano, Tetsuya; Kikuchi, Yuji; Saito, Shigeru; Goto, Fumio

doi:10.1213/00000539-199709000-00006

Cited by 22 publications

(8 citation statements)

References 14 publications

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“…We found that administering PGE 1 suppressed the early phase of pathological changes in MCT-treated rats by inhibiting the production of IL-1, IL-6, and TNF by macrophages immediately after the MCT injection. Concerning the effect of PGE 1 on human pulmonary hypertension, a function of PGE 1 as a vasodilator has been considered by several investigators [16,21,27,33]. The coincidence of suppression of the RV/LV+S ratio and suppression of cytokine production by PGE 1 in MCT-treated rats observed in this study indicates that PGE 1 suppressed pulmonary hypertension by suppression of cytokine production by alveolar macrophages.…”

Section: Discussionsupporting

confidence: 61%

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Suppressive Effect of Prostaglandin E1 on Pulmonary Hypertension Induced by Monocrotaline in Rats

Sakuma

Miyata

Kasukawa

1999

Lung

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The effect of administering prostaglandin E1 (PGE1) on the extent of monocrotaline (MCT)-induced pulmonary hypertension and cytokine production [interleukins (IL) 1 and 6 and tumor necrosis factor (TNF)] by macrophages during MCT induction of pulmonary hypertension was studied. Right ventricle/left ventricle plus septum weight ratios (RV/LV + S) were used as an index of the development of pulmonary hypertension. Administering PGE1 at a dose of 0.2 mg/kg/day for 4 weeks reduced significantly the RV/LV + S ratio from 0.428 +/- 0.070 to 0.243 +/- 0.059 (p < 0.01) and decreased the production of these cytokines: IL-1, from 4.675 +/- 3.558 to 1.800 +/- 0.722 units; IL-6, from 0.322 +/- 0.121 to 0.060 +/- 0.039 units; and TNF, from 0.578 +/- 0.369 to 0.004 +/- 0.004 units. In another series of experiments, a significant reduction of the RV/LV + S ratio was noted for only 1 week when we administered PGE1 immediately after the injection of MCT. We confirmed that histopathologic improvements of lungs were noted by administering 0. 2 mg/kg PGE1 for 4 weeks. In another experiment, PGE1 at a concentration of 2 microg/ml suppressed a rise in the cytosolic Ca2+ concentration of lipopolysaccharide-stimulated peritoneal macrophages of rats in vitro, suggesting that PGE1 suppressed cytokine production by macrophages through the suppression of the Ca2+ influx. These results suggest that administering PGE1 may be effective in the treatment of some forms of pulmonary hypertension in humans.

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Section: Discussionsupporting

confidence: 61%

“…On the other hand, prostaglandin E 1 (PGE 1 ) has been used clinically as a vasodilator to treat vascular occlusion as well as pulmonary hypertension [16,21,27,33]. However, the precise mechanisms of the effect of PGE 1 are not fully understood.…”

Section: Introductionmentioning

confidence: 99%

Suppressive Effect of Prostaglandin E1 on Pulmonary Hypertension Induced by Monocrotaline in Rats

Sakuma

Miyata

Kasukawa

1999

Lung

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“…Our observations are similar to those of Russell et al [9], who showed that a continuous infusion of PGE 1 (30 ng/kg/min) in 17 patients with ARDS had no effect on either oxygen delivery or consumption. Likewise, Kunimoto et al [10], using a dosing range of 20-60 ng/kg/min, failed to show that PGE 1 had an effect on cardiac index or oxygen delivery in 14 patients with ARDS. Our data, however, are different from those reported by a number of other investigators.…”

Section: Discussionmentioning

confidence: 98%

The Effect of Liposome-Encapsulated PGE1 on Systemic Oxygen Delivery and Consumption in Patients With the Acute Respiratory Distress Syndrome

Heard

Longtine

Smyrnios

et al. 2002

J Intensive Care Med

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The goal of this study was to determine the effect of liposome-encapsulated prostaglandin E1(PGE1) on oxygen delivery and consumption and hemodynamics in patients with the acute respiratory distress syndrome (ARDS). Mechanically ventilated patients with ARDS and pulmonary artery catheters who were in the intensive care unit (ICU) were enrolled within 24 hours of diagnosis. Treatment consisted of either liposomal PGE1or placebo every 6 hours in a dose-escalating fashion for up to 7 days. Cardiac index (CI), systemic vascular resistance index (SVRI), oxygen delivery (D2) and consumption (VO2), and oxygen extraction ratio were determined every morning before and after the dose of study drug using arterial and mixed venous blood gases and standard formulas. No significant differences in any of the variables were observed over time or between groups. Liposomal PGE1administered in this fashion does not alter hemodynamic parameters or oxygen transport variables in patients with ARDS.

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“…10 Most of the reports were case reports or uncontrolled, nonrandomized clinical trials with small numbers of patients (Table 4). [10][11][12][13][14][15][16]…”

Section: Intravenous Vasodilatorsmentioning

confidence: 99%

Management of Pulmonary Hypertension in the Operating Room

Subramaniam

Yared

2007

Semin Cardiothorac Vasc Anesth

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Pulmonary artery hypertension is defined as persistent elevation of mean pulmonary artery pressure > 25 mm Hg with pulmonary capillary wedge pressure < 15 mm Hg or elevation of exercise mean pulmonary artery pressure > 35 mm Hg. Although mild pulmonary hypertension rarely impacts anesthetic management, severe pulmonary hypertension and exacerbation of moderate hypertension can lead to acute right ventricular failure and cardiogenic shock. Knowledge of anesthetic drug effects on the pulmonary circulation is essential for anesthesiologists. Intraoperative management should include prevention of exacerbating factors such as hypoxemia, hypercarbia, acidosis, hypothermia, hypervolemia, and increased intrathoracic pressure; monitoring and optimizing right ventricular function; and treatment with selective pulmonary vasodilators. Recent advances in pharmacology provide anesthesiologists with a wide variety of options for selective pulmonary vasodilatation. Pulmonary hypertension is a major determinant of perioperative morbidity and mortality in special situations such as heart and lung transplantation, pneumonectomy, and ventricular assist device placement.

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A Comparative Study of the Vasodilator Effects of Prostaglandin E1 in Patients with Pulmonary Hypertension After Mitral Valve Replacement and with Adult Respiratory Distress Syndrome

Cited by 22 publications

References 14 publications

Suppressive Effect of Prostaglandin E1 on Pulmonary Hypertension Induced by Monocrotaline in Rats

Suppressive Effect of Prostaglandin E1 on Pulmonary Hypertension Induced by Monocrotaline in Rats

The Effect of Liposome-Encapsulated PGE1 on Systemic Oxygen Delivery and Consumption in Patients With the Acute Respiratory Distress Syndrome

Management of Pulmonary Hypertension in the Operating Room

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