Reduction In Mean Pulmonary Artery Pressure Research Articles

Haemodynamic and hormonal effects of captopril in primary pulmonary hypertension.

The treatment of primary pulmonary hypertension is unsatisfactory. Since, in animals, experimental pulmonary vasoconstriction may be mediated in part by angiotensin II, we treated five primary pulmonary hypertensive patients with captopril for four days. To ensure accuracy of haemodynamic and hormone data, the patients were studied under conditions of constant body posture, regulated dietary sodium and potassium intake, and unchanged diuretic therapy. Captopril reduced mean pulmonary arterial pressure in parallel with plasma angiotensin II levels. Right ventricular ejection fraction recordings increased considerably in three of four patients. Systemic arterial pressure fell, but there was no change in right atrial pressure, cardiac output, or heart rate. The decline in plasma (and urine) aldosterone levels presumably contributed to the positive cumulative potassium balance and the rise in plasma potassium (mean 0.7 mmol/1). These encouraging results suggest that converting enzyme inhibitors warrant a formal trial with prolonged follow up in the treatment of primary pulmonary hypertension.

Prostacyclin-induced acute pulmonary vasodilation in primary pulmonary hypertension.

To evaluate the effects of prostacyclin (prostaglandin I2) on pulmonary vascular tone in primary pulmonary hypertension (PPH), we performed right-heart catheterization on seven patients with PPH and made hemodynamic measurements before and after infusing incremental doses of prostacyclin. In maximal doses of 2-12 mg/kg/min (mean 5.7 +/0 3.1 ng/kg/min), prostacyclin reduced mean pulmonary arterial pressure from 62 +/- 15 to 55 +/- 16 mm Hg (p less than 0.05) and total pulmonary resistance from 17.1 +/- 8.7 to 9.7 +/- 5.9 units (p less than 0.005), and increased cardiac output from 4.22 +/- 1.64 to 6.57 +/- 2.04 l/min (p less than 0.01). Heart rate increased from 83 +/- 13 to 94 +/- 11 beats/min (p = 0.1) and mean systemic arterial pressure decreased from 90 +/- 12 to 77 +/- 4 mm Hg (p = 0.055). Three patients who received a continuous infusion of prostacyclin for 24-48 hours had sustained reductions in total pulmonary resistance during the infusion period. These data demonstrate that prostacyclin can increase cardiac output and reduce pulmonary arterial pressure and resistance in PPH.

The effects of a new xanthine derivative, 3,7-dimethyl-1(5-oxohexyl)-xanthin (pentoxifylline) on the general and cardiac haemodynamics of the intact animal.

A study has been made of the effects of xanthine derivative (pentoxifylline) upon the general and cardiac haemodynamics of intact anaesthetised dogs. The drug increased heart-rate, respiration rate, cardiac output and systemic pressure. It reduced mean pulmonary arterial pressure. Coronary flow was increased for only a few minutes, but coronary sinus O2 content increased throughout the study. Lactate and pyruvate values increased in both artery and coronary sinus, as did the cardiac extraction of these substances. Cardiac extraction of non-esterified fatty acid increased.