Why the study?
Does prostacyclin infusion or acute hypoxia alter plasma atrial natriuretic peptide levels in patients with primary pulmonary hypertension and normal subjects?
Does prostacyclin infusion or acute hypoxia alter plasma atrial natriuretic peptide levels in patients with primary pulmonary hypertension and normal subjects?
Plasma ANP is markedly elevated in primary pulmonary hypertension due to altered hemodynamics rather than hypoxia, and is not acutely changed by prostacyclin infusion.
ANP in PPH is unaltered by acute prostacyclin or hypoxia; supports hemodynamic etiology but leaves open therapeutic relevance and requires validation.
Plasma levels of atrial natriuretic peptide (ANP) were determined during cardiac catheterization in nine patients with primary pulmonary hypertension (PPH) and the effect of prostacyclin infusion via a right heart catheter studied. The role of hypoxia on the release of ANP was investigated in a control group of six normal subjects who underwent an acute hypoxic challenge. Patients showed the typical haemodynamic changes of primary pulmonary hypertension with elevation of mean (SD) pulmonary artery pressure, 71.3 (13.8) mmHg, and low cardiac index, 1.9 (0.5) l.min-1.m-2. Plasma ANP was also elevated; mean pulmonary artery plasma ANP was 96.3 (77.6) pmol.l-1 in PPH patients compared with mean venous plasma ANP of 8.9 (5.6) pmol.l-1 in normal subjects. Prostacyclin infusion in PPH patients and hypoxic challenge in normal subjects did not significantly alter plasma ANP levels. The elevated levels of ANP in PPH are due to the altered haemodynamics secondary to increased pulmonary vascular resistance and may be responsible for the lack of peripheral oedema seen in this condition.
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Morice et al. (1990) studied this question.
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