EFFECTS OF MAGNESIUM-SULFATE AND NITRIC-OXIDE IN PULMONARY-HYPERTENSION INDUCED BY HYPOXIA IN NEWBORN PIGLETS

Aim-To examine the haemodynamic effects of intravenous magnesium sulph ate on an animal model of neonatal pulmonary hypertension induced by h ypoxia. Methods-The cardiac index (Q), pulmonary arterial pressure (PA P), systemic arterial pressure (SAP), and pulmonary (PVRI) and systemi c (SVRI) vascular resistance indices were measured in nine newborn pig lets (including three controls). Pulmonary hypertension was induced by lowering the FIO2, to 0.12-0.14, after which there was a significant increase in PAP and PVRI (37% and 142%, respectively; p<0.01) and a si gnificant fall in SAP and Q (30% and 33%, respectively; p<0.01). Resul ts-Magnesium sulphate was infused intravenously as four doses of 25 mg /kg, 15 minutes apart, which resulted in a significant mean (SD) incre ase in serum magnesium (0.83 (0.07) mmol/l to 1.82 (0.19) mmol/l; p<0. 01). After the initial dose SAP, SVRI, PAP and PVRI decreased, but not significantly. Each subsequent dose of (50, 75, 100 mg/kg) was accomp anied by further significant reductions in these variables from contro l baseline (p<0.05). The PVRI:SVRI ratio remained unchanged throughout . Inhaled nitric oxide (NO) 40 ppm was administered after the last dos e of magnesium sulphate. The PVRI:SVRI significantly decreased (p<0.05 ), indicating that reversible pulmonary hypertension remained after a maximum dose of magnesium sulphate. Conclusions-Unlike NO, magnesium s ulphate is not a selective pulmonary vasodilator and may lead to delet erious effects on systemic pressures in critically ill newborns.