Modification of hypoxic pulmonary vasoconstriction by aerosolized cromolyn sodium.

We have previously demonstrated the role of mast cell degranulation in the mediation of hypoxic pulmonary vasoconstriction, and its prevention by intravenous cromolyn sodium. In the present investigation, we studied the modification of the hypoxic pulmonary vascular response by aerosolized cromolyn sodium. In seven conscious sheep on two separate days, pulmonary arterial pressure, pulmonary arterial wedge pressure and cardiac output were measured for the calculation of pulmonary vascular resistance (Rpv) along with arterial oxygen tension (Pao2) during room air breathing and breathing a hypoxic gas mixture (13% O2-87% N2), without and with cromolyn sodium administration. Cromolyn sodium (20 mg X kg-1) was administered as an aerosol before and during 13% O2 breathing. The sheep had comparable degrees of hypoxia during low oxygen breathing on both days (mean PaO2: 43 and 46 mmHg). Breathing hypoxic gas mixture caused pulmonary vasoconstriction, with increases in mean Rpv of 89% (p less than 0.05). Aerosolized cromolyn sodium blunted the hypoxic pulmonary vascular response; mean Rpv increased by 27% (p less than 0.05), which was significantly different from the increase during hypoxia without cromolyn sodium treatment (p less than 0.05). We conclude that aerosolized cromolyn sodium (a mast cell membrane stabilizing agent) modifies hypoxic pulmonary vasoconstriction; however, unlike the intravenous form, aerosolized cromolyn sodium (at the dosage used) offers a partial protection.