The pulmonary vascular effects of prostaglandin E
1 (PGE
1) and isosorbide dinitrate (ISD) on acute hypoxic pulmonary vasoconstriction in conscious sheep were studied. While the animals inhaled room air or hypoxic gas (O
2:N
2 =1.9), PGE
1 (0.5μg/kg/min) and ISD (10μg/kg/min) were administered intravenously for 20 min, using an infusion pump. The changes of pulmonary arterial pressure (P^
-PA) or pulmonary vascular resistance (PVR) in room air due to PGE
1 decreased P^
-PA by 14.7% (p<0.05) and PVR by 14.5% (p<0.05). The effect of PGE
1 in room air on systemic arterial pressure (P^
-SA) remained nearly constant, whereas slight decreases in systemic vascular resistance (SVR) were noticed. In hypoxic condition, P^
-SA levels were slightly decreased by PGE
1, but SVR indicated a slight degree of delayed rise. When ISD in room air was administered, the values of P^
-PA, PVR, P^
-SA and SVR decreased by 9% (p<0.05), 10.4% (p<0.05), 17.7% (p<0.05) and 21.8% (p<0.05), respectively. In hypoxic condition, ISD decreased the values of P^
-PA, PVR, P^
-SA and SVR by 14.7% (p<0.05), 15.8% (p<0.05), 10.2% (p<0.05) and 6.7% (p<0.05), respectively. In summary in hypoxic condition both PGE
1 and ISD cause similar decreases of P^
-PA and PVR. Furthermore, there was a very little decrease in P^
-SA during PGE
1 infusion in the hypoxic condition. These findings may suggest that the vasodilator actions of PGE
1 were not evident in the pulmonary vascular bed under resting conditions, but could be demonstrated in vessels with increased tone produced by hypoxia without a marked fall in the systemic arterial pressure.
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