AN INVESTIGATION OF THE MECHANISMS BY WHICH HYPERVENTILATION DECREASES PULMONARY VASCULAR RESISTANCE IN THE NEWBORN LAMB

Abstract

We have previously reported that hyperventilation decreases pulmonary vascular pressures in the newborn lamb. The following study examined whether these pulmonary vascular effects are due to mechanical effects of hyperventilation or due to the respiratory alkalosis, and whether the effects of hyperventilation are mediated by prostaglandin production. Six newborn lambs were anesthetized and appropriate vascular catheters were placed. Each lamb was studied during three baseline periods separated by two periods of hyperventilation, one with hypocarbia and one with normocarbia. Arterial blood gases were normal during the baseline periods and were unchanged during the hyperventilation with normocarbia. During hyperventilation with hypocarbia, marked respiratory alkalosis was produced. During hyperventilation with hypocarbia, pulmonary artery pressure decreased significantly from 25.8±5.53SD to 17.7±2.66SD (p≤.01) and pulmonary vascular resistance decreased significantly from 0.99±.037 to 0.07±.029 (p≤.03). There was no change in these values during hyperventilation with normocarbia. In preliminary studies on 4 newborn lambs pretreated with indomethacin, pulmonary artery pressure and pulmonary vascular resistance decreased during hyperventilation with hypocarbia. In newborn lambs, the pulmonary vascular effects of hyperventilation are not due to mechanical factors and may not be due to prostaglandin production.

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