ABSTRACT. This report analyzes the effect on pulmonary vascular structure and function in the newborn guinea pig of chronic fetal hypoxemia, induced by maternal hypobaric hypoxia (380-420 torr) without direct interference with the utero-placental blood flow. Six pregnant guinea pigs were maintained in hypobaric chambers, 10 newborns from their litters being the hypoxic group. Twenty newborns from the litters of 10 pregnant guinea pigs maintained in air were the control group. After spontaneous delivery catheters were placed in the left carotid and the main pulmonary arteries of the newborns. Oxygen consumption was measured, pressures recorded from the pulmonary artery, right ventricle, and right atrium, oxygen saturation and hemoglobin concentration estimated on blood from systemic arteries, pulmonary artery, and right atrium, and cardiac output calculated (Fick principle). All data were normalized per kilogram body weight. Morphometric analysis of the pulmonary vasculature after injection of the pulmonary arteries showed no difference between the groups. Contrary to expectation chronic hypoxemia in utero did not cause pulmonary hypertension or the precocious muscularization of the precapillary unit found in human cases of persistent pulmonary hypertension: it caused growth retardation, a feature not typical of the human syndrome. (Pediatr Res 20: 292-295,1986)
Abbreviation v 0 2 , oxygen consumptionAcute alveolar hypoxia in man and experimental animals causes pulmonary hypertension by vasoconstriction that is rapidly reversible on return to air (1-5). Chronic hypoxia causes progressive hypertension and structural changes in the pulmonary vasculature that are only partly reversible (6-8). Morphometric analysis shows that these changes include an increase in the thickness of the arterial medial coat, the appearance of muscle in the smaller more peripheral arteries that are normally not muscular, and a reduction in the density of intraacinar arteries that fill with injection medium (6, 7). In the exteriorized fetal sheep and newborn lamb, numerous studies have demonstrated an increase in pulmonary vascular resistance in response to acute Rcceivcd Junc 13, 1984; accepted November 18, 1985 hypoxia (5, 9, 10). The speculation that chronic fetal hypoxemia causes persistent pulmonary hypertension in the newborn is based on these acute studies in which hypoxemia is caused by a reduction in uterine or placental blood flow. Few investigators have examined the effect of chronic hypoxemia on the intact fetus.Recently we have reported severe structural abnormalities of the microcirculation of the lungs in two series of newborns with fatal persistent pulmonary hypertension (1 1, 12), notably muscularization of the intraacinar pulmonary arteries that normally at this age are free of muscle. Our present study analyzes the effect on the structure and function of the pulmonary vascular bed of the newborn guinea pig after chronic fetal hypoxemia induced by maternal hypoxia without any direct interference with the utero placent...