The Grand Multipara (GM) has almost disappeared in the Western countries due to the advancement of family planning. Having a heterogeneous population, the problem of Grand Multiparity still exists in our country. This study is based on 5785 cases of GM which were treated in our Obstetrical Department during a period of 16 years (1960-1975). We have compared this group to the general obstetrical population in terms of pregnancy and delivery complications. Face and breech presentations as well as transverse lie were twice, brow presentations were three times as frequent in the GM group. Postpartum hemorrhage (P.P.H.) was four times and premature separation of the placenta twice as frequent. Rupture of the uterus was about 20 times more frequent. Forceps delivery and Cesarean section rate were twice, while the vacuum extraction 5-fold more frequent. Though there was no material mortality and perinatal mortality was not higher than in the general population. Even though the percentage of GM in our population has been decreased in the last 10 years, our results suggest that Grand Multiparity is still a high risk obstetrical problem.

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Pulmonary arterial pressure is decreased in pregnant women despite increased cardiac output, suggesting that pulmonary vascular resistance is decreased in pregnancy. To determine if pulmonary vascular reactivity is decreased in pregnant rats, lungs isolated from pregnant rats were perfused with blood from other pregnant rats at constant flow rate, and pressor responses to airway hypoxia and to angiotensin II were measured. Compared with responses obtained in lungs from nonpregnant female rats, hypoxic and angiotensin II pressor responses were blunted in pregnancy. To separate possible effects of pregnancy on the lung from those of substance(s) circulating in the blood in pregnancy, we perfused lungs from nonpregnant rats with blood from pregnant rats. Both the hypoxic and angiotensin II pressor responses were blunted by blood from pregnant rats. The angiotensin II pressor response was blunted also in lungs from pregnant rats perfused with blood from nonpregnant rats. These results suggest that a circulating substance is responsible for blunting of pulmonary vascular reactivity in pregnancy and that changes in the lung induced by pregnancy also depress angiotensin II responses. It is unlikely that estrogen and progesterone were responsible for these effects, since lungs and blood obtained from animals treated with these hormones did not have blunted pulmonary vascular reactivity.

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