Uterine tone may be the most important predictor of success when selecting candidates for external cephalic version.

Monoamniotic twin pregnancies and cord entanglement in such twins were diagnosed reliably by ultrasound. Abnormal tracings prompting cesarean delivery occurred in two of the five pregnancies with cord entanglement. Amniocentesis reflected pulmonary maturity of both twins in all pregnancies so assessed, and delivery after 32 weeks' gestation, with lung maturity, resulted in good perinatal outcomes. Statistical validity of these findings is limited by our small sample size.

The mechanism whereby glucocorticoid deficiency impairs renal water excretion was studied in the conscious mineralocorticoid-replaced, adrenalectomized rat. Control animals received physiologic replacement with prednisolone, and experimental animals were deprived of glucocorticoid hormone for either 1 or 14 days. The control animals excreted 95 +/- 1.9% of an acute water load (30 ml/kg) in 3 hours, a value significantly higher than the volume excreted by animals deprived fo glucocorticoid hormone for 1 day (70.0 +/- 3.6%, P less than 0.01) and 14 days (40.0 +/- 3.9%, P less than 0.01). Following the acute water load, plasma vasopressin levels, as measured by radioimmunoassay, was 1.08 pg/ml in the control rats, a value significantly lower than values obtained after the water load in rats deprived of glucocorticoid hormone for 1 day (2.5 +/- 0.2 pg/ml, P less than 0.01) and 14 days (2.4 +/- 0.3 pg/ml, P less than 0.01). To further examine the effect of plasma vasopressin in the impaired water excretion of glucocorticoid deficiency, we performed studied in Brattleboro rats with central diabetes insipidus. In these animals with absence of vasopressin, a defect in water excretion was observed after 14 days, but no 1 day, of glucocorticoid deficiency. In Sprague-Dawley rats, the impaired water excretion after 14 days of glucocorticoid deficiency was associated with a significantly lower cardiac index (209 +/- 14 vs. 291 +/- 11 ml/min/kg, P less than 0.01) and renal blood flow (3.8 +/- 0.3 vs. 5.7 +/- 0.2 ml/min/g, P less than 0.01) than that observed after 1 day of glucocorticoid deficiency. In diabetes insipidus rats, after 14 days of glucocorticoid deficiency, the percentage of an acute water load excreted (121 +/- 7% vs. 158.7 +/- 7.0%, P less than 0.01) was lower than that observed after 1 day of glucocorticoid deficiency. In summary, the present results indicate that glucocorticoid deficiency impairs renal water excretion by both vasopressin-dependent and vasopressin-independent mechanisms. The vasopressin-dependent renal mechanism is associated with a marked decrease in both systemic and renal hemodynamics.

A B S T R A C T The vascular effects of arginine vasopressin (AVP) were examined in conscious SpragueDawley rats. In six control rats, synthetic AVP at a dose of40 ng/kg, injected as an intravenous bolus, resulted in a rise in mean arterial blood pressure (BP) from 127 to 149 mm Hg (P < 0.005). No tachyphylaxis was observed after a second AVP bolus administered 30 min later, as BP increased from 125 to 150 mm Hg, P < 0.005. In a second group of six rats, 1-deamino penicillamine, 2-(O-methyl) tyrosine AVP ([dPTyr (Me) To eliminate the possibility that this AVP analogue was antagonistic to endogenous pressor substances other than AVP, additional studies were performed. In homozygotis Brattleboro (diabetes insipidus) rats receiving exogenous AVP, the vasopressin analogue lowered BP (133 to 112 mm Hg, P < 0.001), but failed to lower BP (112 vs. 112 mm Hg) in rats not receiving AVP. BP in a group of bilaterally nephrectomized Sprague-Dawley rats, after 24 h of fluid deprivation, fell from 130 to 118 mm Hg (P < 0.02) after the AVP analogue, precluding an effect of the analogue on lowering BP by inhibiting the renin-angiotensin system. Finally, the AVP analogue failed to alter the pressor response to exogenous infusions of either norepinephrine or angiotensin II. These results demonstrate that (a) the AVP analogue [dPTyr (Me)]AVP abolishes the pressor effect of large exogenous doses of AVP; (b) the analogue has no effect on BP in rats with suppressed or absent endogenous AVP; (c) the depressor effect of the analogue does not involve antagonism of the vasoconstrictors, norepinephrine or angiotensin; and (d) most importantly, BP fell significantly after AVP antagonist administration in intact, conscious, fluid-deprived rats with elevated endogenous AVP levels. This effect of the AVP antagonist to block endogenous AVP and lower BP was primarily due to a fall in peripheral vascular resistance.