David B. Schwartz

Genital condylomas in pregnancy: Use of trichloroacetic acid and laser therapy☆

Genital condylomas in pregnancy pose several management problems for the obstetrician, including the mechanical problems of large condylomas and the issues relating to transmission of the human papillomavirus to the fetus during delivery. Transmission of papillomavirus occurs infrequently, but respiratory papillomatosis can result in mortality or lifelong morbidity. We evaluate our experience in treating condylomas in 32 pregnant women, using carbon dioxide laser therapy and 85% trichloroacetic acid. Condylomas in 31 (97%) of 32 women were controlled with this combination therapy. The only maternal complication was an episode of acute pyelonephritis secondary to urethral catheterization. One patient had premature rupture of the membranes 4 days after laser therapy and subsequently was delivered of a healthy neonate at 36 4/7 weeks. Prenatal photovaporization of condylomas appears to offer a method of treatment with a low complication and recurrence rate and helps avert the dilemma of whether patients with extensive genital condylomas should be delivered by cesarean section.

Effect of PGI2 on the response of the ovine placenta to norepinephrine

We have examined the effects of PGI2, 50 microgram/kg, on norepinephrine induced placental vasoconstriction in 6 chronically catheterized near-term sheep. Regional blood flows were measured with radioactive microspheres. Control flows were measured. Norepinephrine was than infused at 50 microgram/min throughout the experiment. After 15 min the blood flows were again measured and PGI2 was then added to the infusate at 50 microgram/min. In 15 min regional blood flows were again measured and the PGI2 infusion was stopped. Regional blood flows were measured for the last time 15 min later. The renal and nonplacental uterine vasculatures behaved in a predictable manner. There was constriction with norepinephrine but PGI2 opposed the effects of norepinephrine and decreased the resistance towards the normal levels. The placenta did not behave as did the other organs. Norepinephrine increased placental resistance but PGI2 did not decrease the resistance and severely depress the placental blood flows. PGI2 does not appear to oppose norepinephrine induced placental vasoconstriction.

Placental vascular responses to 6-keto-prostaglandin E1 in the near-term sheep.

6-Keto-prostaglandin E1 (6-keto-PGE1) is a biologically active, stable metabolite of prostaglandin I2 (PGI2). It has vasoactive properties similar to those of PGI2 and it has been shown to decrease the resistance of the renal, mesenteric, and pulmonary vascular beds. PGI2 is synthesized by the pregnant uterus and is vasoactive in the ovine placenta. The effects of 6-keto-PGE1 on uterine and placental blood flow in pregnant ewes were determined for comparison with those of PGI2. Near-term ewes and their fetuses were chronically catheterized to permit the measurement of regional blood flow by the radioactive microsphere method. In six sheep a 5-minute maternal jugular infusion of 3.25 micrograms/kg/min of 6-keto-PGE1 decreased mean arterial blood pressure from 89 +/- 4.8 to 63 +/- 7.1 mm Hg. Uterine vascular resistance decreased from 0.55 +/- 0.11 to 0.35 +/- 0.05 peripheral resistance units (PRU), but maternal cotyledonary resistance increased from 0.19 +/- 0.04 to 0.27 +/- 0.03 PRU. In five sheep a fetal intravenous infusion of 18 micrograms/min of 6-keto-PGE1 decreased mean fetal blood pressure from 43 +/- 2 to 29 +/- 2 mm Hg. Cotyledonary vascular resistance increased from 0.30 +/- 0.02 to 0.55 +/- 0.09 PRU . kg-1. In these sheep there were no significant changes in maternal uterine, renal, or cotyledonary blood flows. These results indicate that 6-keto-PGE1 is similar to PGI2 in that it produces maternal cotyledonary vasoconstriction, hypotension, and vasodilation in other organs.

The stability of phospholipids in amniotic fluid.

A systematic study of amniotic fluid phospholipids including phosphatidylcholine (PC, lecithin), saturated phosphatidylcholine, and phosphatidylglycerol was undertaken to evaluate the stability of these surfactant indices as a function of temperature and time. The purpose of the study was to determine optimum conditions for storage and for transport of specimens to centralized laboratories performing comprehensive analyses of amniotic fluid phospholipids for improved assessment of fetal lung development. Remarkable stability was found for the above phospholipids, as well as for the more commonly employed ratio of lecithin to sphingomyelin. We determined that room temperature more commonly employed ratio of lecithin to sphingomyelin. We determined that room temperature storage is acceptable for periods up to 24 hours; however, when longer delays before lipid extraction are anticipated, it is essential that specimens be frozen or that refrigeration or wet-ice storage (4 degrees C) be employed. Results of this study indicate that when amniotic fluid samples are stored frozen and strict quality control is maintained in analytic procedures, only minimal changes occur in phospholipid concentrations over 12 months.

Ovine maternal and fetal circulatory responses to an endoperoxide analog.

Abstract There are extensive data on the circulatory responses to prostaglandins during pregnancy, but little is known about the precursor endoperoxides. The endoperoxide analog (15S)-hydroxy-9α, 11α-(epoxymethano)prosta-5Z, 13E-dienoic acid (EPA1) was used to evaluate the circulatory effects of endoperoxides in pregnant sheep. Ten near-term ewes and their fetuses were chronically catheterized to permit the measurement of regional blood flows by the radioactive microsphere method. In five sheep a fetal IV bolus injection of 12.5 μg/kg EPA1 produced a significant increase in fetal blood pressure from 43 to 51 mm Hg, vascular resistance of the cotyledons from 0.06 to 0.09 PRU·kg−1, membranes from 0.84 to 3.15 PRU·kg−1, and kidneys from 1.18 to 1.94 PRU·kg−1. In five sheep a 10-min maternal infusion of 0.5 μg/kg/min EPA1 produced a significant increase in blood pressure from 89.0 to 115.0 mm Hg, resistance of the uterus from 0.49 to 1.10 PRU, and kidneys from 0.13 to 0.20 PRU. There was no significant change in maternal cotyledonary resistance. It is evident from these results that EPA1 causes widespread vasoconstriction. In the placenta, however, there is vasoconstriction on the fetal side but the resistance of the maternal vascular bed is unaltered.