Robert L. Andres

Cessation of cocaine use during pregnancy: effects of contingency management interventions on maintaining abstinence and complying with prenatal care

Previous studies have reported cessation of cocaine use in pregnant women prior to treatment entry. This study examined the relative effectiveness of adjunctive contingency management interventions in maintaining abstinence and enhancing compliance with prenatal care in this unique population. Pregnant cocaine-dependent women who had used the drug during this pregnancy but had ceased use prior to study entry (N = 12) were randomly assigned to one of two treatment groups. All patients received a multifaceted treatment including behaviorally based drug counseling and weekly prenatal visits. Patients in the experimental condition also received contingent reinforcement for cocaine abstinence and attendance at prenatal visits. There was a high rate of retention and abstinence from cocaine in both groups. However, patients in the experimental group had a higher rate of attendance at prenatal visits, and none of the patients in this group experienced adverse perinatal outcome(s), compared to 80% of patients in the control group. This finding has important implications for cost-effective treatments and prevention of illness.

The association of cigarette smoking with placenta previa and abruptio placentae

Smoking was recognized as having an adverse effect of pregnancy outcome as early as the mid 1950s. Smoking is a well recognized risk factor for low birthweight infants and has been implicated in preterm birth. The increased risk of both placenta previa and abruptio placentae among women who continue to smoke during pregnancy, is in general, less well recognized, but supported by numerous studies. The purpose of this article is to review the published literature dealing with the risk of placenta previa and abruptio placentae in women who smoke during their pregnancy.

VENOUS THROMBOEMBOLISM AND PREGNANCY

Venous thromboembolism remains a major cause of maternal morbidity and mortality. Pregnancy is a thrombogenic state; therefore, clinicians must be familiar with the diagnosis and treatment of acute VTE. It is of paramount importance when caring for pregnant women to understand which patients are at risk for VTE and to use thromboprophylactic heparin accordingly.

Cocaine alters placental production of thromboxane and prostacyclin

OBJECTIVE The objective of this study was to test the hypothesis that cocaine alters placental prostaglandin production in vitro. STUDY DESIGN Placentas were obtained from healthy women (n = 6) after normal vaginal delivery at term. Placental explants (300 mg) were incubated in duplicate at 37 degrees C in the presence of 0, 30, 300, or 3000 ng/ml cocaine. Thromboxane and prostacyclin production was measured by radioimmunoassay of their stable metabolites (thromboxane B2 and 6-keto-prostaglandin F1 alpha) at 0, 0.5, 1.0, 1.5, 2, 4, 8, and 12 hours. Analysis of variance with Newman-Keuls test was used for statistical analysis. RESULTS Cocaine increased thromboxane production in a dose-dependent manner (p < 0.001) and decreased prostacyclin production (p < 0.05). Cocaine increased the ratio of thromboxane/prostacyclin production (p < 0.05). CONCLUSION Cocaine alters the placental production of prostaglandins in vitro, favoring thromboxane production, which may cause vasoconstriction and decrease uteroplacental blood flow.

The acute effect of cocaine exposure on pregnant human myometrial contractile activity

OBJECTIVE The objective of this study was to test the hypothesis that cocaine acutely increases contractile activity in isolated pregnant human myometrium. STUDY DESIGN Myometrial samples were obtained from the lower uterine segment at elective cesarean section from five women at term who were not in labor and who had no perinatal risk factors. Myometrial strips were suspended in contractile buffer, and isometric contractions were measured. Frequency, amplitude, duration, and integrated area (mean +/- SE) were compared before and after the addition of cocaine (10(-6) to 10(-4) mol/L) by means of analysis of variance and Duncans multiple range test. RESULTS Contraction duration, expressed relative to control, increased acutely after addition of cocaine (10(-5) mol/L, 2.0 +/- 0.29; 10(-4) mol/L, 2.8 +/- 0.64) (p < 0.001). Integrated area of contractions also increased relative to control (10(-6) mol/L, 1.6 +/- 0.18, p < 0.05; 10(-5) mol/L, 2.4 +/- 0.16 and 10(-4) mol/L, 3.5 +/- 0.23, p < 0.001). These effects were dose dependent. CONCLUSION Cocaine acutely increases contractile activity in myometrium isolated from pregnant women.

Teratogenic potential of cocaine

Cocaine has been implicated as a potential cause of congenital abnormalities since the mid 1980s. Clinical studies have reported an increased risk of cardiovascular and central nervous system abnormalities as well as an increased incidence of limb reduction defects and intestinal atresias. The published data have not established an unequivocal link between cocaine and these abnormalities. The most compelling evidence for the role of cocaine as a teratogen is the increased risk of genitourinary tract defects. Although animal models have also yielded contradictory conclusions, it is intriguing to note that the abnormalities observed in these models are similar to those seen clinically. This review summarizes the clinical and basic research relating to the teratogenic potential of cocaine.

Cocaine acutely increases rat myometrial contractile activity by mechanisms other than potentiation of adrenergic pathways

OBJECTIVE We hypothesized that cocaine acutely increases contractile activity in isolated rat myometrium and that this effect is solely caused by potentiation of adrenergic pathways. STUDY DESIGN Isometric contractions were measured in myometrium isolated from virgin and day-18 pregnant Sprague-Dawley rats. Frequency, duration, amplitude, and integrated area were compared before and after the addition of cocaine (10(-6) to 10(-4) mol/L) by means of analysis of variance and Duncans multiple-range test. The effects of alpha-adrenergic receptor antagonists (prazosin 10(-6) mol/L and yohimbine 10(-6) mol/L) and beta-adrenergic receptor antagonist (DL-propranolol 2 x 10(-6) mol/L) were assessed. RESULTS Contraction duration, expressed relative to control, increased acutely after cocaine (10(-5) mol/L) administration in pregnant (1.70 +/- 0.20) and nonpregnant (1.36 +/- 0.24) myometrium (mean +/- SE, p < 0.05), as did integrated area (pregnant 3.47 +/- 0.97, nonpregnant 2.48 +/- 0.66) (mean +/- SE, p < 0.05). These effects were not completely inhibited by adrenergic blockade. CONCLUSION Cocaine acutely increases the duration and integrated area of spontaneous contractions in isolated rat myometrium by mechanisms not completely explained by inhibition of catecholamine reuptake and potentiation of adrenergic pathways.

Left thoracic duct lymph flow responses to angiotensin II or atrial natriuretic factor infusion in the ovine fetus

In the ovine fetus it is known that left thoracic duct lymph flow rate relative to body weight is four to five times adult levels, but it is not known whether the circulating hormones modulate fetal lymph flow. To explore this, we intravenously infused either angiotensin II (10 to 400 ng/min, n = 8) or atrial natriuretic factor (500 to 1000 ng/min, n = 8) into chronically catheterized fetal sheep for 30 minutes. Significant increases occurred in fetal arterial (p less than 0.0001) and venous (p = 0.018) pressures during the angiotensin II infusion, and thoracic duct lymph flow rate underwent a dose-dependent increase (r = 0.888, p = 0.0033). With termination of the angiotensin II infusion, fetal vascular pressures rapidly returned to control levels, and lymph flow fell from 18.8% +/- 10.1% (mean +/- SE) above control to 13.7% +/- 7.7% below preinfusion levels (p less than 0.01). During the atrial natriuretic factor infusion, fetal arterial pressure and circulating blood volume decreased significantly (p less than 0.01), whereas thoracic duct lymph flow was unchanged. After termination of the atrial natriuretic factor infusion, fetal arterial pressure returned toward control, blood volume remained reduced, and lymph flow rate underwent a transient rise to 35.6% +/- 15.7% (p less than 0.05) above control levels. These data suggest that angiotensin II and atrial natriuretic factor have significant but opposite effects on fetal thoracic duct lymph flow rate, with angiotensin II stimulating and atrial natriuretic factor suppressing lymph flow.