Biomedical subjects

D S Lambers

Publications and source records attributed to D S Lambers.

4 recordsLinked to original sources

PubMed2000

Functional role of angiotensin II type 1 and 2 receptors in regulation of uterine blood flow in nonpregnant sheep.

The objective was to determine the receptor subtype of angiotensin II (ANG II) that is responsible for vasoconstriction in the nonpregnant ovine uterine and systemic vasculatures. Seven nonpregnant estrogenized ewes with indwelling uterine artery catheters and flow probes received bolus injections (0.1, 0.3 and 1 microg) of ANG II locally into the uterine artery followed by a systemic infusion of ANG II at 100 ng x kg(-1) x min(-1) for 10 min to determine uterine vasoconstrictor responses. Uterine ANG II dose-response curves were repeated following administration of the ANG II type 2 receptor (AT(2)) antagonist PD-123319 and then repeated again in the presence of an ANG II type 1 receptor (AT(1)) antagonist L-158809. In a second experiment, designed to investigate the mechanism of ANG II potentiation that occurred in the presence of AT(2) blockade, nonestrogenized sheep received a uterine artery infusion of L-158809 (3 mg/min for 5 min) prior to the infusion of 0.03 microg/min of ANG II for 10 min. ANG II produced dose-dependent decreases in uterine blood flow (P < 0.03), which were potentiated in the presence of the AT(2) antagonist (P < 0.02). Addition of the AT(1) antagonist abolished the uterine vascular responses and blocked ANG II-induced increases in systemic arterial pressure (P < 0.01). Significant uterine vasodilation (P < 0.01) was noted with AT(1) blockade in the second experiment, which was reversed by administration of the AT(2) antagonist or by the nitric oxide synthetase inhibitor N(omega)-nitro-L-arginine methyl ester. We conclude that the AT(1)-receptors mediate the systemic and uterine vasoconstrictor responses to ANG II in the nonpregnant ewe. AT(2)-receptor blockade resulted in a potentiation of the uterine vasoconstrictor response to ANG II, suggesting that the AT(2)-receptor subtype may modulate uterine vascular responses to ANG II potentially by release of nitric oxide.

Angiotensin II↗

PubMed1996

The maternal and fetal physiologic effects of nicotine.

The effects of nicotine are seen in every trimester of pregnancy, from increased spontaneous abortions in the first trimester, to increased premature delivery rates and decreased birth weights in the final trimester. The birth weight of a baby is dependent on two factors: the gestational age of the fetus at the time of delivery and the rate of fetal growth. Nicotine has been shown to affect both of these factors. Carbon monoxide, also found in tobacco, forms carboxyhemoglobin, which inhibits the release of oxygen into fetal tissues. Nicotine readily gains access to the fetal compartment via the placenta, with fetal concentrations generally 15% higher than maternal levels. The primary metabolite of nicotine, cotinine, has a half-life of 15 to 20 hours and serum concentrations that are 10-fold higher than nicotine; thus, cotinine provides a better index of nicotine exposure because of its longer half-life. Nicotine concentrates in fetal blood, amniotic fluid, and breastmilk. The fetus and neonate may also have environmental tobacco exposure that may be significant. In animal models and humans, nicotine increases maternal blood pressure and heart rate, with a concomitant reduction in uterine blood flow. An increase in fetal heart rate is also seen, which is thought to be caused by catecholamine release. The impact of nicotine on the respiratory and central nervous system is also reviewed. In conclusion, the physiological effect of tobacco on fetal growth seems to be a culmination of both the vasoconstrictive effects of nicotine on the uterine and potentially the umbilical artery and the effects on oxygenation by carboxyhemoglobin.

Embryonic and Fetal Development↗

PubMed1996

Hyperreactio luteinalis complicating a normal singleton pregnancy.

Hyperreactio luteinalis is a rare, usually self-limited syndrome with bilaterally enlarged ovaries containing multiple theca lutein cysts. It is usually associated with gestational trophoblastic disease and/or pregnancies that have elevated maternal serum hCG levels. Hyperreactio luteinalis with maternal anasarca was diagnosed at 19 weeks in a spontaneously conceived gestation, in a 16-year-old primigravida. A second trimester termination for maternal respiratory decompensation secondary to pleural effusions and ascites was required. There was no evidence of trophoblastic disease on pathological examination of the products of conception. Hyperreactio luteinalis may be diagnosed prenatally by ultrasound, and intervention may be necessary for maternal indications. Following termination of pregnancy, spontaneous resolution and regression of ovarian size may be expected.

Abortion, Induced↗

PubMed1995

Ability of normal vaginal flora to produce detectable phosphatidylglycerol in amniotic fluid in vitro.

OBJECTIVE: To determine if bacteria are capable of producing phosphatidylglycerol in amniotic fluid (AF) and the number of colony forming units (CFU) of bacteria necessary to produce this result. METHODS: Eleven species of bacteria and one species of yeast, common to the female genital tract and implicated in chorioamnionitis, were selected. Amniotic fluid was collected from 21 women and inoculated with 10(8) CFU/mL of each isolate. Aliquots of AF were tested at 0, 4, 12, and 24 hours for colony counts and the presence of phosphatidylglycerol by thin-layer chromatography. RESULTS: The mean gestational age (+/- standard deviation) of the 21 study patients was 33 weeks and 1 day (+/- 4 weeks). Among the 12 species studied, Escherichia coli produced phosphatidylglycerol, at a concentration of 1.75 x 10(8) CFU/mL, beginning 12 hours after incubation. CONCLUSION: Escherichia coli is capable of producing phosphatidylglycerol in AF in vitro and is present in the vagina in 24% of normal pregnant patients. Our findings question the validity of using vaginal pool AF specimens for phosphatidylglycerol determination. Therefore, we recommend that patients presenting with preterm premature rupture of membranes be evaluated by amniocentesis to determine fetal lung maturity with phosphatidylglycerol and the lecithin-sphingomyelin ratio.

Amniotic Fluid↗