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Biomedical subjects

R C Goodlin

Publications and source records attributed to R C Goodlin.

At least 91 records · Page 5Linked to original sources
PubMed1988

Blow-blow-blow.

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Delivery, Obstetric↗
PubMed1988

Fetal endoxin and pregnancy complication.

Digoxin-like substances (endoxin) are found in increasing concentrations in serum and urine with advancing pregnancy. Some high-risk pregnant women with hypertension and/or in premature labor have increased levels of endoxin. Both nifedipine and antidigoxin serum are proposed as specific therapy in abnormal pregnancies with high levels of endoxin. Urinary endoxin levels may indicate otherwise unsuspected high-risk pregnancies.

Blood Proteins↗
PubMed1988

Fetal endoxins and complications of pregnancy.

Maternal endoxin (digoxinlike substance) is proposed as arising in the fetal area of the fetal adrenal cortex. Its function may be to sensitize the uterus for labor, much as does cortisol in the sheep fetus. Because endoxin is a sodium-potassium-adenosine triphosphatase inhibitor, however, it may also induce maternal vasoconstriction. On our service, normal pregnant women have detectable endoxin after 35 weeks with increasing amounts at term. Specimens of cord blood often have "digoxin" in the therapeutic range. We find that about 40% of women in premature labor and 65% of pregnant women with hypertension have elevated levels of serum endoxin. Postdate gravid women sometimes have very low endoxin levels. Pregnant women with complications and elevated digoxin (endoxin) levels could have specific antidigoxin therapy if endoxin proves to be a modulator of their symptoms. Digoxinlike substances are also sometimes elevated in ill nonpregnant persons, such as those with renal, liver, or heart failure, or hypertension.

Blood Proteins↗
PubMed1987

Evaluation of platelet function in pregnancy. Comparative studies in non-smokers and smokers.

We have evaluated the possible role of platelet functional abnormalities as a contributory cause of thrombosis during pregnancy and to the increased fetal mortality and morbidity among women who smoke. Fifty-three pregnant women were enrolled and evaluated on two separate prenatal visits held between the 20th and 36th week of pregnancy and, when possible, post partum. Smoking status was evaluated by personal statement and alveolar carbon monoxide levels. Women in the smoking group deliberately avoided cigarettes for at least 20 minutes before sampling. Plasma levels of beta-thromboglobulin, thromboxane B2, and 6-Keto PGF1 alpha were evaluated. A significant increase in 6-Keto PGF1 alpha was noted among smoking women as pregnancy advanced. 6-Keto PGF1 alpha levels decreased among non-smoking women while beta-thromboglobulin increased significantly between the 20th and 33rd week of pregnancy in non-smokers. Platelet aggregation, both in platelet rich plasma and in whole blood (by impedance aggregometry), was evaluated by five different parameters and four different aggregating agents. Significant differences between the non-smoking and smoking pregnant women were noted for selected age cohorts and aggregating agents. An increase in platelet reactivity among smokers was observed in whole blood by impedance aggregometry with adenosine diphosphate and in two age cohorts using platelet rich plasma. In two groups in which aggregation was significantly accelerated among non-smokers, epinephrine was used as the aggregating agent.

6-Ketoprostaglandin F1 alpha↗