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Biomedical subjects

G H Nelson

Publications and source records attributed to G H Nelson.

At least 73 records · Page 4Linked to original sources

Observations on maternal dietary fat intake and fetal pulmonary maturation in rats.

Pregnant rats were maintained on one of the following dietary regimes: (1) low fat through gestation; (2) low fat to gestational age 15, then high fat until term; or (3) high fat throughout gestation. Fetal pulmonary maturation (as measured by the lung content of acetone-precipitable lecithin) was accelerated in rats on the high-fat diet, was intermediate in the group on low fat later switched to high fat and was retarded in rats on the low-fat diet. We feel that these data, as well as previous reports from our laboratory, justify additional experiments on human subjects.

Animals↗

5-methoxy-2-methyl-3-indole acetic acid, a metabolite and alkali hydrolysis product of indomethacin, inhibits platelet aggregation, in vivo.

Previous studies suggested that one of the hydrolysis products of indomethacin, either 4-chlorobenzoic acid or 5-methoxy-2-methyl-3-indole acetic acid, can inhibit platelet aggregation in vivo. If correct, this hypothesis explains the apparent action of indomethacin dissolved at high pH where hydrolysis rapidly occurs. Moreover, if the indole is the active product, the hypothesis in addition suggests a possible role for the indole following the use of indomethacin dissolved at lower pH, since the indole is also an important natural metabolite of indomethacin in man. We induced platelet aggregation in cerebral and mesenteric microvessels and inhibited this aggregation with the indole (25 mg/kg i.p. one hour before test). The 4-chlorobenzoic acid was inactive. The indole had a modest but statistically significant inhibitory effect in vitro, when added to platelet rich plasma stimulated to aggregate by arachidonic acid (0.5 mM). Thus the action of indomethacin dissolved at high pH is explained, and a pharmacologic action of a metabolite of indomethacin becomes a possibility.

Animals↗

Method for calculating blood loss at vaginal delivery.

We describe a method for calculating blood loss at vaginal delivery using a special plastic drape. Blood loss is calculated from the sum of three components: (1) blood lost in sponges, (2) blood loss represented by clots, and (3) blood loss represented by unclotted RBC. The procedure has been used in ten patients and the results are presented. The obstetrician would know the maximal potential blood loss immediately after delivery. If this figure is less than 15% of the estimated blood volume, further calculation might be deemed unnecessary. If this figure exceeds 15% of the estimated blood volume, however, the full procedure described should be done. The final result could be available to the obstetrician within approximately four hours after delivery.

Blood Volume↗

Consideration of blood loss at delivery as percentage of estimated blood volume.

It is recommended that blood loss at delivery be evaluated in terms of percentage of estimated blood volume rather than in terms of volume only. Estimated blood volume in milliliters per kilogram may be calculated by the following formula: (formula: see text). It is recommended that postpartum hemorrhage be defined as a loss of blood at delivery of greater than 15% of the total estimated blood volume.

Blood Volume↗

Timing of postpartum hematocrit determinations.

Postpartum hematocrit determinations have been done at eight, 16, and 24 hours after vaginal deliveries. We studied 23 patients in whom the hematocrit level dropped at least 10% from control value with a range of 10% to 32%. The peak drop in hematocrit occurred at eight hours in four patients, at 16 hours in nine patients, and at 24 hours in ten. Therefore, no single timed hematocrit determination in the first 24 hours post partum will detect the peak drop in a vast majority of patients. A proposed plan for timing of hematocrit determinations in the postpartum period is presented.

Female↗

Unusual amniotic fluid spectral analysis in Rh sensitization.

In our experience delta 450 millimicron OD measurements have shown a progressive decline during the latter half of gestation in pregnancies unaffected by fetal hemolytic disease. However, we have seen two Rh-negative patients in whom there was a rise in delta 450 millimicron OD between 24 and 27 weeks' gestation and who subsequently bore Rh-negative infants. In these two cases the increase between 24 and 27 weeks was from approximately 0.140 to about 0.200. Both infants were unaffected with fetal hemolytic disease. Therefore, we recommend caution in interpreting modest increases in delta 450 millimicron OD during this period of gestation.

Amniotic Fluid↗

Body temperature recordings during oral prostaglandin E2 induction of labor.

Body temperature measurements have been recorded in 99 patients during the course of labor induction with oral prostaglandin E2 (PGE2). From the data obtained, there is no evidence that oral PGE2, in the usual dosage for induction of labor, acts as a pyretic agent. If fever is encountered during the course of an oral PGE2 induction, the obstetrician would be advised to look for some other cause for the temperature elevation.

Administration, Oral↗

Induction of labor with oral prostaglandin E2 in normal and high-risk pregnancies.

There were 153 oral prostaglandin (PG) E2 inductions attempted in 149 patients. For various reasons nine cases were dropped from the study. Of the remaining 144 induction attempts, 96 were judged successful, with a success rate of 67 per cent. Details of these inductions are presented, including summaries of three patients with uterine hypertonus and three with uterine hyperstimulation. As a rule, the labor pattern established with oral PGE2 was effective and indistinguishable from normal spontaneous labor. After review of the data we feel that induction of labor with oral PGE2 is no more hazardous to mother or infant than with other oxytocic agents. In our opinion oral PGE2 offers the obstetrician an additional means for induction of labor in normal and high-risk pregnancies. The need for close observation of the progress of labor during PGE2 inductions is emphasized.

Administration, Oral↗

Acquired resistance in turkey poults to Pasteurella multocida (P-1059 strain) during aflatoxin consumption.

The potential for impairment by aflatoxin of the development of acquired immunity to fowl cholera in 8 week old turkey poults from a commercial flock was investigated by challenge of vaccinated poults at 10, 12, and 16 weeks of age. Sixty poults were allotted to 4 groups: A) aflatoxin fed, nonvaccinated; B) aflatoxin fed, vaccinated; C) control fed, nonvaccinated; and D) control fed, vaccinated. Aflatoxin B-1 (.5 ppm) was added to the control ration of groups A and B from 49 to 70 days of age. The avirulent CU (Clemson University) strain of Pasteurella multocida drinking water vaccine was given for one day to groups B and C. Challenge (5 poults from each group) was by administration of the virulent (P-1059) strain of P. multocida in the drinking water for 4 consecutive days. The presence of aflatoxin B-1 (.5 ppm) in the feed during oral vaccination with the avirulent strain of P. multocida did not impair the development of acquired resistance to later challenge with the virulent strain. Results indicate that age of poults and method of vaccination may be important factors in the development of acquired resistance to fowl cholera when aflatoxin is present in the diet.

Administration, Oral↗

A comparison of oral prostaglandin E2 and intravenous oxytocin for induction of labor in normal and high-risk pregnancies.

The efficacy of oral prostaglandin E2 (PGE2) for induction of labor has been compared to that of intravenous oxytocin. There were 49 patients in each series. The over-all success rate with PGE2 is 82 per cent; with oxytocin, 65 per cent. PGE2 is at least as effective as oxytocin regardless of Bishop score or gravidity. There was no difference in the duration of labor in successful inductions with PGE2 or oxytocin. Nausea and diarrhea are more common with PGE2 but in only one case was this severe enough to warrent discontinuing the medication. One case of uterine hypertonus occurred in each series. No serious harmful effects on mother or fetus were noted with PGE2. These data support the concept that oral PGE2 administration is a safe and effective alternative to intravenous oxytocin for induction of labor in normal and high-risk pregnancies.

Administration, Oral↗