James N. Pasley

Effects of various doses of estradiol on chlamydial genital infection in ovariectomized guinea pigs.

The effect of various doses of estradiol on genital tract infection by the chlamydial agent of guinea pig inclusion conjunctivitis (GPIC) was investigated in ovariectomized guinea pigs. Prolongation of infection, as determined by chlamydial inclusion counts of cells in Giemsa-stained smears of vaginal scrapings, was observed in animals receiving daily doses of 1.0, 10.0, 100.0, or 1000 μg of estradiol. In contrast to controls, ascending infection resulting in endometritis was found in animals receiving doses of ≥1.0 μg of estradiol per day. Response to estradiol treatment was reflected in an increase in cervical-uterine wet weight and uterine wall thickness. No differences were observed in time of appearance of antibody titers to GPIC in serum, but a delay in appearance of IgA antibody to GPIC in genital secretions was found in estradiol-treated animals receiving doses of ≥1.0 μg per day.

Absence of progesterone effects on chlamydial genital infection in female guinea pigs

The effect of progesterone alone and in combination with estradiol was investigated in ovariectomized and gonadally intact female guinea pigs infected with the chlamydial agent of guinea pig inclusion conjunctivitis (GPIC). The course of the infection, as determined by the percentage of cells with GPIC (chlamydia) inclusions in Giemsa-stained vaginal scrapings, was not affected in animals receiving 5.0 mg of progesterone daily. Progesterone had no influence on the enhancement of infection by estradiol. In comparison with sesame oil-treated controls, infection was prolonged by four to six days (P less than .05) in animals receiving a combination of 5.0 mg of progesterone plus 1.0 microgram of estradiol or 1.0 microgram of estradiol alone each day. In ovariectomized animals, estradiol delayed the appearance of IgA antibody in genital secretions, whereas progesterone alone had no effect. Guinea pigs treated with estradiol or progesterone plus estradiol manifested an acute endometritis not observed in animals treated with progesterone alone or in controls receiving sesame oil. Although cervical ectopy, analogous to that seen in women with high levels of progesterone, was identified by histopathology in animals treated with progesterone, no enhancement of the chlamydial infection was observed.

Chlamydial salpingitis in female guinea pigs receiving oral contraceptives.

Female guinea pigs were given daily doses of a combination of oral contraceptive (OC) agents, consisting of mestranol and norethynodrel suspended in sesame oil or distilled H2O, and were infected in the genital tract with the chlamydial agent of guinea pig inclusion conjunctivitis (GPIC). Counts of chlamydial inclusions in cells of vaginal smears collected during infection, showed prolongation and enhancement of infection in OC-treated animals as compared with controls. Appearance of IgG and IgA antibodies to GPIC in genital secretions, as determined by enzyme-linked immunosorbent assay (ELISA), was also delayed in OC-treated animals as compared with controls. OC-treated infected animals were killed on days 15 and 43, and gross pathological evidence for ascending infection culminating in salpingitis was found in all of five and four of five animals, respectively. On the other hand, among untreated infected controls on each sacrifice day, only one of five animals had any evidence for ascending infection. Chlamydiae were detected by light and electron microscopy in fallopian tube tissue collected on day 15 following OC-treatment but not in tissue from control animals.

Exogenous administration of estradiol and cholecystokinin alters exocrine pancreatic function in rats

SummaryThis study was conducted in rats to investigate the influence of exogenously administered estradiol (ESD) and/or cholecystokinin (CCK) on components and secretions of the pancreatic acini. Intact male rats were treated for 14 d with exogenous administration of ESD, CCK, or ESD+CCK. After 14 d CCK treatment induced significant increases in DNA and RNA contents, and DNA/RNA ratio in the pancreas, indicating hyperplasia and hypertrophy of the pancreas, however, ESD treatment did not have these effects. Both ESD treatment and CCK treatment induced significant increases in amylase and trypsinogen contents in pancreatic acini and each decreased secretion from acini in response to CCK. Combined treatment with ESD plus CCK augmented these effects on enzyme contents and secretion. The results indicate that exogenous administration of CCK has trophic effects on the exocrine pancreas, increasing effects on enzyme contents and inhibitory effects on amylase secretion. In contrast, exogenous administration of ESD had no trophic effects on pancreas, but had increasing effects on enzyme contents and inhibitory effects on amylase secretion. The results suggest that the effects of exogenous ESD and CCK on pancreas are not similar to each other, but both ESD and CCK may be involved in regulating pancreatic exocrine functions.

Humoral factors that induce alterations of the pancreas in rats with obstructive jaundice

This study was conducted to investigate the role of humoral factors in pancreatic alterations induced by obstructive jaundice (OJ) in rats. OJ in male Sprague-Dawley rats induced significant increases in pancreatic weight, DNA content, and RNA content of acinar cells. These changes were accompanied by enlargement of eosinophilic granules and compressed nuclei. Protein, amylase, and trypsinogen contents of pancreas were also increased in OJ rats. In addition, plasma levels of bilirubin, cholecystokinin (CCK), and estradiol increased in OJ rats and were correlated positively with each other and with pancreatic weights. Administration of a specific CCK receptor, L-364,718, to OJ rats partly attenuated the changes of the pancreas, indicating that CCK is involved in these changes. These findings suggest that estradiol may be involved in regulating the pancreatic changes induced by OJ in rats.

Zinc concentrations in two strains of mice after free choice and forced ethanol exposure

from lack of control over the specific radioactivity of the precursor amino acid during the incorporation period. In the present study the rate of protein synthesis was measured in anaestheiized rats, using a continuous, intravenous infusion of valine (specific radioactivity 3.33 pCi/mol), lasting for 30 min. The specific radioactivity of valine was measured to be fairly constant from 11 min onwards. Liver specimens were taken at 11, 20 and 30 min. The protein synthesis rate was calculated from valine-specific radioactivity in protein and in the intracellular precursor pool measured from 11 to 30 min. The rats were pair-fed either a diet containing ethanol (9.2 g/kg per rat per day) or a control diet, in which lipid replaced ethanol isoenergetically, for 58 65 days. The animal growth rate was not significantly different between the groups (2.8 g/day in the ethanol-treated US. 2.9 g/day in controls). All animals were fasted for approximately 16 h before measurement of protein synthesis. In addition, some rats received an i.p. injection (1 ml/kg) of either saline or dexamethasone (4 mg/kg) 1 h prior to measurement of protein synthesis. Chronic ethanol treatment reduced the in uiuo protein synthesis rate by 37% from a control rate of 86.0 + 5.9 nmoles valine per 100 g body weight per min (a = 0.002). This reduction became less marked when the rats received an i.p. injection of saline and disappeared completely when given dexamethasone i.p. 1 h before measurement of protein synthesis. Thus ethanol-treated rats given dexamethasone i.p. had a significantly higher rate of protein synthesis than ethanol-treated rats given nothing or saline (a < 0.05). Our observations demonstrate that the handling procedure preceding the measurement of protein synthesis could be of critical importance to the outcome of the experiments. This could explain some of the controversies in the literature on ethanol effects on rates of protein synthesis.