Accelerated ovum transport in rabbits induced by endotoxin 1. Changes in prostaglandin levels and reversal of endotoxin effect (original) (raw)
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Endotoxin-induced interruption of early pregnancy in the rabbit
Reproduction, 1978
Endotoxin derived from Salmonella enteritidis (Boivin) completely interrupted pregnancy in the rabbit when given as a single dose (10 or 20 \g=m\g/kgintravenously on Day 4 or Day 8 of pregnancy. Indomethacin (2 or 10 mg/kg) was unable to prevent this effect.
Domestic Animal Endocrinology, 2001
The effect of endotoxin on follicular growth and on secretion of LH, estradiol-17, progesterone and cortisol during the proestrous phase in cattle was investigated. Holstein heifers were treated with PGF 2␣ at 11-13 d after ovulation to induce luteolysis. At 42 hr after PGF 2␣ treatment, heifers were administered either lipopolysaccharide (LPS; Escherichia coli, O111:B4, 5 g/kg, n ϭ 6) or saline (control; n ϭ 6) by i.v. bolus injection. Ovarian structures were monitored daily by transrectal ultrasonography, and blood samples were collected at various times for hormonal analysis. The duration from PGF 2␣ treatment to ovulation was significantly longer in the LPS group (8.0 Ϯ 1.3 d) than in the control group (4.2 Ϯ 0.2 d). LPS significantly reduced the pulse frequency of LH for 6 hr after the administration, and increased the mean concentration and pulse amplitude of LH from 3 to 6 hr after the administration. The plasma concentrations of progesterone and cortisol were transiently increased after LPS administration. The plasma concentration of estradiol-17 was significantly decreased at 24 hr after LPS administration compared to that in the controls. Five of six LPS-treated heifers exhibited no preovulatory LH surge until 120 hr after PGF 2␣ treatment and the remaining heifer exhibited the surge at 108 hr after PGF 2␣ treatment, while the LH surge was observed at 54 -78 hr after PGF 2␣ treatment in control heifers. These results suggest that endotoxin disrupts progression of the proestrous phase of cattle, interrupting the preovulatory estradiol rise and thus delaying the LH surge and the subsequent ovulation.
American Journal of Obstetrics and Gynecology, 2000
OBJECTIVE: In the current study the role of developing ovarian follicles in the control of the endotoxin-induced pregnancy-specific inflammatory reaction was evaluated. STUDY DESIGN: Follicular development was induced in pregnant rats (n = 20) by means of daily intraperitoneal injections of follicle-stimulating hormone from day 11 of pregnancy until the end of the experiment. Control pregnant rats (n = 20) received daily sodium chloride injections. All pregnant rats were infused for 1 hour with either 2 mL endotoxin solution (1.0 µg/kg body weight) or 2 mL sodium chloride solution on day 14 and killed 4 hours or 3 days later. At death, the left kidneys were snap-frozen and immunohistologically stained for the presence of polymorphonuclear leukocytes and monocytes. RESULTS: The results show that in control pregnant rats endotoxin significantly increased glomerular polymorphonuclear leukocyte and monocyte numbers at both 4 hours and 3 days after endotoxin infusion. Induction of follicular development did not affect glomerular polymorphonuclear leukocyte number after endotoxin infusion but significantly decreased the number of monocytes in the glomeruli at both 4 hours and 3 days after endotoxin infusion. CONCLUSION: We conclude that follicles stimulated with follicle-stimulating hormone produce a follicular factor or factors that are able to prevent the endotoxin-induced influx of monocytes into the glomeruli of pregnant rats. It is suggested that these factors play a role in the control of inflammatory processes associated with reproduction, including the disease of pregnancy, preeclampsia.
Endocrinology, 1999
Three experiments were conducted to investigate whether the immune/inflammatory stimulus endotoxin disrupts the estradiolinduced LH surge of the ewe. Ovariectomized sheep were set up in an artificial follicular phase model in which luteolysis is simulated by progesterone withdrawal and the follicular phase estradiol rise is reproduced experimentally. In the first experiment, we tested the hypothesis that endotoxin interferes with the estradiol-induced LH surge. Ewes were either infused with endotoxin (300 ng/kg/h, iv) for 30 h beginning at onset of a 48-h estradiol stimulus or sham infused as a control. Endotoxin significantly delayed the time to the LH surge (P Ͻ 0.01), but did not alter surge amplitude, duration, or incidence. The second experiment tested the hypothesis that the delaying effects of endotoxin on the LH surge depend on when endotoxin is introduced relative to the onset of the estradiol signal. Previous work in the ewe has shown that a 14-h estradiol signal is adequate to generate GnRH and LH surges, which begin 6-8 h later. Thus, we again infused
Domestic Animal Endocrinology, 1995
The mechanism for the luteolytic release of prostaglandin (PG)F2, ~ in swine is not known. This study examined the potential role of oxytocin (OT)-induced phosphoinositide (PI) hydrolysis in promoting PGF2, ~ secretion in vitro from the endometrium of cyclic gilts on Day 15 postestrus. In Experiment 1, endometrial PI hydrolysis was increased (P < 0.05) by 100 nM OT and was increased quadratically (P < 0.05) by LiCI, but was not affected by the LiC1 x OT interaction (P > 0.30). PI hydrolysis was maximal at 50 mM LiCI and declined at 100 mM LiC1. In Experiment 2, endometrial PI hydrolysis and PGF2, ~ secretion were similarly increased (P < 0.01) by 0, 0.1, 1, 10, and 100 nM OT in a dose-dependent manner. In Experiment 3, the linear increase in PI hydrolysis occurring 0, 3, 5, 10, and 20 min after treatment was greater (P = 0.01) for tissue treated with 100 nM OT than for the tissue treated with 0 nM OT. The quadratic increase (P < 0.05) in PGF2~ secretion occurring 0, 3, 5, 10, and 20 min after treatment was greater (P < 0.05) for tissue treated with 100 nM OT than for the tissue treated with 0 nM OT. In Experiment 4, A1F4-(an activator of G o and phospholipase C) similarly increased (P < 0.01) PI hydrolysis and PGF2, ~ secretion. In Experiment 5, PI hydrolysis (P < 0.01) and PGF2, ~ secretion (P < 0.05) were increased by 100 nM OT but were not stimulated by cholera toxin (an activator of G S and adenylate cyclase). Cholera toxin also did not enhance PI hydrolysis and PGF2, ~ secretion in response to 0.1 or 100 nM OT. These results are consistent with the hypothesis that OT may induce PI hydrolysis to stimulate the endometrial secretion of PGF2~ during corpus luteum regression in swine.
Biology of Reproduction, 1997
These experiments were designed to study the increased sensitivity of pregnant rats to endotoxin. Pregnant (Pr), cyclic (C), and progesterone (P)-treated pseudopregnant rats with or without a decidualized uterus (PSP and DEC rats, respectively) received infusions of an ultra-low dose of endotoxin (1.0 Rig/kg BW) and were killed 3 days later. Pr, PSP, and DEC rats were infused on Day 14, C rats on diestrus. Endotoxin-infused rats were compared with saline-infused rats in the same reproductive conditions. The inflammatory reaction of the glomeruli of the kidneys was studied by immunohistochemical methods using 4-pIm cryostat sections stained with specific monoclonal antibodies against neutrophils (polymorphonuclear cells, PMNs) and monocytes (MOs), and against the adhesion molecules ICAM-1 and VCAM-1 on the endothelium, and LFA-1, MAC-1, and VLA-4 on the leukocytes. Endotoxin infusion increased glomerular PMN and MO number in Pr, PSP, and DEC rats, all of which have elevated P levels, but not in C rats, which do not. The endotoxin-induced expression of adhesion molecules, associated with this influx of inflammatory cells, varied with the reproductive condition. In C rats there was no increased adhesion molecule expression after endotoxin treatment, in Pr rats there was increased expression of both the combinations ICAM-1/LFA-1 and VCAM-1/VLA-4. DEC rats did not express either of these combinations (although there was expression of ICAM-1); PSP rats expressed the combination ICAM-1/MAC-1. Adhesion molecule expression thus seems to be regulated by ovarian (e.g., P) and placental factors (e.g., of trophoblastic and decidual origin). Because the different combinations of adhesion molecules in the various reproductive conditions after exposure to endotoxin led to more or less the same leukocyte influx under these conditions, the increased sensitivity to endotoxin of pregnant individuals cannot be reduced to differences in leukocyte influx into the glomeruli.
Theriogenology, 2000
Changes in prostaglandin and progesterone concentrations after ovulation seem to affect reproductive functions in the sow. The influence of lowered prostaglandin levels on ova transport velocity through the isthmus part of the oviduct, and on progesterone concentrations, was studied during the second estrus after weaning in thirteen purebred Yorkshire multiparous sows. To determine the time of ovulation transrectal ultrasonographic examination was performed. In the second estrus, six sows were given intravenous injections of flunixin meglumine (2.2 mg/kg body weight) every sixth hour from 4 to 8 h after time of ovulation until about 48 h after ovulation, at which time the sows were slaughtered. Blood samples were collected every second hour from about 12 h before ovulation until slaughter. Progesterone and prostaglandin Fru (PGFr,) metabolite levels were determined. Immediately after slaughter the isthmus part of the oviducts were cut into 3 equally long segments and the number of ova in each segment, and in the upper part of the uterine horns, was determined. Before start of treatment, PGF2, metabolite levels were similar in the 2 groups (P=O.84). In the treatment group, PGFr, values dropped to below the detection limit immediately after start of treatment, whereas in the control group the concentrations were quite stable throughout the sampling period (P=O.OOS). Ova recovery rate was 94 % in the treatment group and 95 % in the control group. At time of slaughter, in the treatment group ova had on average passed 2.1 segments whereas in the control group the ova had passed 2.5 segments (P=O.57). The progesterone levels increased continuously in both groups after ovulation but there was no difference in the mean progesterone concentrations between the two groups before (P=O.96) or after (P=O.58) ovulation. It can be concluded that the transport of ova through the isthmus part of the oviduct is unaffected by an inhibition of prostaglandin synthesis immediately after ovulation. Furthermore, the post-ovulatory progesterone profile seems unaffected by lowered PGFza levels.