Abstract:The purpose of this experiment was to determine whether surgical stress on the morning of proestrus would elicit an early release of gonadotropin from the pituitary. Animals exhibiting 5-day estrous cycles underwent bilateral sham-ovariectomy under ether anesthesia at 0800 h of proestrus. These animals had high levels of progesterone and estradiol following the surgery. These steroids were thought to be adrenal in origin, since animals adrenalectomized at 0800 h of proestrus had low progesterone levels and est… Show more
“…The high P4 concentration and low GnRH as a result of metritis might be responsible for ovarian quiescence. However, Nequin et al [14] reported that E2 concentration also increased in addition to P 4 concentration under a surgical stress condition, although this was not observed in this study.…”
Section: Discussioncontrasting
confidence: 82%
“…This shows that the lifespan of the corpus luteum was not prolonged and that pseudopregnancy was not induced. Alternatively, stress stimulates progesterone secretion from the adrenal cortex in rats [7,14] and this secretion depends on corticotrophin releasing hormone (CRH) from the hypothalamus [22] . CRH also acted on cells directly producing GnRH and suppressed secretion of GnRH [9,13].…”
Abstract. To investigate how uterine inflammation affects ovarian activity in rats, endometritis was induced and changes in the length of estrous cycle and serum concentrations of estradiol-17β (E2) and progesterone (P4) were examined. A suspension of Staphylococcus aureus (bacterial solution) or iodine solution was infused into the uterine lumen at various estrous phases. When the bacterial solution was infused at estrus, metestrus, or the first day of diestrus, the following diestrus continued for 5 to 12 days. In the case of the iodine solution, regardless of the estrous phase of the infusion, the following diestrus continued for approximately 6 days. E2 concentration after infusion of each solution did not fluctuate largely and remained at a low concentration (around 5 pg/ml). P4 concentration was high (35-45 ng/ml) on the day following infusion, but decreased rapidly to base line values within a few days and remained thereafter at a low level (around 5 ng/ml). It is assumed that the endometritis caused by biological or chemical stimulation raises the concentration of P4 to depress gonadotrophic hormone secretion, and hence this high P4 concentration might inhibit the growth of ovarian follicles.
“…The high P4 concentration and low GnRH as a result of metritis might be responsible for ovarian quiescence. However, Nequin et al [14] reported that E2 concentration also increased in addition to P 4 concentration under a surgical stress condition, although this was not observed in this study.…”
Section: Discussioncontrasting
confidence: 82%
“…This shows that the lifespan of the corpus luteum was not prolonged and that pseudopregnancy was not induced. Alternatively, stress stimulates progesterone secretion from the adrenal cortex in rats [7,14] and this secretion depends on corticotrophin releasing hormone (CRH) from the hypothalamus [22] . CRH also acted on cells directly producing GnRH and suppressed secretion of GnRH [9,13].…”
Abstract. To investigate how uterine inflammation affects ovarian activity in rats, endometritis was induced and changes in the length of estrous cycle and serum concentrations of estradiol-17β (E2) and progesterone (P4) were examined. A suspension of Staphylococcus aureus (bacterial solution) or iodine solution was infused into the uterine lumen at various estrous phases. When the bacterial solution was infused at estrus, metestrus, or the first day of diestrus, the following diestrus continued for 5 to 12 days. In the case of the iodine solution, regardless of the estrous phase of the infusion, the following diestrus continued for approximately 6 days. E2 concentration after infusion of each solution did not fluctuate largely and remained at a low concentration (around 5 pg/ml). P4 concentration was high (35-45 ng/ml) on the day following infusion, but decreased rapidly to base line values within a few days and remained thereafter at a low level (around 5 ng/ml). It is assumed that the endometritis caused by biological or chemical stimulation raises the concentration of P4 to depress gonadotrophic hormone secretion, and hence this high P4 concentration might inhibit the growth of ovarian follicles.
“…Recent evidence has indicated that control of pituitary secretion of follicle stimulating hormone (FSH, follitropin) may differ from that of pituitary secretion of luteinizing hormone (LH, lutropin) (1)(2)(3)(4)(5), in spite of the failure to find more than one hypothalamic decapeptide releasing factor acting on the pituitary-LH/FSH-RF (6). FSH is secreted in high amounts without LH, beginning [5][6][7][8][9][10][11][12] hr after ovariectomy in the rat (3,4) or following hypothalamic electrochemical stimulation in the specific locus (5).…”
mentioning
confidence: 99%
“…FSH is secreted in high amounts without LH, beginning [5][6][7][8][9][10][11][12] hr after ovariectomy in the rat (3,4) or following hypothalamic electrochemical stimulation in the specific locus (5).…”
Margoliash, September 20, 1977 ABSTRACT The present studies were carried out to see if porcine follicular fluid could inhibit increases in serum follicle stimulating hormone (FSH) levels when injected into the rat. For these studies the pentobarbital-treated proestrous rat was chosen as the major test animal model. If an artificial surge of luteinizing hormone (LH) is administered to these rats, it can induce a synchronized secondary rise in FSH secretion rate. Normal saline-treated rats were also used as test animals. They exhibit preovulatory endogenous "surges" of LH and FSH, and also a secondary FSH rise.Porcine follicular fluid was harvested from medium-sized and large (3-to 10-mm diameter) follicles and treated with charcoal to remove endogenous steroids. Charcoal-treated porcine serum served as a control solution. The fluid was injected intraperitoneally in two 0.5-ml doses into pentobarbital-treated proestrous rats immediately and 3 hr after LH injection. Follicular fluid, but not the serum, suppressed the secondary, LH-induced FSH rise (P < 0.01) in a dose-dependent manner, without altering the effects of LH upon serum ovarian steroid levels or follicular rupture. It was effective down to a total dose of 200 Al. Porcine follicular fluid also blocked the secondary FSH surge in normal proestrous rats exhibiting endogenous LH/FSH primary surges. Thus, it would appear that porcine follicular fluid contains a non-steroidal substance~s) that can block the secretion of FSH that is secondary to a natural or artificial LH surge.
“…Although there were no significant differences between the group that underwent ECS at 13.00 h and the controls, there was an ap parent reduction in the mean ova per rat in this group. This could be due to the possibility that some of the rats in this group may have not fully recovered from the stressful ef- fects of stereotaxic surgery by the time that the critical peri od started (14.00h) and this may have had an effect on the preovulatory LH surge and ovulation [18,29]. Only when bilateral ECS was followed by the procedure for blood sam pling from the external jugular vein under ether anesthesia were the LH surge and ovulation significantly inhibited (ta ble II, fig-2).…”
Bilateral electrochemical stimulation (ECS) of the ventral hippocampus (VHPC) or dorsal hippocampus (DHPC) under acute conditions at 10.00, 12.00 or 13.00 h on proestrus did not interfere with ovulation. When the same ECS of the VHPC was repeated at 12.00 h of proestrus followed by the taking of blood samples at 14.00, 16.00 and 18.00 h under ether anesthesia from the jugular vein, the LH surge and ovulation were significantly (p < 0.05) inhibited. Acute unilateral ECS of the VHPC or passing the same current through a platinum electrode had no effect on the LH surge. When large electrolytic lesions were bilaterally made in the VHPC with a platinum electrode at 12.00 h of proestrus followed by blood samples, the LH surge and ovulation were also inhibited (p < 0.05). Large lesions in the caudate putamen also resulted in a significant (p < 0.05) suppression of the LH surge and the number of ova. These data suggest that (1) electrochemical stimulation of the hippocampus is not inhibitory to ovulation, and (2) acute procedures on the day of proestrus can inhibit LH secretion.
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