Biomedical subjects
Publications and source records attributed to C A Blake.
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Further analysis has been made of the response of the rat pituitary gland to LHRH during the 4-day estrous cycle. LHRH was infused iv at a constant rate (50 ng/h) into phenobarbital-treated rats at different times during the estrous cycle. Infusion at this rate in proestrous rats simulates the rising and plateau phases of the spontaneous proestrous surges of LH and FSH in plasma. Plasma LH rose to similar heights during the "initial phase" of LH release (during the first 40 min of infusion) on the afternoons of estrus, diestrous day one, and proestrus and during the morning of proestrus. The increase during the afternoon of diestrous day two was significantly less than that in all the other groups. A similar response was seen in the case of FSH release. A "rapid rising" or "augmented" phase of LH release (during 40-120 min of infusion) was present in all groups and the magnitude of the response was greatest during the afternoon of proestrus. In the case of FSH, an augmented phase of release started 60 min after the start of infusion, and the response during the afternoon of proestrus was slightly greater than the responses measured at the other times tested. The responses on diestrous day one were not altered when phenobarbital was omitted or when rats were ovariectomized shortly before LHRH infusion. Other differences in the LH and FSH responses during both initial and augmented phases of release were seen in rats tested at different times during the estrous cycle with an LHRH infusion rate which caused a supraphysiological response on proestrus. The results suggest that 1) the initial rising phases in plasma LH and FSH during the spontaneous surges during proestrus are not the result of an increase in pituitary responsiveness to LHRH during the estrous cycle, 2) augmented phases of LH and FSH release can be elicited on all days of the estrous cycle, and 3) the increases in magnitude of the augmented phases of LH and FSH release on proestrus, as compared to those on other days of the cycle, are the result of an increase in pituitary responsiveness to LHRH during the estrous cycle.
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UNLABELLED: Catecholamines were infused through an atrial cannula in unanesthetized rats on the afternoon of proestrus and blood was withdrawn through a second cannula for radioimmunoassay of LH and prolactin. Infusion of epinephrine, but not of norepinephrine or dopamine, blocked spontaneous pituitary LH release and ovulation. Ultimately, this effect appears to be exerted on the brain and not on the pituitary or through changes in pituitary blood flow. Pituitary LH release in response to exogenous LHRH, when administered in an amount that simulated the proestrous LH surge in phenobarital-treated rats, was unaltered by epinephrine infusion. In addition, epinephrine infusion did not alter the timing of the rise in plasma prolactin. Infusion of dopamine blocked the spontaneous rise in plasma prolactin and depressed basal prolactin levels. After the end of infusion, plasma prolactin rose rapidly. Infusion of norepinephrine or epinephrine partially suppressed the prolactin rise but only after 2 h of infusion. THE RESULTS: 1) point out the possibility that chronic release of epinephrine from the adrenal medulla may be involved in phenomena in which "stress" inhibits reproductive function; and 2) are consistent with the view that dopamine, but not norepinephrine, may be PIF.
Four-day cycling rats were kept in a room with the light on from 0500-1900 h. Plasma LH concentrations in blood withdrawn through atrial cannulas at hourly intervals from 1400-2000 h on proestrus were very similar to serum LH concentrations in blood collected from uncannulated rats by decapitation at these times. Additional cannulated rats were bled (0.1 ml) at 5 min intervals from 1400-1600, 1600-1800, or 1800-2000 h. After each bleeding, 0.1 ml of heparinized saline was injected through the cannula. Following a rise (rate unknown) to detectable levels of about 200 ng/ml, plasma LH displayed a rapid linear increase to 1538 +/- 118 ng/ml, starting between 1445 and 1650 h and lasting 20 to 50 min. Over the next 110 min plasma LH at first rose erratically by about another 200 ng/ml and then fluctuated around an apparent plateu. It then dropped rapidly but the declines were commonly interrupted by one or more rapid increases in plasma LH. A generalized pattern of the proestrous LH surge has been constructed from the data.
Four-day cycling rats were kept in a room with the lights on from 0500-1900 h. Injection of an ovulation-blocking dose of phenobarbital at 1230 h on proestrus did not alter the rise in plasma LH concentration in response to rapid injection of 12.4, 124, or 1240 ng of LHRH at 1300 h. In additional blocked rats, blood was rapidly withdrawen through one of two indwelling atrial cannulas while LHRH was infused at a constant rate through the other. Administration of a given amount of LHRH by slow infusion was much more effective in elevating plasma LH than was rapid injection of the same amount of releasing hormone. The pattern of plasma LH concentration after infusion of approximately 50 ng of LHRH per hour from 1500-1810 h was remarkably similar to that of the spontaneous LH surge, i.e., a gradual rise in plasma LH concentration followed by a steep linear increase to high levels which remained elevated for a period of approximately 2 h before declining rapidly soon after the end of infusion. In rats given a second 3 h infusion of LHRH at the same rate, from 2200 to 0100 h, a different response pattern was seen: the initial increase in plasma LH was greater, but the linear rise, which ensued after a lag period of similar duration (about 45 min), was less marked. Prolongation of the first infusion beyond 1800 h did not prolong the plateau: plasma LH levels declined before the infusion was terminated. This decline was less rapid than that seen at the end of a spontaneous LH surge, which in turn was less rapid than that seen after termination of a 3 h and 10 min infusion starting at the same time (1500 h), suggesting that both LHRH release and pituitary responsiveness are diminished (but not abolished) at this time. These findings clearly indicate that, in phenobarbital-blocked proestrous rats, the major part of the proestrous LH surge (including rising and plateau phases) can be simulated by a constant-rate infusion of about 150 ng of LHRH over the 3 h and 10 min period beginning at 1500 h. Since the data also suggest that LHRH release is reduced and/or occurs sporadically during the terminal phase of the surge (when plasma LH levels are declining), these experiments imply that the LH surge is caused by a properly timed, nearly constant-rate release of LHRH for about 3 h (beginning about 1500 h of proestrus) followed by a period of diminished LHRH release.
Four-day cycling rats were kept in a room with the lights on from 0500-1900 h. Plasma FSH concentrations in blood withdrawn through atrial cannulas at hourly intervals from 1400-2000 h on proestrus were very similar to serum FSH concentrations in blood collected by decapitation. Additional cannulated rats were bled at 20 min intervals from 1400-1600, 1600-1800, or 1800-2000 h. In most rats, plasma FSH concentration rose gradually to approximately three times pre-rise levels by 1900 h. It then decreased slightly by 2000 h. Injection of an ovulation-blocking dosage of phenobarbital at 1345 h blocked the FSH rise. Rapid injection of 124 or 1240 ng of LHRH at 1300 h did not elevate plasma FSH by 1315 h but the 1240 ng dose did by 1400 h. Phenobarbital injection at 1230 h did not alter this response. In additional blocked rats, blood was rapidly withdrawen through one of two indwelling atrial cannulas while LHRH was infused at a constant rate through the other. Administration of LHRH by infusion was much more effective in elevating plasma FSH than was rapid injection of the releasing hormone. The pattern of plasma FSH concentration after infusion of about 50 ng of LHRH per hour from 1500-1810 h and then about 12 ng of LHRH per hour from 1810-1920 h was remarkably similar to that of the spontaneous FSH rise. These experiments imply that the early phase of the FSH surge (the one associated with the proestrous LH surge) is caused by a properly timed, nearly constant-rate release of LHRH for about 3 h (beginning about 1500 h of proestrus) followed by a period of diminished LHRH release.
In 4-day cyclic rats kept in a room with the lights on from 05.00 to 19.00 h, sham pinealectomy or pinealectomy on the morning of pro-oestrus did not alter the length of the oestrous cycle for 44 days or the time and magnitude of the rises in LH, FSH and prolactin in the circulation in the afternoon on pro-oestrous days 0, 20 or 44. On day 45, the light schedule was set forward 4 h to run from 09.00 to 23.00 h. The rats continued to have seven additional consecutive 4-day oestrous cycles. On day 27 after the resetting of the light schedule, the pro-oestrous rises in serum LH, FSH and prolactin were delayed 4 h in all rats and a normal quota of eggs was ovulated that night. Other 4- and 5-day cyclic rats which had been made persistently oestrous by anterior deafferentation of the medial basal hypothalamus (AC) underwent pinealectomy. These AC-pinealectomized rats were ovariectomized 60 days later and histological examination of the ovaries revealed no evidence of recent ovulation. Five to six weeks after ovariectomy, sequential blood samples were withdrawn through indwelling atrial cannulas in the AC-pinealectomized-ovariectomized rats and in ovariectomized, pinealectomized-ovariectomized and AC-ovariectomized rats. Regular pulsatile rhythms in plasma LH were measured in all rats. Subcutaneous injection of 50 mug mug oestradiol benzoate in oil lowered plasma LH levels in all four groups but caused an LH surge in the afternoon 2 days later only in the ovariectomized and pinealectomized-ovariectomized rats. The results indicate that the pineal gland in rats kept on a 14 h light: 10 h darkness schedule does not play an active or premissive role in the timing or magnitude of LH, FSH or prolactin release at pro-oestrus, the length of the oestrous cycle, or LH release in ovariectomized rats.
Five male rabbits were actively immunized against testosterone to determine if this procedure could permanently inactivate circulating testosterone. To assess the response to immunization, serum LH, serum testosterone and antitestosterone titer (titer) were measured by radioimmunoassay at various times after immunization. All rabbits produced antisera to testosterone and developed serum LH levels similar to those measured in castrated males. The rise in serum LH was particularly pronounced after a booster immunization but these elevated levels were not maintained which suggests that biological neutralization was only transient. Serum testosterone rose dramatically after immunization and was directly correlated with titer. High serum testosterone concentrations were associated with both high and low serum LH. No correlation existed between titer ans serum LH. It is concluded that active immunization against testosterone does not necessarily result in a permanent neutralization of circulating testosterone and that titer alone is an inadequate criterion of neutralization.
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The effects ov various "stresses" on pulsatile LH release in ovariectomized rats were investigated. Blood was withdrawn through atrial cannulas and replaced with saline at 10 min intervals for 190 min. Plasma LH concentration was suppressed in rats subjected to 30 or 60 min of immobilization during the collection period. On the contrary, sham ovariectomy 4 hr prior to blood collection, leg break or iv injection of ACTH or corticosterone during the collection period did not alter pulsatile patterns in LH release. The results indicate that LH release mechanisms are highly resistant to "stresses" but that immobilization can suppress LH release by an unknown mechanism.