Efficacy of intermittent or continuous administration of GnRH in inducing ovulation in early and late seasonal anoestrus in the Père David's deer hind (Elaphurus davidianus)

Père David's deer hinds were treated with GnRH, administered as intermittent i.v. injections (2.0 micrograms/injection at 2-h intervals) for 4 days, or as a continuous s.c. infusion (1.0 micrograms/h) for 14 days. These treatments were given early (February-March) and late (May-June) in the period of seasonal anoestrus. The administration of repeated injections of GnRH increased mean LH concentrations from pretreatment values of 0.54 +/- 0.09 to 2.10 +/- 0.25 ng/ml over the first 8 h of treatment in early anoestrus, and from 0.62 +/- 0.11 to 2.73 +/- 0.49 ng/ml in late anoestrus. The mean amplitude of GnRH-induced LH episodes was greater (P less than 0.01) in late (4.03 +/- 0.28 ng/ml) than in early (3.12 +/- 0.26 ng/ml) anoestrus, but within each replicate (early or late anoestrus), neither mean LH episode amplitude nor mean plasma LH concentrations differed significantly between the four periods of intensive blood sampling. On the basis of their progesterone profiles, 6/12 hinds had ovulated in response to treatment with injections of GnRH (1/6 in early anoestrus and 5/6 in late anoestrus), and oestrus and a preovulatory LH surge were recorded in all of these animals. Oestrus and a preovulatory LH surge were also recorded in one other animal treated in early anoestrus in which progesterone concentrations remained low. The mean times of onset of oestrus (91.0 +/- 1.00 and 62.4 +/- 0.98 h) and of the preovulatory LH surge (85.8 +/- 3.76 and 59.4 +/- 0.25 h) both occurred significantly earlier (P less than 0.001) in animals treated in late anoestrus. Continuous infusion of GnRH to seasonally anoestrous hinds resulted in an increase in mean plasma LH concentrations, but this response did not differ significantly between early (2.15 +/- 0.28 ng/ml) and late (2.48 +/- 0.26 ng/ml) anoestrus. Ovulation, based on progesterone profiles, occurred in 2/7 hinds in early anoestrus and in 4/6 hinds in late anoestrus. Oestrus was detected in all except one of these hinds. The mean time of onset of oestrus occurred earlier in animals treated in late anoestrus (66.2 +/- 0.32 h and 46.7 +/- 0.67 h, P less than 0.01). The administration of GnRH, given either intermittently or continuously, will induce ovulation in a proportion of seasonally anoestrous Père David's deer. However, more animals ovulate in response to this treatment in late than in early anoestrus (75% compared with 23%).     

A role for alternative pathway catecholamines in the regulation of steroidogenesis in cow luteal cells

Incubation of bovine luteal cells with the alternative pathway catecholamines octopamine, synephrine and deoxyadrenaline at concentrations of 10(-6) to 10(-3) M enhanced the production of progesterone (P less than 0.05). Tryamine did not alter basal progesterone production (P greater than 0.05). Addition of noradrenaline and adrenaline at concentrations of 10(-4) to 10(-7) M significantly elevated the production of progesterone (P less than 0.05). The steroidogenic response to noradrenaline and adrenaline was greater than that for octopamine, synephrine and deoxyadrenaline (P less than 0.05). Response to both primary (10(-6) M) and alternative (10(-4) M) pathway catecholamines was inhibited by propranolol (10(-5) M, P less than 0.05) but not phentolamine (10(-5) M, P greater than 0.05). These results demonstrate that octopamine, synephrine and deoxyadrenaline can affect steroidogenesis by bovine luteal cells, and their action is mediated by beta-adrenergic receptors.     

Indomethacin reversal of ethanol-induced suppression of ovine fetal breathing movements and relationship to prostaglandin E2

The effects of indomethacin on the ethanol-induced suppression of fetal breathing movements and fetal arterial plasma and cerebrospinal fluid (CSF) PGE2 concentrations and maternal arterial plasma PGE2 concentration were determined in the near-term fetal lamb. Eight conscious instrumented pregnant ewes (between 130 and 133 days of gestation; term, 147 days) received 1-h maternal intravenous infusion of 1 g ethanol/kg total body weight, and the fetus received 6-h intravenous infusion of indomethacin (1 mg/h per kg fetal body weight) commencing 30 min later. Serial fetal and maternal arterial blood samples (n = 8) and fetal CSF samples (n = 5) were collected at selected times throughout the 12-h study for the determination of PGE2 concentration. Fetal breathing movements were monitored continuously throughout the experimental period. Maternal ethanol infusion resulted in initial suppression (P less than 0.05) of fetal breathing movements for 2 h below pretreatment value, followed by a rapid increase in the incidence of fetal breathing movements after the onset of fetal indomethacin treatment. Fetal and maternal plasma PGE2 concentrations and fetal CSF PGE2 concentration were increased (P less than 0.05) above the pre-infusion value during the administration of ethanol and 1 h thereafter. Fetal indomethacin treatment suppressed (P less than 0.05) to undetectable levels fetal plasma and CSF PGE2 concentrations, which then became similar (P greater than 0.05) to pretreatment by 12 h. There was a positive correlation between fetal plasma and CSF PGE2 concentrations. There was an inverse correlation between the incidence of fetal breathing movements and fetal CSF PGE2 concentration.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of buserelin injection and deslorelin (GnRH-agonist) implants on plasma progesterone, LH, accessory CL formation, follicle and corpus luteum dynamics in Holstein cows

The influence of Buserelin injection and Deslorelin (a GnRH analogue) implants administered on Day 5 of the estrous cycle on plasma concentrations of LH and progesterone (P4), accessory CL formation, and follicle and CL dynamics was examined in nonlactating Holstein cows. On Day 5 (Day 1 = ovulation) following a synchronized estrus, 24 cows were assigned randomly (n = 4 per group) to receive 2 mL saline, i.m. (control), 8 micrograms, i.m. Buserelin or a subcutaneous Deslorelin (DES) implant in concentrations of 75 micrograms, 150 micrograms, 700 micrograms or 2100 micrograms. Blood samples were collected (for LH assay) at 30-min intervals for 2 h before and 12 h after GnRH-treatment from cows assigned to Buserelin, DES-700 micrograms and DES-2100 micrograms treatments and thereafter at 4-h intervals for 48 h. Beginning 24 h after treatment, ovaries were examined by ultrasound at 2-h intervals until ovulation was confirmed. Thereafter, ultrasonography and blood sampling (for P4 assay) was performed daily until a spontaneous ovulation before Day 45. A greater release of LH occurred in response to Deslorelin implants than to Buserelin injection (P < 0.01). Basal levels of LH between 12 and 48 h were higher in DES-700 micrograms group than in DES-2100 micrograms and Buserelin (P < 0.05). The first wave dominant follicle ovulated in all cows following GnRH treatment. Days to CL regression did not differ between treatments, but return to estrus was delayed (44.2 vs 27.2 d; P < 0.01) in cows of DES-2100 micrograms group. All GnRH treatments elevated plasma P4 concentrations, and the highest P4 responses were observed in the DES-700 micrograms and DES-2100 micrograms groups. The second follicular wave emerged earlier in GnRH-treated than in control cows (9.9 vs 12.8 d; P < 0.01). However, emergence of the third dominant follicle was delayed in cows of DES-2100 micrograms treatment (37.0 d) compared with DES-700 micrograms (22.2 d), Buserelin (17.8 d) or control (19.0 d). In conclusion, Deslorelin implants of 700 micrograms increased plasma P4 and LH concentrations and slightly delayed the emergence of the third dominant follicle. On the contrary, Deslorelin implants of 2100 micrograms drastically altered the P4 profiles and follicle dynamics.     

Urinary dopamine, noradrenaline and adrenaline in type 2 diabetic patients with and without nephropathy

We measured the urinary excretions of dopamine, noradrenaline and adrenaline, their conjugated metabolites, urinary excretion of sodium and creatinine clearance simultaneously in 21 patients with Type 2 (non-insulin-dependent) diabetes and 6 normal subjects. The mean (+/- SEM) value for urinary excretion of dopamine (52.4 +/- 8.8 micrograms/day) in diabetic patients with nephropathy (Group C, n = 12) was significantly lower (P less than 0.01) than in the normal subjects (Group A, 179.7 +/- 15.5 micrograms/day) and in diabetic patients without nephropathy (Group B, n = 9, 131.5 +/- 16.5 micrograms/day). The mean values for the urinary excretions of noradrenaline and adrenaline were also significantly lower (P less than 0.01) in Group C than in Groups A and B. In addition, the mean urinary excretion of conjugated metabolite of dopamine in Group C was significantly lower (P less than 0.05) than in Group A. There was a trend toward the observation that the mean 24-h urinary excretion of sodium in Group C (121.6 less than 12.9 mEq) was lower as compared with that in Group A (140.8 +/- 8.9 mEq) or B (150.7 +/- 17.9 mEq). A multiple regression analysis revealed that the 24-h urinary excretion of dopamine correlated significantly with creatinine clearance, systolic (P less than 0.01) and diastolic (P less than 0.05) blood pressures. The results indicate that synthesis or secretion of renal dopamine might decrease with a progression of diabetic nephropathy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of inhibition of prostaglandin F2α biosynthesis during preluteolysis and luteolysis in heifers

Flunixin meglumine (FM; 2.5 mg/kg) was given to heifers at three 8-h intervals, 16 d after ovulation (first treatment = Hour 0) to inhibit the synthesis of prostaglandin F_2α (PGF), based on plasma concentrations of a PGF metabolite (PGFM). Blood samples were collected at 8-h intervals from 15 to 18 d in a vehicle (control) and FM group (n = 16/group). Hourly samples were collected from Hours −2 to 28 in 10 heifers in each group. Heifers that were in preluteolysis or luteolysis at Hour 0 based on plasma progesterone (P4) concentrations at 8-h intervals were partitioned into subgroups. Concentration of PGFM was reduced (P < 0.05) by FM treatment in each subgroup. For the preluteolytic subgroup, the first decrease (P < 0.05) in P4 concentration after Hour 0 occurred at Hours 24 and 40 in the vehicle and FM groups, respectively. Plasma P4 concentrations 32 and 40 h after the beginning of luteolysis in the luteolytic subgroup were greater (P < 0.05) in the FM group. Concentration at the peak of a PGFM pulse in the FM group was greater (P < 0.05) in the luteolytic than in the preluteolytic subgroup. The peak of a PGFM pulse occurred more frequently (P < 0.001) at the same hour as the peak of an LH fluctuation than at the ending nadir of an LH fluctuation. In conclusion, a reduction in prominence of PGFM pulses during luteolysis delayed completion of luteolysis, and treatment with FM inhibited PGFM production more during preluteolysis than during luteolysis.     

Release of histamine and adrenaline in vivo following intravenous administration of neurotensin

Plasma histamine levels of rats anesthetized with pentobarbital sodium were significantly increased by intravenous administration of neurotensin (NT, 1 nmole/kg) with the maximum effect at 3 min, and a return to the initial levels in 20 min. Treatment of animals with compound 48/80 or disodium cromoglycate completely inhibited the elevation of histamine level by NT, however, treatment with reserpine or diphenhydramine and adrenalectomy did not affect the elevation. Plasma adrenaline levels increased transiently 1 min after NT injection, and adrenalectomy and treatment with compound 48/80 or diphenhydramine markedly reduced the elevation of adrenaline levels after NT injection. Plasma levels of noradrenaline were unchanged upon NT injection. These results provide direct evidence of the release of endogenous histamine and adrenaline following NT administration, and suggest the contribution of these amines to the NT-induced triphasic blood pressure responses (the first depressor, second pressor and third depressor responses) reported previously.     

Effect of mouse epidermal growth factor on plasma concentrations of LH, FSH and testosterone in rams

Two experiments were conducted to examine the effects of mouse epidermal growth factor (EGF) on the concentrations of testosterone, LH and FSH in jugular blood plasma and on the pituitary responsiveness to LHRH. In 20 rams treated with subcutaneous doses of EGF at rates of 85, 98 or 113 micrograms/kg fleece-free body weight, mean plasma LH and testosterone concentrations were significantly reduced (P less than 0.05) at 6 h after treatment but not at 24 h. EGF treatment at 130 micrograms/kg fleece-free body weight suppressed the plasma content of these hormones for up to 48 h. Mean plasma FSH concentrations decreased significantly (P less than 0.05) for up to 48 h after EGF treatment, the effect being most pronounced in rams with mean pretreatment FSH values greater than or equal to 0.5 ng/ml. Intravenous injections of 1.0 micrograms LHRH given to each of 5 rams before and at 6 h, 24 h and 72 h after EGF treatment produced LH and testosterone release patterns which paralleled those obtained in 5 control rams similarly treated with LHRH. These results suggest that, in rams, depilatory doses of mouse EGF temporarily impair gonadotrophin and androgen secretion by inhibiting LHRH release from the hypothalamus. Such treatment appears to have no effect on the responsiveness of the pituitary to LHRH.     

Relationships between LH, FSH and prolactin secretion and reproductive activity in the weaned sow

Blood samples were collected from primiparous sows via indwelling jugular cannulae at 15-min intervals for 12 h before and for 24 h (2 sows) or 48 h (10 sows) after weaning and then every 4 h until behavioural oestrus. Weaning to oestrus intervals ranged from 3 to 10 days and 2 sows showed no signs of oestrus and had not ovulated by Days 11 and 16 after weaning. Prolactin concentrations in plasma decreased significantly (P less than 0.001) and reached basal levels 1-2 h after weaning in all sows whilst plasma progesterone concentrations remained basal until approximately 30 h after the preovulatory LH surge in sows that ovulated. Elevated concentrations of prolactin or progesterone during the post-weaning period were, therefore, not responsible for delayed restoration of cyclicity. Overall, mean LH concentrations rose significantly (P less than 0.001) from 0.22 +/- 0.02 during the 12-h period before weaning to 0.38 +/- 0.03 ng/ml during the 12-h post-weaning period. After weaning, pulsatile and basal LH secretions were markedly increased for sows that showed an early return to oestrus (less than or equal to 4 days) compared with sows showing a longer weaning to oestrus interval but a correlation did not exist between either of these LH characteristics and the time taken to resume cyclicity. Mean LH concentrations before weaning were, however, inversely related (r = -0.649; P less than 0.05) to the weaning to oestrus interval. Overall, mean FSH concentrations rose significantly (P less than 0.001) from 151.1 +/- 6.2 (s.e.m.) ng/ml in the 12-h period immediately before weaning to 187.7 +/- 9.7 ng/ml in the subsequent 12-h period but there was no correlation between FSH concentrations, before or after weaning, and the interval from weaning to oestrus. However, a significant correlation was apparent between ovulation rate and peak concentrations of the rise in FSH after weaning (r = 0.746; P less than 0.05) and overall mean FSH values (r = 0.645; P less than 0.05). It is concluded that both LH and FSH concentrations in peripheral blood rose in response to removal of the suckling stimulus at weanling. The increase in LH pulse frequency associated with weaning was not directly related to the weaning to oestrus interval although a specific pattern of LH secretion was observed in sows showing an early return to oestrus (less than or equal to 4 days).(ABSTRACT TRUNCATED AT 400 WORDS)     

The effect of cyproheptadine on plasma growth hormone (GH) and on somatostatin response to GH-releasing hormone in man

Cyproheptadine (CPH)--a putative serotonin antagonist--is known to inhibit growth hormone (GH) response to various pharmacological stimuli, as well as during sleep. To elucidate the possible site at which this drug takes effect, we examined plasma GH and somatostatin response to i.v. GHRH1-44 (1 microgram/kg body wt.) before and after CPH treatment in 10 healthy volunteers. The oral administration of CPH (8-12 mg daily for 5 days; total dose 56 mg) significantly curbed GH response to GHRH as expressed in peak plasma GH values (32.0 +/- 6.1 micrograms/l vs. 12.6 +/- 3.2 micrograms/l; P less than 0.01) and in integrated GH response area (2368 +/- 517 micrograms x l-1 x 2 h vs. 744 +/- 172 micrograms x l-1 x 2 h; P less than 0.01). Plasma somatostatin levels did not change in response to GHRH.     

Function of abnormal corpora lutea in vivo after GnRH-induced ovulation in the anoestrous ewe

Anoestrous Romney Marsh ewes with and without progesterone treatment (+P, -P) were treated with small-dose (250 ng) multiple injections of GnRH at 2-h intervals for 48 h. Animals were slaughtered on Days 4, 5, 7 and 11 after the end of GnRH treatment and luteal function was assessed by the measurement of daily plasma progesterone concentrations. In all animals which ovulated (29/32, 91%) peripheral progesterone concentrations rose to 0.5-1.0 ng/ml within 3 days of the end of GnRH treatment. In 7/7 (100%) +P animals and 5/22 (23%) -P animals, progesterone concentrations continued to rise and were maintained at levels greater than 1.5 ng/ml until slaughter. In the remaining -P animals, plasma progesterone concentrations declined to reach basal levels by Day 5. Corpora lutea recovered from these animals showed signs of premature regression on Day 5 and were fully regressed by Day 7. Progesterone priming delayed the occurrence of the LH surge which occurred 39.1 +/- 3.6 h after the end of GnRH treatment in the +P animals compared to 20.2 +/- 1.74 h (P less than 0.001) in the -P animals in which luteal function was abnormal and 22.4 +/- 4.35 h in the -P animals in which luteal function was normal. These results show that abnormal luteal function occurs in the majority of GnRH-treated ewes in the absence of progesterone pretreatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ability of cortisol and progesterone to mediate the stimulatory effect of adrenocorticotropic hormone upon testosterone production by the porcine testis

The influence of corticosteroids and progesterone upon porcine testicular testosterone production was investigated by administration of exogenous adrenocorticotropic hormone (ACTH), cortisol and progesterone, and by applying a specific stressor. Synthetic ACTH (10 micrograms/kg BW) increased (P less than 0.01) peripheral concentrations of testosterone to peak levels of 5.58 +/- 0.74 ng/ml by 90 min but had no effect upon levels of luteinizing hormone (LH). Concentrations of corticosteroids and progesterone also increased (P less than 0.01) to peak levels of 162.26 +/- 25.61 and 8.49 +/- 1.00 ng/ml by 135 and 90 min, respectively. Exogenous cortisol (1.5 mg X three doses every 5 min) had no effect upon circulating levels of either testosterone or LH, although peripheral concentrations of corticosteroids were elevated (P less than 0.01) to peak levels of 263.57 +/- 35.03 ng/ml by 10 min after first injection. Exogenous progesterone (50 micrograms X three doses every 5 min) had no effect upon circulating levels of either testosterone or LH, although concentrations of progesterone were elevated (P less than 0.01) to peak levels of 17.17 +/- 1.5 ng/ml by 15 min after first injection. Application of an acute stressor for 5 min increased (P less than 0.05) concentrations of corticosteroids and progesterone to peak levels of 121.32 +/- 12.63 and 1.87 +/- 0.29 ng/ml by 10 and 15 min, respectively. However, concentrations of testosterone were not significantly affected (P greater than 0.10). These results indicate that the increase in testicular testosterone production which occurs in boars following ACTH administration is not mediated by either cortisol or progesterone.     

Studies on the immediate and delayed leucocytosis elicited by brief (30-min) strenuous exercise

Eight healthy male volunteers exercised for two 30-min sessions starting 3 h apart on an electronically braked cycle ergometer at a work load (mean 155.9 W, SD 33.4 W) which required an oxygen consumption that was 70% of their maximal rate of oxygen uptake. Venous blood samples were taken through an indwelling cannula over a period of 6 h beginning shortly before the first bout of exercise and were analysed for routine haematological parameters and for lactate, noradrenaline, adrenaline and cortisol. Both bouts of exercise induced an immediate leucocytosis due to rises in lymphocytes and neutrophils but only the first exercise bout induced a substantial delayed neutrophilia. In at least five subjects, changes in lymphocyte and platelet numbers were correlated (Spearman's rank procedure, P less than 0.05) with simultaneous changes in the plasma concentrations of lactate, noradrenaline and adrenaline over the 6-h period studied. Increases in the plasma concentration of cortisol due to exercise correlated positively with the percentage changes in neutrophil numbers at 3 h and 6 h. These results are consistent with the suggestion that the immediate and delayed leucocytosis induced by exercise are mediated respectively by catecholamine and by cortisol.     

Effect of soman (pinacolyl methylphosphonofluoridate) on the blood levels of corticosterone and adrenocorticotropin in mice

Mice were poisoned by an extremely toxic organophosphate anticholinesterase soman (pinacolyl methylphosphonofluoridate), 50 or 100 micrograms/kg at 1000, and the serum concentrations of corticosterone were determined fluorometrically at 3-h intervals for at least 24 h. The lower soman dose (50 micrograms/kg) produced a modest increase in serum corticosterone concentrations but by 24 h the levels were not significantly different from control. Following the higher soman dose (100 micrograms/kg) the serum corticosterone levels were elevated significantly (p less than 0.05), for at least 27 h. However, ACTH concentrations were not elevated. It is possible that the elevated levels of corticosterone were due to a reduced metabolism and excretion of corticosterone resulting from the intense hypothermia, following soman poisoning which may change cardiac output and organ (liver and kidney) perfusion and not due to an enhanced release from the adrenal gland.     

Prolactin administration during the luteal and follicular phase of the oestrous cycle of gilts

In Exp. I infusions of prolactin (0.5 mg in 2 ml sterile saline) were repeated every 2 h for 36 h on Days 12-13 of the cycle. In Exp. II infusions of prolactin were administered from Days 17 to 19 (60 h) at 2-h intervals. Control gilts were given 2 ml sterile saline at similar intervals during the same period. Basal prolactin concentrations before initiation of infusions ranged from 1.3 +/- 0.1 to 5.6 +/- 2.2 ng/ml in both experiments. By 5 min after a prolactin infusion, mean plasma prolactin concentration ranged from 74.9 +/- 5.8 to 113.0 +/- 9.5 ng/ml, but then declined to approximately equal to 10 ng/ml just before the next infusion of prolactin. Administration of prolactin during the luteal phase of the oestrous cycle of the gilts had no effect on basal levels of progesterone, oestradiol or LH. During the follicular phase there were no differences (P greater than 0.05) between control and prolactin-treated gilt progesterone and LH concentrations, but oestradiol plasma values were decreased (P less than 0.05) on the 2nd and 3rd day of prolactin treatment. Our results would indicate that prolactin does not play a major role in the regulation of the oestrous cycle of the pig.     

Left ventricular systolic time intervals and plasma noradrenaline concentrations during acute hypovolaemia in newborn infants

Left ventricular systolic time intervals and plasma noradrenaline concentrations were determined in twelve newborn infants during acute moderate hypovolaemia. Rapid withdrawal of 8.5 ml of blood per kg body weight shortened the left ventricular ejection time from 204 to 176 msec (P less than 0.001) and increased the plasma noradrenaline concentration from 3.4 to 4.0 nmol/l (P less than 0.05). Systemic blood pressure was unchanged. It is concluded that even a moderate reduction in blood volume is associated with marked changes in left ventricular dynamics. The shortening of left ventricular ejection time during hypovolaemia probably reflects left ventricular adaptation to decreased volumes and response to increased noradrenaline release.     

Adrenal-pituitary-gonadal relationships and ejaculate characteristics in captive leopards (Panthera pardus kotiya) isolated on the island of Sri Lanka

In Study 1, semen was collected using a standardized electroejaculation procedure. Males (N = 8) produced ejaculates with a high incidence of sperm abnormalities (77 +/- 3.3%). After electroejaculation under anaesthesia, serum cortisol concentrations increased (P less than 0.05), while testosterone concentrations decreased (P less than 0.05) and LH and FSH concentrations were unchanged (P less than 0.05) over a 2-h bleeding period. In Study 2, male and female leopards were bled at 5-min intervals for 3 h and given (i.v.): (1) saline (N = 2/sex); (2) GnRH (1 microgram/kg body weight) 30 min after the onset of sampling (N = 5/sex); or (3) ACTH (250 micrograms) at 30 min followed by GnRH 1 h later (N = 5/sex). Basal concentrations of serum LH, FSH and cortisol were comparable (P greater than 0.05) between male and female leopards. After GnRH, peak LH concentrations were 2-fold greater (P less than 0.05) in males than females while FSH responses were similar. In males, testosterone concentrations increased 2-3-fold following GnRH. After ACTH, serum cortisol concentrations doubled within 15 min in both sexes. Administration of ACTH 1 h before GnRH did not affect GnRH-induced LH or FSH release (P greater than 0.05); however, testosterone secretion was only 30% of that observed after GnRH alone (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Prostaglandin E2 counteracts the effects of PGF2 alpha in indomethacin treated cycling gilts

Twenty crossbred gilts with at least 2 consecutive estrous cycles of 18 to 21 days in length were used to study the effects of prostaglandins E2 and F2 alpha (PGE2 and PGF2 alpha) on luteal function in indomethacin (INDO) treated cycling gilts. Intrauterine and jugular vein catheters were surgically placed before day 7 of the treatment estrous cycle and gilts were randomly assigned to 1 of 5 treatment groups (4/group). With exception of the controls (Group I) all gilts received 3.3 mg/kg INDO every 8 h, Groups III, IV and V received 2.5 mg PGF2; 2.5 mg PGF2 alpha + 400 micrograms PGE2 every 4 hr, or 400 micrograms PGE2 every 4 h, respectively. All treatments were initiated on day 7 and continued until estrus or day 23. Jugular blood for progesterone analysis was collected twice daily from day 7 to 30. Estradiol-17 beta (E2-17 beta) concentrations were determined in samples collected twice daily, from 2 d before until 2 d following the day of estrus onset. When compared to pretreatment values, estrous cycle length was unaffected (P greater than 0.05) in Group I, prolonged (P less than 0.05) in Groups II, IV and V; and shortened (P less than 0.05) in Group III. The decline in plasma progesterone concentration that normally occurs around day 15 was unaffected (P greater than .05) in Group I; delayed (P less than 0.05) in Groups II, IV and V; and occurred early (P less than 0.05) in Group III. Mean E2-17 beta remained high (31.2 +/- 4.9 to 49.3 +/- 3.1 pg/ml) in Groups III and IV, while the mean concentrations in Groups III and V varied considerably (17.0 +/- 2.0 to 52.2 +/- 3.5 pg/ml). The results of this study have shown that PGE2 will counteract the effects of PGF2 alpha in INDO treated cycling gilts. The inclusion of PGF2 alpha appeared to either stimulate E2-17 beta secretion or maintain it at a higher level than other treatments.     

Hormonal regulation of potassium shifts during graded exhausting exercise

Serum potassium, aldosterone and insulin, and plasma adrenaline, noradrenaline and cyclic adenosine 3':5'-monophosphate (cAMP) concentrations were measured during graded exhausting exercise and during the following 30 min recovery period in six untrained young men. During exercise there was an increase in concentration of serum potassium (4.74 mmol.l-1, SEM 0.12 at the end of exercise vs 3.80 mmol.l-1, SEM 0.05 basal, P less than 0.001), plasma adrenaline (2.14 nmol.l-1, SEM 0.05 at the end of exercise vs 0.30 nmol.l-1, SEM 0.02 basal, P less than 0.001), plasma noradrenaline (1.10 nmol.l-1, SEM 0.64 at the end of exercise vs 1.50 nmol.l-1, SEM 0.05 basal, P less than 0.001), serum aldosterone (0.92 nmol.l-1, SEM 0.14 at the end of exercise vs 0.36 nmol.l-1, SEM 0.05 basal, P less than 0.01), and plasma cAMP (35.4 nmol.l-1, SEM 2.3 at the end of exercise vs 21.4 nmol.l-1, SEM 4.5 basal, P less than 0.05). While concentrations of serum potassium, plasma adrenaline and cAMP returned to their basal levels immediately after exercise, those of plasma noradrenaline and serum aldosterone remained elevated 30 min later (1.90 nmol.l-1, SEM 0.01, P less than 0.01; and 0.85 nmol.l-1, SEM 0.12, P less than 0.01, respectively). Serum insulin concentration did not change during exercise (6.47 mlU.l-1, SEM 0.58 at the end of exercise vs 5.47 mlU.l-1, SEM 0.41 basal, NS) but increased significantly (P less than 0.02) at the end of the recovery period (7.12 mlU.l-1, SEM 0.65).(ABSTRACT TRUNCATED AT 250 WORDS)     

Catecholamine release and interrenal response of brown trout, Salmo trutta, exposed to aluminium in acidic water

Cannulated brown trout, Salmo trutta , were exposed for 36 h to synthetic water with a low calcium content of pH 5 and similar synthetic water dosed with aluminium to raise the filterable A1 from 5 to 290 μg 1⁻¹ over the 36-h period. There were no significant disturbances of plasma concentrations of glucose, cortisol or catecholamine (adrenaline and noradrenaline) in fish held in water of pH 5. The addition of aluminium to this acidic synthetic water resulted in a generalized endocrine stress response with a four-fold increase in plasma glucose concentration after 18 h and a significant increase in plasma cortisol concentration from 24 h onwards when filterable A1 exceeded 200 μg 1⁻¹. Plasma catecholamine concentration indicated an adrenergic stress response in aluminium-exposed brown trout. A transient doubling in noradrenaline after 6 h in A1 was followed by a larger increase in both plasma adrenaline and noradrenaline concentrations in fish surviving the 36-h exposure to A1.