Investigations of antithrombin III-activity in patients after myocardial infarction and a long-term coumarin therapy

In 40 M.I. patients with long-term anticoagulant treatment, (Falithrom), the AT III-activity was determined at an interval of three years by means of Chromozym TH. We have found a mean AT III-value in the first testing period of 79.67 (+/- 14.16) per cent and in the second assessment of 82.5 (+/- 10.42) per cent. The difference is not significant. However, we were unable to confirm the comparatively marked increase AT III for dicoumarol treatment found by Roka and Bleyl. In acute M.I.-patients was demonstrated a decreased AT III-activity in the first 3-4 days and a normalisation tendency in the next 10-14 days. Our values of the mean AT III-activity were in the lower normal range for patients with long-term coumarin therapy. In dead patients (average age 70 years) there is a trend of a risk to an untimely death in the presence of pathologic AT III-activity (despite a good anticoagulation of an individual mean quick test from greater than or equal to 0.20 to less than or equal to 0.30) or a bad anticoagulation (mean individual quick tests greater than or equal to 0.30 to 0.35), but a normal AT III-activity. The three dimensional analysis was not significant.     

Therapeutic results in acute myelogenous leukemia in the years from 1970 to 1982

In a retrospective study, three groups of patients with acute myeloid leukaemia were analyzed in respect to the outcome of remission induction therapy: group I (vincristine, daunorubicin and prednisone) was treated between 1970 and 1976, group II (daunorubicin and cytosine-arabinoside) between 1976 and 1980 and group III (daunorubicin, cytosine-arabinoside, 6-thioguanine and consolidation therapy with cyclophosphamide, vincristine, cytosine-arabinoside and prednisone) between 1980 and 1982. Complete remissions were achieved in 49% (group I), 46% (group II) and 65% (group III) of the patients (p greater than 0.05, chi-square test). The mortality rate of the remission induction therapy was significantly reduced from 27% in group I to 15% and 13% in group II and III, respectively (p less than 0.05, chi-square test). The median remission duration increased significantly from four months (group I) to nine months (group III) (p less than 0.05, log-rank test). The long term results were about the same in the three groups. After three years, the proportion of patients being still in first remission was less than 10% in group I and II 13% in group III.     

The effects of dietary manipulation on blood acid-base status and the performance of high intensity exercise

The effect of a pattern of exercise and dietary modification, which is normally used to alter muscle glycogen content, upon the acid-base status of the blood and the ability to perform high intensity exercise was studied. Eleven healthy male subjects cycled to exhaustion on an electrically braked cycle ergometer at a workload equivalent to 100% of their maximal oxygen uptake (VO2max) on three separate occasions. The first exercise test took place after a normal diet (46.2 +/- 6.7% carbohydrate (CHO)), and was followed by prolonged exercise to exhaustion to deplete muscle glycogen stores. The second test was performed after three days of a low carbohydrate diet (10.1 +/- 6.8% CHO) and subsequently after three days of a high CHO diet (65.5 +/- 9.8% CHO) the final test took place. Acid-base status and selected metabolites were measured on arterialised venous blood at rest prior to exercise and during the post-exercise period. Exercise time to exhaustion was longer after the normal (p less than 0.05) and high (p less than 0.05). CHO dietary phases compared with the low CHO phase. Resting pre-exercise pH was higher after the high CHO diet (p less than 0.05) compared with the low CHO diet. Pre-exercise bicarbonate, PCO2 and base excess measurements were higher after the high CHO treatment compared with both the normal (p less than 0.01, p less than 0.05, p less than 0.01 respectively) and low CHO phases (p less than 0.001, p less than 0.01, p less than 0.001 respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in serum T4, T3 and TSH concentrations in newborns and infants with congenital goiter from the Mazovia region.

Thyroid function was investigated in a group of 61 newborns with congenital goiter before starting the therapy with thyroid hormones. The group included 19 girls and 42 boys, of which 27 were of age not exceeding one week (group I), 19 were between the first and the second week (group II), and 15 were between the second week and the third month of life (group III). The concentrations of the thyroid hormones were determined by radioimmunoassay. The values obtained have been compared with the local reference range obtained for the newborns of the Mazovia region. The values remaining outside the reference range were found in 47.5% of the newborns studied. The elevated values of TSH were observed mainly in group I newborns (12 from 27); among group II newborns there was only one with the elevated values, and none among the newborns of group III. thyroxine (T4) values were lowered in 14 among 27 newborns of group I, and in 2 among 19 newborns of group II; all T4 values were normal in group III. The percentage of the elevated values of triiodothyronine (T3) was higher in older newborns (group III). The elevated level of T3 accompanied by the lowered level of T4 with the normal or moderately elevated level of TSH is characteristic for the adaptation to the deficiency of iodine. There is preferential secretion of T3 aimed at maintaining euthyreosis. The elevated levels of T3 found in 30% of newborns with untreated goiter suggest an intrauterine deficit of iodine as a cause of the goiter appearance.(ABSTRACT TRUNCATED AT 250 WORDS)     

Response of thyrotropin, prolactin and free thyroid hormones to graded exercise in normal male subjects

Serum levels of thyrotrophin (TSH), prolactin (PRL), free thyroxine (FT4) and free triiodothyronine (FT3) were determined before and after physical exercise in 21 normal male subjects. The subjects were divided into 3 groups as follows: group I--light exercise (exercise on the Mijnhardt bicycle ergometer at 100 Watts for 15 min); group II--moderate exercise (a 5 km marathon); group III--heavy exercise (a 10 km marathon). In group I, TSH level rose from 1.96 +/- 0.42 mu u/ml (mean +/- SEM) to 2.52 +/- 0.30 mu u/ml (p less than 0.01), and PRL levels rose from 11.0 +/- 2.0 ng/ml to 19.0 +/- 5.2 ng/ml (p less than 0.01). In group II, TSH rose from 2.11 +/- 0.51 mu u/ml to 2.62 +/- 0.56 mu u/ml (p less than 0.05), and PRL rose from 11.2 +/- 1.6 ng/ml to 24.0 +/- 5.2 ng/ml (p less than 0.01). In group III, TSH rose from 2.01 +/- 0.41 mu u/ml to 2.36 +/- 0.45 mu u/ml (p less than 0.02), and PRL rose from 12.1 +/- 2.0 ng/ml to 47.7 +/- 9.3 ng/ml (p less than 0.01). The serum levels of FT4 showed different results among the three groups: Group I showed an increased response from 1.60 +/- 0.12 ng/dl to 1.72 +/- 0.12 ng/dl (p less than 0.01); Group II showed no significant difference; and group III demonstrated a diminished response from 1.61 +/- 0.14 ng/dl to 1.45 +/- 0.16 ng/dl (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Growth hormone secretion during sleep. II. Interrelationships between growth hormone secretion, insulin-like growth factor I and sex steroids

The serum levels of insulin-like growth factor I (IGF I), dehydroepiandrosterone sulfate (DHAS), testosterone (T) and estradiol (E2) have been measured in 78 prepubertal and 57 early pubertal patients referred for short stature, at the same time when their secretion of GH was evaluated both during nocturnal sleep and by two conventional stimulation tests. According to the results of GH measurements they were considered as having a normal secretion of GH (group I), a complete GH deficiency (group II), a partial GH deficiency (group III), low responses to stimuli with normal secretion during sleep (group IV) or a nocturnal neurosecretory dysfunction (group V). Though widely scattered, the IGF I levels showed the following characteristics: a significant increase at puberty from 0.77 to 1.29 U/ml (p less than 0.001) in the so-called endocrinologically normal patients of group I, not in the other groups; in the prepubertal patients of group I, a correlation of IGF I with chronological age (r = 0.47, p less than 0.005) and bone age (r = 0.52, p less than 0.002); significantly reduced IGF I levels in patients of group II having complete GH deficiency (p less than 0.001); no significant differences between prepubertal patients with partial or atypical GH deficiency from groups III, IV, V and prepubertal patients from group I; lower pubertal levels in groups III, IV, V than in pubertal patients from group I (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of the prostaglandin E1 analog enisoprost on glucose and lipid metabolism in patients with type II diabetes mellitus.

Short-term studies have suggested that analogs of prostaglandin E may have favorable effects on the carbohydrate and lipid metabolism in patients with type II diabetes mellitus. The present study was undertaken to investigate the long-term effects of a prostaglandin E1 analog on the regulation of glycemic control and plasma lipids. Twenty patients with type II diabetes received enisoprost, 300 mcg/day, for three months. Fasting serum glucose, glycosylated hemoglobin, insulin and C-peptide levels as well as triglyceride, total cholesterol, high density lipoprotein cholesterol and its subfractions, apolipoproteins B and AI and post-heparin lipoprotein lipase and hepatic triglyceride lipase activities were determined. During the first month, enisoprost treatment caused significant decreases in plasma glucose (baseline = 8.72 +/- 0.39 mmol/L, 4 week = 7.78 +/- 0.5 mmol/L, change = -0.94 +/- 0.28 mmol/L, p less than 0.01) and total cholesterol (baseline = 5.30 +/- 0.23 mmol/L, 4 week = 5.01 +/- 0.26 mmol/L, change = -0.28 +/- 0.06 mmol/L, p less than 0.05). The decrease in cholesterol level was due to a reduction in high density lipoprotein, specifically in high density lipoprotein2 fraction (baseline = 1.29 +/- 0.1 mmol/L, 4 week = 1.12 +/- 0.08 mmol/L, change = -0.018 +/- 0.04 mmol/L, p less than 0.05 for the former and baseline = 0.40 +/- 0.06 mmol/L, 4 week = 0.27 +/- 0.03 mmol/L, change = -0.12 +/- 0.03 mmol/L, p less than 0.05 for the latter): All of these values returned to the pretreatment levels despite continuation of enisoprost.(ABSTRACT TRUNCATED AT 250 WORDS)     

Recovery from heart failure: structural and functional analysis in a canine model

Chronic, rapid ventricular pacing produces congestive heart failure in the dog. Using echocardiography, the features of developing heart failure were analysed and the capacity of this model for recovery was assessed once pacing had been discontinued. Fifteen dogs were studied; nine were paced at 250 beats/min (bpm) to severe heart failure (5.0 +/- 1.8 weeks) and six served as sham controls. In the paced animals at severe heart failure, two-dimensional echocardiography demonstrated a significant increase in diastolic cross-sectional cardiac area (from 11 +/- 3 to 16 +/- 2 cm2, p less than 0.05), associated with a marked fall n area ejection fraction (54 +/- 8 to 21 +/- 8%, p less than 0.05), and significant left ventricular wall thinning (from 6.0 +/- 0.7 to 4.7 +/- 0.9 mm, p less than 0.05). In addition, significant increases in heart rate (77 +/- 7 to 126 +/- 13 bpm, sinus rhythm; p less than 0.05), respiratory rate (41 +/- 13 to 80 +/- 20 cycles/min, p less than 0.05), and body weight (21 +/- 1 to 24 +/- 3 kg, p less than 0.05) were noted. Serum sodium fell (146 +/- 3 to 140 +/- 8 mmol/L, p less than 0.05), while blood urea nitrogen (6 +/- 2 to 10 +/- 2 mmol/L, p less than 0.05) and creatinine (86 +/- 12 to 101 +/- 15 mmol/d, p less than 0.05) increased. Recovery was characterized by rapid improvement such that all measured parameters normalized by 1 week, except for cross-sectional cardiac area which remained dilated up to 4 weeks (14 +/- 3 cm2, p less than 0.05 versus control).(ABSTRACT TRUNCATED AT 250 WORDS)     

Characterization of a more electronegatively charged LDL subfraction by ion exchange HPLC

Low density lipoproteins (LDL), collected from 32 normal male subjects (aged 30-60), were subfractionated by high resolution ion exchange chromatography (IE-HPLC). By this procedure two LDL subfractions were eluted. The first corresponds to normal LDL (nLDL); while the second one corresponds to a more electronegative subfraction, called LDL-. The mean percentage contribution of LDL- to native plasma LDL was of 3.9% (range 0.5-9.8%). The percentage concentration of LDL- in total native LDL did not correlate with plasma total cholesterol, triglycerides, and LDL cholesterol, whereas a significant negative correlation with high density lipoprotein cholesterol was found (r = -.38; p less than .05). LDL- was negatively correlated with LDL phospholipids (r = -.59; p less than .001), and with the LDL vitamin E content (r = -.63; p less than .001), and positively correlated with LDL proteins (r = -.35; p less than .05) and the content of thiobarbituric acid reactive substances (TBARS) in total LDL (r = .43; p less than .05). The TBARS molar content of LDL- was three times higher than in nLDL, with a mean concentration in LDL- of 7.3 mol/mol lipoprotein. By preparative IE-HPLC significant differences of the LDL- chemical composition were observed. The percentage content of cholesterol esters and of phospholipids was decreased, whereas proteins and free cholesterol were increased. Analysis by sodium dodecyl sulphate polyacrylamide gel electrophoresis revealed that besides apolipoprotein B-100 there was evidence of peptides with a higher molecular weight in LDL-.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effects of dietary manipulation upon the respiratory exchange ratio as a predictor of maximum oxygen uptake during fixed term maximal incremental exercise in man

This study examined the effects of dietary manipulation upon the respiratory exchange ratio (R = VCO2/VO2) as a predictor of maximum oxygen uptake (VO2max). Seven healthy males performed fixed term maximal incremental treadmill exercise after an overnight fast on three separate occasions. The first test took place after the subjects had consumed their normal mixed diet (45 +/- 5% carbohydrate (CHO] for a period of three days. This test protocol was then repeated after three days of a low CHO diet (3 +/- 2% CHO), and again after three days of a high CHO diet (61 +/- 5% CHO). Respiratory gases were continuously monitored during each test using an on-line system. No significant changes in mean exercise oxygen uptake (VO2), VO2max or maximum functional heart rate (FHRmax) were found between tests. Mean exercise carbon dioxide output (VCO2) and R were significantly lower than normal after the low CHO diet (both p less than 0.001) and significantly higher than normal after the high CHO diet (both p less than 0.05). Moreover, compared with the normal CHO diet, the R-time relationship during exercise was at all times significantly (p less than 0.001) shifted to the right after the low CHO diet, and shifted to the left, being significantly so (p less than 0.05) over the final 5 min of exercise, after the high CHO diet.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sheep plasma protease inhibitors influencing protease activity and growth of Lucilia cuprina larvae in vitro

The enzyme inhibitors alpha 2-macroglobulin (alpha 2M), anti-thrombin III (AT III) and alpha 1-proteinase inhibitor (alpha 1PI) were isolated from sheep plasma and tested for their ability to affect L. cuprina larval proteases and larval growth in vitro. Casein radial diffusion gels indicated that both alpha 2M and alpha 1PI completely inhibited the protease activity of a larval excretory-secretory preparation, while AT III had a partial effect. Casein zymograms revealed that alpha 2M inhibited all of the larval proteases, while AT III was able to modify the normal plaque pattern; alpha 1PI inhibited all plaques except a doublet present at pI 8.5. Larval growth in vitro was significantly inhibited by alpha 2M and AT III (P less than 0.05) when compared to albumin controls but was not affected by alpha 1PI. The levels of alpha 2M in sheep serum were monitored over the course of a larval fly infection. A significant increase in alpha 2M (P less than 0.05) was recorded in the serum of flystruck sheep. It is suggested that, under certain circumstances, these inhibitors may be involved in influencing flystrike through reducing the activity of larval proteases necessary for wound formation and larval nutrition.     

Endocrine studies in postmenopausal women during oral replacement therapy with unconjugated oestrogens

Two groups of postmenopausal women were seen at monthly intervals during a three-month trial of continuous therapy with oral unconjugated oestrogens. Ten women in the first group were administered daily Hormonin No. 1 containing oestriol (E3) 0.135 mg, oestradiol (E2) 0.3 mg and oestrone (E1) 0.7 mg. Eight women in the second group received Hormonin No. 2 containing E3 0.27 mg, E2 0.6 mg and E1 1.4 mg. E1, E2, E3 and dehydroepiandrosterone (DHA) as well as follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were measured by radioimmunoassay. Maturation index of vaginal smears and clinical effects were also evaluated. Oral replacement therapy with these unconjugated oestrogens produced a significant elevation of E1 (p less than 0.05) and E2 (p less than 0.05) to values corresponding well with the premenopausal range measured in our laboratory. Postmenopausal levels of FSH and LH showed only a moderate but significant decrease (p less than 0.05). There was consistent relief of vasomotor symptoms. One case of endometrial focal adenomatous hyperplasia uncovered during the period of treatment was transformed to functional secretory endometrium after an appropriate course with progestogens. Oral administration of unconjugated oestrogens and periodic withdrawal bleeding induced with a progestational agent seems to be an effective method of replacement therapy in postmenopausal women.     

Regulation of canine skeletal muscle and hindlimb blood flow in acute anemia

Redistribution of blood flow away from resting skeletal muscles does not occur during anemic hypoxia even when whole body oxygen uptake is not maintained. In the present study, the effects of sympathetic nerve stimulation on both skeletal muscle and hindlimb blood flow were studied prior to and during anemia in anesthetized, paralyzed, and ventilated dogs. In one series (skeletal muscle group, n = 8) paw blood flow was excluded by placing a tourniquet around the ankle; in a second series (hindlimb group, n = 8) no tourniquet was placed at the ankle. The distal end of the transected left sciatic nerve was stimulated to produce a maximal vasoconstrictor response for 4-min intervals at normal hematocrit (Hct.) and at 30 min of anemia (Hct. = 14%). Arterial blood pressure and hindlimb or muscle blood flow were measured; resistance and vascular hindrance were calculated. Nerve stimulation decreased blood flow (p less than 0.05) in the hindlimb and muscle groups at normal Hct. Blood flow rose (p less than 0.05) during anemia and was decreased (p less than 0.05) in both groups during nerve stimulation. However, the blood flow values in both groups during nerve stimulation in anemic animals were greater (p less than 0.05) than those at normal Hct. Hindlimb and muscle vascular resistance fell significantly during anemia and nerve stimulation produced a greater increase in vascular resistance at normal Hct. Vascular hindrance in muscle, but not hindlimb, was less during nerve stimulation in anemia than at normal Hct.(ABSTRACT TRUNCATED AT 250 WORDS)     

Self-priming effect of LH-RH on pituitary gonadotropins in hyperprolactinemic women

To investigate how various concentrations of serum prolactin (PRL) influence the priming effect of luteinizing hormone releasing hormone (LH-RH) on the pituitary gland, 24 women with various blood PRL concentrations received intravenous injections of 100 micrograms of synthetic LH-RH twice at an interval of 60 minutes and their serum LH and follicle-stimulating hormone (FSH) were measured and analysed. In the follicular phase with a normal PRL concentration (PRL less than 20 ng/ml, n = 6), marked first peaks of the two hormones following the first LH-RH stimulation and enhanced second peaks after the second LH-RH administration were observed, indicating a typical priming effect of LH-RH on gonadotropins, though the second response of FSH was more moderate than that of LH. In hyperprolactinemia, in which the serum PRL concentration was higher than 70 ng/ml (n = 13), the basal concentration of gonadotropins was not significantly changed but the priming effect of LH-RH on LH and FSH was significantly decreased (p less than 0.01). No marked second peaks of LH and FSH were observed, suggesting an inhibitory effect of hyperprolactinemia on the second release of LH and FSH. In contrast, this effect was restored in a group of women whose serum PRL concentration was between 30 and 50 ng/ml (n = 5). Furthermore, enhanced second peaks of both LH and FSH were noted after successful bromocriptine therapy reduced hyperprolactinemia (PRL greater than 70 ng/ml) to less than 25 ng/ml (n = 5).(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in the hypothalamic-hypophyseal axis of mares associated with seasonal reproductive recrudescence

Four groups of mares, representing anestrus (AN; n = 8), early transition (ET; n = 7), late transition (LT; n = 8) and estrus (EST; n = 12) were used to examine changes in the hypothalamus and anterior pituitary during the period of transition from winter anestrus into the breeding season. Mares were of mixed breeding, between the ages of 3 and 20 years, and had shown normal patterns of estrous behavior and ovulation during the breeding season previous to this experiment. Hypothalamic content of gonadotropin-releasing hormone (GnRH) and anterior pituitary content of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were determined by radioimmunoassay. The number of receptors for GnRH in anterior pituitary tissue was also determined. There was no effect of stage of transition into the breeding season on receptors for GnRH or content of FSH (p greater than 0.05). Likewise, content of GnRH in the hypothalamus did not differ between the four groups (p greater than 0.05). However, pituitary content of LH increased progressively from anestrus to the breeding season (p less than 0.05). Means for the AN, ET, LT and EST groups were 1.1 +/- 0.2, 2.2 +/- 0.3, 6.3 +/- 1.4 and 15.2 +/- 1.8 micrograms LH/mg pituitary, respectively. In addition, serum concentrations of LH associated with the first ovulation of the year for 5 of the EST mares were significantly lower (p less than 0.01) than those associated with the second ovulation of the year.(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in cerebrospinal fluid and plasma amino acid concentrations with elevated dietary protein concentration in dogs with portacaval shunts

Effects of dietary protein concentration on plasma and cerebrospinal fluid (CSF) amino acids (AA) in dogs with portacaval shunts (PCS) were examined. An 18% protein purified diet (18P) was fed to 4 PCS dogs and 2 controls; at week 10, 2 of the PCS dogs were switched to 36% protein (36P) until week 28. Effects of the diet switch on plasma and CSF AA in 8 normal dogs were determined in another experiment. Neither surgery nor protein level significantly affected average food intake (weeks 10-28). Plasma amino acid patterns typical of PCS animals were observed: phenylalanine and tyrosine increased and branched chain AA decreased with shunting (p less than 0.05). Plasma phenylalanine increased further with 36P in PCS dogs (p less than 0.05), but was not affected by dietary protein concentration in controls. With 36P: CSF arginine, serine, histidine, tryptophan, phenylalanine, glutamate and glutamine increased in PCS dogs; but only arginine decreased in CSF of controls (p less than 0.05). In PCS dogs, significant CSF AA changes with elevated dietary protein were unrelated to plasma AA changes.     

Beta cell response to the hyperglycaemic clamp in three patients with insulinoma: a study using a hyperglycaemic glucose clamp

To determine the mechanism responsible for deficient carbohydrate metabolism in patients with insulinoma, we studied three affected patients and seven normal controls using the hyperglycaemic clamp method (8.4 mmol/l) with the BIOSTATOR (GCIIS). In insulinoma patients, the amount of glucose necessary to reach the hyperglycaemic clamp was less than that required in normal controls (6.19 +/- 1.19 mg/min/kg vs. 9.95 +/- 0.53 mg/min/kg) (p less than 0.05). There was no significant difference in metabolized glucose (M) in the stable phase of the hyperglycaemic clamp; however, the M/IRI in this phase was less in those with insulinoma (7.9 +/- 0.50) than in controls (22.26 +/- 4.14) (p less than 0.05). There was no difference in beta cell secretory response to hyperglycaemic stimulus (defined as the increase in the concentration of C-peptide from the basal state to the stable phase of the hyperglycaemic clamp) between the two groups. Hepatic insulin extraction was significantly lower in patients with insulinoma than in normal controls (+0.72 +/- 0.07 vs. +0.85 +/- 0.01). Finally, the ratios of fractional turnover of glucose (K/IRI); glucose clearance/IRI and total rate of elimination of glucose from the extracellular pool/IRI were also all lower in patients with insulinoma than in controls (p less than 0.05). These data support the conclusion that deficient glucose metabolism seen in these patients is not related to a lack of response to glucose on the part of normal or neoplastic islet tissue.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of an antiandrogen, flutamide, on oocyte quality and embryo development in rats superovulated with pregnant mare's serum gonadotropin

Increased oocyte degeneration in rats is associated with enhanced ovarian androgen secretion following superovulation with pregnant mare's serum gonadotropin (PMSG). To determine whether androgens may be causally related to oocyte degeneration, we examined the effects of an antiandrogen, flutamide, on oocyte quality and embryo development after induction of superovulation with PMSG. Immature female Sprague-Dawley rats were used for two experiments. In the first experiment, the females received either 5 mg flutamide or vehicle alone 30 and 36 h after 40 IU PMSG and were killed at 48, 60, and 72 h. Although total number of oocytes was not significantly different between the two groups, flutamide significantly reduced the percentage of degenerate oocytes ovulated at all the time intervals examined (p less than 0.01). In the second experiment, the females were given 4 IU PMSG (control) or 40 IU PMSG with either 5 mg flutamide or vehicle. The rats were mated and then killed on Days 2, 3, 4, and 5 of pregnancy. Compared to control, flutamide did not effectively prevent the early loss of preimplantation embryos nor the developmental retardation which took place in the vehicle-treated rats after Day 2. However, flutamide treatment was associated with a significant decrease in embryo degeneration and a significant increase in the percentage of cleaved embryos on Day 2 (p less than 0.01). Compared to levels associated with the vehicle regimen, ovarian and/or serum androgen levels in the flutamide-treated rats significantly decreased at 60 h (p less than 0.01) and on Day 2 (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Time course of muscle adaptation after high force eccentric exercise

The repeated bout effect on changes in muscle damage indicators was examined in two groups of subjects following two bouts of 70 maximal eccentric actions of the forearm flexors. Fourteen college age female subjects were placed into two groups. The two bouts were separated by 6 weeks (n = 6), and 10 weeks (n = 8). The subjects performed the same amount of work for the bouts. The muscle damage indicators were isometric strength (STR), relaxed elbow joint angle (RANG), flexed elbow joint angle (FANG), perceived muscle soreness ratings (SOR), and plasma creatine kinase activity (CK). These measures were obtained pre-exercise and 5 days following each bout. The first bout showed significant changes in all measures over time for both groups (P less than 0.01). For the 6-week group, significantly smaller changes in RANG (P less than 0.01), SOR (P less than 0.05), and CK (P less than 0.01), as well as significantly faster recoveries (P less than 0.05) for STR and FANG were produced in the second bout. For the 10-week group, significantly smaller changes in RANG (P less than 0.05) and CK (P less than 0.01) were demonstrated by the second bout, but not significant difference was found for STR, FANG, and SOR between bouts 1 and 2. Changes in CK were still significantly smaller than that of the first bout when 6 subjects (3 subjects from each group) performed the same exercise 6 months after the second bout, but no difference in other measures.(ABSTRACT TRUNCATED AT 250 WORDS)     

Central nervous system mediated vasodepressor action of atrial natriuretic factor

Administration of 20, 4 or 2.5 micrograms/kg of atriopeptin III (AT III) into the fourth ventricle of the brain of spontaneously hypertensive rats produced a 13, 14 and 7 mm Hg decrease in MAP respectively, while 1 microgram/kg had no effect on MAP and was significantly different from 20 or 4 micrograms/kg (p less than 0.025). In contrast, injection of AT III 20 micrograms/kg into the lateral ventricle did not produce a change in MAP. To examine an interaction of AT III with the opioidergic system, the opiate antagonist, naloxone HCl, 10 micrograms, was given by ICV injection 10 minutes prior to AT III, and significantly prevented the depressor response to AT III (p less than 0.025 compared with AT III alone). Injection of specific anti-sera to beta-endorphin failed to prevent the AT III-induced depressor response. Our results demonstrate that AT III can act within the central nervous system to decrease the MAP of rats, most likely at a locus in proximity to the fourth ventricle of the brain. Further, an interaction with the central opioidergic nervous system underlies the central effects of AT III.