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Biomedical subjects

E Ramey

Publications and source records attributed to E Ramey.

18 recordsLinked to original sources
PubMed1984

Sex differences in arachidonate cyclo-oxygenase products in elicited rat peritoneal macrophages.

Peritoneal macrophages were elicited by Freund's incomplete adjuvant from adult male and female Fisher 344 rats. The release of prostaglandin E2 and thromboxane B2 from these macrophages was determined by radioimmunoassay. The basal release of these products was the same for males and females. The macrophages of the female rats released, in a dose-dependent manner, significantly more prostaglandin E2 and thromboxane B2 than macrophages from the male, following challenge with either a particulate stimulus, zymosan (25-150 micrograms/ml) or a soluble stimulus, calcium ionophore A23187 (1 X 10(-7) -1 X 10(-6) M). These results may relate to gender differences in immune responses.

Animals↗
PubMed1983

Glucocorticoid protection against PAF-acether toxicity in mice.

Intravenous platelet activating factor (PAF-acether, 10 to 25 micrograms/kg body weight) produced dose-dependent mortality in both male and female mice. Pretreatment with indomethacin (50 mg/kg), verapamil (40 mg/kg) or nifedipine (4 mg/kg) failed to inhibit the lethal effect of 20 micrograms/kg PAF-acether. This suggests that neither arachidonate cyclo-oxygenase products nor availability of extracellular Ca2+ mediate the toxic action. In contrast, pretreatment with 100 mg/kg cortisone acetate (s.c.) daily for four days exerted a highly protective effect, i.e. 100% and 93% survival in males and females, compared to 13% and 7% respectively, in untreated animals. PAF-acether-induced death may be a useful model for the in vivo evaluation of pharmacological agents in anaphylactic shock.

Animals↗
PubMed1983

Thromboxane agonism and antagonism in a mouse sudden death model.

The effects of the stable thromboxane agonist, U46619, and sodium arachidonate were tested by i.v. injection into male and female mice. U46619 produced dose-dependent mortality in both sexes equally, in contrast to the gender-differentiated effects of arachidonic acid. The thromboxane receptor antagonist, SQ 26,536, protected in a dose-dependent manner against both arachidonate and U46619. The thromboxane antagonist was more effective against arachidonate toxicity in male than in female mice, but was equiactive against U46619 in both sexes. Neither the thromboxane synthetase inhibitor, OKY-1581, nor the cyclooxygenase inhibitor, indomethacin, protected against U46619-induced sudden death. However, cortisone acetate increased survival of mice challenged with U46619. The results support the hypothesis that thromboxane A2 mediates arachidonate-induced sudden death. The effects of arachidonate can be mimicked by the thromboxane agonist and are attenuated by the thromboxane antagonist. The gender difference in arachidonate toxicity is apparently not due to differences in sensitivity to thromboxane A2, as the thromboxane agonist was equally toxic in males and females. The greater protective effect of the thromboxane antagonist against arachidonate toxicity in males suggests that thromboxane A2 is a more important mediator of arachidonate-induced sudden death in males compared to female mice.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1982

Sexual differentiation of arachidonate toxicity in mice.

Mature male and female mice 50 days of age were challenged with i.v. sodium arachidonate at doses of 12.5, 25, 50 and 100 mg/kg. A dose-dependent response in terms of mortality was observed. Males were significantly more susceptible to arachidonate-induced mortality than females at the 25 and 50 mg/kg doses (P less than .05). The 100 mg/kg dose produced 100% mortality in both sexes. When mice aged 23, 29, 35 and 50 days were challenged with 50 mg/kg of arachidonate, no gender difference was observed until mice were 35 days of age, at which time the male mortality was 80%, compared to 57% for female mice (P less than .05). Mice gonadectomized at 23 days and intact mice 23 days of age were treated with s.c. estradiol, testosterone or vehicle for 7 days before arachidonate challenge. Among these groups, the gonadectomized females and intact males were significantly protected by estradiol when compared to the appropriate controls (P less than .05). In contrast, testosterone pretreatment had no significant effect on mortality. These results demonstrate that the development of the gender difference in arachidonate-induced mortality in mice is dependent upon the presence of gonadal hormones in the immature stages.

Adrenal Glands↗
PubMed1981

Acute protection against arachidonate toxicity by hydrocortisone and dexamethasone in mice.

1. Pharmacologic doses of hydrocortisone sodium succinate (100 mg/kg) has a rapid protective action against arachidonate-induced mortality in mice when administered intravenously 5 to 60 min before intravenous infusion of arachidonate. 2. Intravenous dexamethasone sodium phosphate (4 mg/kg) has a similar protective effect. 3. The time course of the development of the protective effect of intravenous glucocorticoids suggests that DNA transcription and protein synthesis are not involved in the mechanism of this action. 4. Longer pretreatment with glucocorticoids are required to reduce mortality when subcutaneous or intraperitoneal routes of administration of the steroids used.

Animals↗
PubMed1979

Effect of corticosteroids on arachidonate induced mortality in male and female mice.

Sodium arachidonate (50 mg/kg) given intravenously to male and female mice induces pulmonary emboli followed by respiratory distress and cyanosis. Female mice are significantly more resistant to this treatment than male mice. Cortisone pretreatment for four days to intact mice (10 mg/kg/day/4 days) had a significant protective effect in both males and females against arachidonate toxicity, eliminating the sex difference previously observed. Adrenalectomy four days before arachidonate infusion increased the sensitivity to SA and resulted in 100% mortality in both sexes. Pretreatment of adrenalized animals with cortisone significantly reduced to some degree the mortality rate in both sexes. Castration of male and female mice three weeks before adrenalectomy did not affect the mortality rate seen following adrenalectomy alone. In conclusion, exogenous cortical steroids augment the resistance of even intact mice and are absolutely necessary for survival in adrenalectomized animals. The observed sex differences in untreated intact animals is not seen after treatment with cortisone or adrenalectomy.

Adrenal Medulla↗
PubMed1977

Androgen-mediated sensitivity in platelet aggregation.

Platelet responsiveness to an aggregating stimulus (ADP) was greater (X10) in male than in female rats. Castration reduced aggregability in males (X4) and increased it in females (X3). Pretreatment with testosterone (1 mg/kg, sc) enhanced platelet aggregability in both sexes and restored the diminished responsivity observed in castrated males. Incubation of platelets with testosterone (1-10 ng/ml) potentiated rat (18.0 +/- 1.5%) and guinea pig (40.0 +/- 5.0%) aggregability when compared with vehicle-treated platelets. Estradiol (1 mg/kg, sc) in vivo or estradiol, progesterone, and deoxycorticosterone (1 microng/ml) in vitro had the opposite effect and decreased aggregability. The rank order of effectiveness of androgens in vitro was dihydrotestosterone, testosterone, methyltestosterone, androstendione, and androsterone, which correlates with their androgenicity. The effect of androgens was antagonized in vitro by the antiandrogen (Flutamide) and by estradiol. These data suggest that gonadal steroids may play a role in regulating platelet function in the rat and guinea pig.

Adenosine Diphosphate↗
PubMed1976

Studies on the extra-hepatic effects of glucagon in the eviscerated rat.

The in vivo effects of glucagon on the metabolism of extra-hepatic tissues have been investigated in eviscerated, functionally hepatectomized rats with intact kidneys. In these animals, even pharmacological amounts of exogenous glucagon did not significantly alter plasma glucose, FFA, or amino acids, compared with saline treatment. The possible secondary release of adrenal catecholamines following such doses of glucagon appeared to be similarly ineffective in increasing the peripheral tissue mobilization of substrates. It was only when the eviscerated animals were pretreated with insulin that the subsequent administration of glucagon or epinephrine elicited significant elevations in plasma FFA. The concomitant evisceration and adrenalectomy did not produce results which were significantly different from evisceration alone. Both kinds of animals required insulin pretreatment before a lipolytic response to glucagon or epinephrine could be demonstrated. This suggests that severe insulin insufficiency itself elicits almost maximum catabolism in these animals and that the further addition of other catabolic hormones such as glucagon or epinephrine cannot increase these catabolic effects, as manifest in plasma concentrations of FFA. These data show an extra-hepatic lipolytic effect of glucagon in vivo, but do not illuminate the significance of this effect in the intact animal.

Amino Acids↗