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Biomedical subjects

G T Peake

Publications and source records attributed to G T Peake.

At least 19 recordsLinked to original sources
PubMed1979

Indomethacin fails to alter basal or phenothiazine-induced prolactin concentrations in man.

In order to evaluate the possible role of prostaglandins in pituitary prolactin (PRL) secretion, PRL was serially measured following perphenazine (Trilafon) ingestion in 8 men before and after 5 days of indomethacin administration. Since estrogens have been shown to modulate prolactin secretion in man, serum steroids including estrone (E1), estradiol (E2), progesterone (P) and testosterone (T) were measured before and after indomethacin ingestion. Serum E1, P and T levels were similar during the pre- and post-indomethacin study periods: 56 +/- 4 (1 SEM) vs 48 +/- 5 pg/ml, 298 +/- 28 vs 315 +/- 32 pg/ml, and 8.1 +/- 0.7 vs 8.6 +/- 0.7 ng/ml, respectively. Serum E2 levels were slightly, but significantly, lower following indomethacin treatment at 30 +/- 3 vs 37 +/- 3 pg/ml (p less than .01). Basal serum PRL concentrations were unaffected by indomethacin administration (9 +/- 3 pre- vs 8 +/- 2 ng/ml post-drug treatment). Integrated perphenazine-induced PRL responses were likewise similar during the 2 study periods: 101 +/- 16 ng . hr/ml during the control period and 104 +/- 14 ng . hr/ml following indomethacin. Thus, short-term indomethacin treatment had no effect on basal or perphenazine-stimulated PRL secretion in men.

Adolescent↗
PubMed1979

Suppressor cell function in sarcoidosis.

We investigated the role of suppressor cells in the depressed cellular immunity of patients with sarcoidosis. The mean response in 16 patients with active sarcoidosis to three concentrations of phytohemagglutinin was significantly (P less than 0.01) less than control values. Passage of the cells over glass wool resulted in a 116% increase in response to phytohemagglutinin in patients and a 39% decrease in control subjects. Addition of indomethacin to phytohemagglutinin cultures increased the response of cells in patients with sarcoidosis by 192% +/- 32% versus a 112% +/- 18%-increase for control subjects (mean +/- SEM, P less than 0.05). Patients had an increased percentage of monocytes in peripheral blood mononuclear cell preparations, and the percent monocytes correlated with the percent increase in phytohemagglutinin response after glass wool passage (r = 0.62, P less than 0.05). Thus, several factors contribute to the depressed phytohemagglutinin response in sarcoidosis patients: an increased suppression by the prostaglandin-producing suppressor cell, an increased percentage of monocytes, and an as yet undefined factor.

Adult↗
PubMed1978

Prostaglandin suppression of mitogen-stimulated lymphocytes in vitro. Changes with mitogen dose and preincubation.

In this study we further characterize the properties of the prostaglandin-producing suppressor cell. Overnight preincubation of peripheral blood mononuclear cells results in an increased response of the cells to phytohemagglutinin or Concanavalin A compared to the response of fresh cells. This increase in mitogen response with preincubation was similar in magnitude to the increase in mitogen response of fresh cells after the addition of indomethacin. The two manipulations were not additive; that is, after preincubation, indomethacin caused much less enhancement of mitogen stimulation of peripheral blood mononuclear cells (100 +/- 12% increase before preincubation vs. 12 +/- 6% after preincubation; mean+/-SEM, P < 0.001). Preincubated cells also lose sensitivity to inhibition by exogenous prostaglandin E(2). It requires the addition of 100- to > 1,000-fold more exogenous PGE(2) to produce comparable inhibition of phytohemagglutinin-stimulated preincubated cells than is required for inhibition of phytohemagglutinin-stimulated fresh cells. The enhancing effect of indomethacin increases with decreasing doses of phytohemagglutinin. Indomethacin causes a 1,059+/-134% increase in [(3)H]thymidine incorporation at the lowest dose of phytohemagglutinin (0.2 mug/ml), and a 4+/-3% increase at the highest dose (20 mug/ml). This increase in response to indomethacin with a lower dose of phytohemagglutinin is due to increased sensitivity to inhibition by PGE(2) at lower mitogen doses. The prostaglandin-producing suppressor cell assay and the short-lived suppressor cell assay measure over-lapping phenomena. The increased suppressive effect of the prostaglandin-producing suppressor at suboptimal mitogen dose must be taken into account in the interpretation of any study where the response to a range of mitogen doses is studied.

Adult↗
PubMed1977

Prostaglandin-producing suppressor cells in Hodgkin's disease.

We examined the role of a prostaglandin-producing suppressor cell in the hyporesponsiveness to phytohemagglutinin seen in Hodgkin's disease. Addition of indomethacin to phytohemagglutinin cultures of lymphocytes from six patients with Hodgkin's disease resulted in an increase of 182 +/- 60 per cent in 3H-thymidine incorporation versus a 44 +/- 18% increase in 29 controls (mean +/- S.D., P less than 0.001). Without indomethacin the mean response of the lymphocytes in Hodgkin's disease was 48% of that of control. With indomethacin it was 94% of the control value. Phytohemagglutinin cultures of Hodgkin-disease lymphocytes produced approximately fourfold more prostaglandin E2 after 48 hours than did normal lymphocytes (P less than 0.02). Removal of glass-adherent cells markedly decreased the enhancement seen with indomethacin; it reduced prostaglandin E2 production by more than 80% and eliminated the differences in response to phytohemagglutinin between Hodgkin-disease and normal lymphocytes. Thus, a glass-adherent, prostaglandin-producing suppressor cell is responsible for the hyporesponsiveness to phytohemagglutinin seen with Hodgkin-disease lymphocytes.

Adult↗
PubMed1977

Direct immunochemical detection of prostaglandin-E and cyclic nucleotides in human malignant tumors.

Immunofluorescent localization of prostaglandin-E (PGE), cyclic AMP (CAMP), and cyclic GMP (cGMP) was studied in tumor tissues from 40 patients with a variety of solid tumors. Representative normal tissues served as controls. Rabbit antisera specific for PGE or the cyclic nucleotides were used, and the reactions observed were correlated with the degree and type of lymphocytic reaction at the tumor margins. Strong PGE immunofluorescence was detected in tumor cells in 27 of 42 malignancies; by contrast nine of 13 normal tissues showed weak PGE reactions, cAMP was detected in 30 of the 42 malignancies; cGMP was noted in only seven of the 42 malignant tissues and in none of the normal tissues studied. The most common malignant tumor profile (17/42) was that of positive PGE and cAMP and negative cGMP staining. Tumors showing strong staining with anti-PGE or cAMP demonstrated a distinct trend towards heavier lymphocytic infiltration with a predominance of T cells at their margins, although this association did not reach statistical significance in the present material.

B-Lymphocytes↗
PubMed1977

Chlorpropamide-induced hypoglycemia: successful treatment with diazoxide.

A healthy adolescent boy was treated on two occasions for an overdose of chlorpropamide (Diabinese). Glucose therapy alone was not sufficient to control the hypoglycemia, but the administration of glucose plus diazoxide raised the blood sugar to supranormal levels. A bolus of intravenous glucagon briefly raised the blood sugar level to within normal limits, increased the blood ketones but also augmented insulin secretion. An overdose of sulfonylurea may cause prolonged and fatal hypoglycemia. Rational therapy, both in diabetic and normal persons, is glucose plus an "insulin antagonist." The administration of diazoxide was effective in our patient, substantially reducing the plasma insulin level; this agent may be the "insulin-antagonist" of choice for use in sulfonylurea-induced hypoglycemia.

Adolescent↗
PubMed1976

Primary empty sella syndrome with visual field defects.

A patient with an enlarged, asymmetric sella turcica and visual field defects suggestive of a pituitary or parasellar tumor underwent extensive roentgenographic and pituitary function studies. No abnormalities in pituitary luteinizing hormone, follicle-stimulating hormone, thyroid-stimulating hormone, ACTH, prolactin or vasopressin secretion were detected. Growth hormone secretion was provoked by arginine infusion but not by hypoglycemia. Pneumoencephalography revealed air in the sella turcica, and no evidence of tumor. Thus, an enlarged sella turcica in a patient with visual field defects but normal pituitary function may suggest the presence of an "empty sella syndrome."

Humans↗
PubMed1976

Hyperprolactinemia influences renal function in man.

Renal handling of solute and water following oral water loading was determined in six subjects with small pituitary adenomas associated with nonsuppressible hyperprolactinemia. Compared to control subjects, urine volume and solute excretion were significantly diminished in the hyperprolactinemic group. This was attributable to a decrease in osmolar clearance. Free water clearances were not different from control subjects. Hypothyroidism and adrenal insufficiency as an explanation for the antidiuresis were excluded in each patient. The data supports the suggestion that prolactin influences renal function in man.

Adenoma↗
PubMed1976

Dissociation between LH release and pituitary cyclic nucleotide accumulation in response to synthetic LH-releasing hormone in vivo.

In order to clarify the role of cyclic nucleotides in the mediation of LH-releasing hormone (LH-RH) action on LH release, the effect of LH-RH on LH release and pituitary cyclic AMP and cyclic GMP accumulation was studied in vivo. Pituitary cyclic AMP levels were increased 10 min after the intraveneous injection of 2 mg dibutyryl cyclic AMP (db-cyclic AMP) or 25 mg aminophylline. However, serum LH levels were not altered at 10, 30 or 60 min after the administration of either agent. Synthetic LH-RH (100 ng/rat) increased serum LH levels as measured 10 min after injection, but no effect on either pituitary cyclic AMP or cyclic GMP was seen 1, 5 or 10 min after LH-RH administration. These in vivo results are contradictory to the second messenger hypothesis for either cyclic AMP or cyclic GMP in the mediation of LH-RH-induced LH released and suggest that further work must be done in order to confirm or reject this hypothesis.

Aminophylline↗
PubMed1976

Endogenous estrogen modulates phenothiazine stimulated prolactin secretion.

The role of endogenous estrogen in the regulation of serum prolactin concentration in man is controversial. To evaluate the possible effect of endogenous fluctuations in serum estrogen on the regulation of prolactin secretion, the authors determined phenothiazine stimulated prolactin secretion in 12 women in the early follicular phase of the menstrual cycle when estrogen levels were low (mean +/- SE E1 + E2 = 82 +/- 7 pg/ml) and compared it to the response during the late follicular phase when estrogen levels were higher (mean E1 + E2 = 320 +/- 63 pg/ml). Mean basal serum prolactin concentrations were similar in the early and late follicular phases of the cylcle (17 +/- 4 and 20 +/- 2 ng/ml, respectively). The integrated prolactin response following phenothiazine administration was significantly higher at mid-cycle (402 +/- 46 ng-hr/ml) than in the early follicular phase (317 +/0 46 ng-hr/ml, P less than .02). Thus, these studies suggest that endogenous estrogen secretion may play a role in the regulation of serum prolactin concentration in man.

Adult↗