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Biomedical subjects

E del Pozo

Publications and source records attributed to E del Pozo.

At least 55 records · Page 3Linked to original sources
PubMed1983

Nitrate and nitrite contents in Cuban cheese of the Gouda type.

The nitrate and nitrite contents in cheese of the Gouda type, produced by the Milk Complex of Havanna, were investigated and compared with those found in 5 types of imported cheese consumed in Cuba. No significant differences were found in the mean value (mean) of NaNO3, whereas in the mean value (mean) of NaNO2 differences were found when comparing all cheeses against each other. From these results it is inferred that the consumption of Gouda type cheese does not represent an important contribution to the daily intake of nitrates and nitrites, precursors in the synthesis of cancerogenic N-nitroso compounds.

Cheese↗
PubMed1980

Failure of oxytocin and lysine-vasopressin to stimulate prolactin release in humans.

In order to test a possible stimulatory effect of oxytocin and lysine-vasopressin on prolactin (PRL) release six female volunteers received either saline or 1 IU oxytocin (Syntocinon) i.v.. Blood sampling was performed at intervals over 90 minutes. Nine puerperae were treated with oral oxytocin (Sandopart) 50 IU t.i.d. for seven days. Nine other untreated postpartum women served as controls. Blood was collected before delivery and on subsequent postpartum days, and the milk volumes produced were estimated by increases in the babies' weight. In addition, seven volunteers received 5 or IU lysine-vasopressin (Vasopressin) i.m. Blood was withdrawn at regular intervals for 180 minutes, the urine volumes excreted in 30-minute intervals were measured and the clearance of free water calculated. Oxytocin failed to modify basal plasma PRL in the acute trial and in the post-partum women, and milk amounts produced were not influenced by treatment. Vasopressin did not change the PRL plasma profile despite a significant (p less than 0.05) reduction in the excretion of free water. Results indicate that neuropeptides are not implicated in the control of PRL release.

Arginine Vasopressin↗
PubMed1980

Endocrine effect of a methionine-enkephalin derivative (FK 33-824) in man.

The endocrine profile of FK 33-824, 0.5 mg i.m., was determined in comparison with placebo or pretreatment with naloxone, 4 mg i.v., in 14 healthy men. Prolactin (PRL), growth hormone (GH), ACTH, cortisol, gonadotropins (LH, FSH), thyrotropin (TSH), thyroxine (T4), triiodothyronine (T3), insulin and glucagon were measured and free water clearance was calculated from urine volumes and osmolar clearances. FK 33-824 increased PRL and GH (p less than 0.001). ACTH was below assay sensitivity but cortisol was significantly lowered (p less than 0.001). Free water clearance was enhanced (p less than 0.01) and the remaining parameters were unchanged. Naloxone alone had no hormonal effect but abolished the increase in PRL and GH following injection of FK 33-824 without modifying the decrease in plasma cortisol or the increase in free water clearance following the same treatment. The results indicate that the effect of FK 33-824 on PRL and GH release is mediated by opiate receptors. Other mechanisms or naloxone nonsensitive receptors may be implicated in the effects recorded on cortisol and FWC.

Adrenocorticotropic Hormone↗
PubMed1980

Inhibitory action of a met-enkephalin on ACTH release in man.

In order to study the mechanism of action of a Met-enkephalin (FK 33824) on the pituitary-adrenal axis eight normal male volunteers were subjected to an ACTH stimulation test. Lysine-vasopressing (LVP), 5 IU, was injected intramuscularly after pretreatment with 0.5 mg FK 33824 i.m. or a placebo. In six of the subjects the opiate was again administered preceding a single injection of 0.25 mg ACTH beta 1-24 i.m. Blood was collected at regular intervals and ACTH and cortisol concentrations analyzed in all samples. LVP induced significant plasma ACTH (P < 0.05) and cortisol (P < 0.001) increases. Pretreatment with FK 33824 completely antagonized the effect of LVP. Furthermore, the cortisol elevation after exogenous ACTH was not modified by previous administration of FK 33824. It is concluded that the Met-enkephalin derivative FK 33824 directly suppresses ACTH release from the pituitary without influencing adrenal synthesis of cortisol.

Adrenal Glands↗
PubMed1980

Induced human gestational hypoprolactinemia: lack of action on fetal adrenal androgen synthesis.

To investigate the possible role of PRL in the control of fetal adrenal function, blood samples were collected from maternal peripheral and cord blood from six women at delivery, who had received treatment with bromocriptine (3.75--35 mg daily) for the entire gestation. A group of eight untreated parturients served as control. Parameters measured were PRL and dehydroepiandrosterone, the latter as an indicator of fetal adrenal function. PRL was significantly suppressed (P < 0.002), whereas dehydroepiandrosterone was not influenced by bromocriptine treatment. The results indicate that the control of fetal production of androgenic substrate by the adrenals is not specifically PRL dependent.

Adrenal Glands↗
PubMed1980

Inhibition of vasopressin secretion by a met-enkephalin (FK 33-824) in humans.

To investigate the effect of a met-enkephalin analogue, FK 33-824, on renal handling of water, 8 subjects were given 0.5 mg im of the drug or placebo in a cross-over study. In a second trial under the same testing conditions, a 4 mg dose of naloxone iv was given to 6 subjects immediately preceding 0.5 mg FK 33-824 im. Urine and blood samples were collected at hourly intervals. Urinary vasopressin (AVP) and plasma prolactin (Prl) were assayed, and free water clearance (FWC) was calculated. Following the same protocol, a further 6 subjects received 5 IU of lysine vasopressin im 5 min preceding administration of FK 33-824. FK 33-824 significantly (P < 0.001) increased Prl and FWC and reduced urinary concentrations of AVP (P < 0.01). Naloxone pre-treatment failed to modify significantly the latter two responses, while Prl stimulation was inhibited. Lysine vasopressin pre-treatment abolished the effect of FK 33-824 on FWC while the stimulating action on Prl was preserved. These results indicate that in humans FK 33-824 reduces AVP secretion and that this effect is not mediated by naloxone sensitive opiate receptors.

Adult↗
PubMed1980

Prolactin release in polycystic ovary.

Ten normoprolactinemic and 10 hyperprolactinemic patients, all with polycystic ovary syndrome (PCO), were subjected to prolactin (PRL) stimulatory tests with thyrotropin-releasing hormone (TRH), 200 microgram intravenously, and haloperidol (a dopamine-blocking agent), 1 mg intramuscularly. The results were compared with those of 8 women with idiopathic hyperprolactinemia and 10 normal female volunteers. Distinctive features of PCO were elevated plasma concentrations of luteinizing hormone, estrone, and testosterone in the presence of normal estradiol, whereas in idiopathic hyperprolactinemia estradiol was reduced. Both groups of patients with PCO exhibited responses to TRH and haloperidol significantly higher than the controls (P less than .001), whereas only the hyperprolactinemic PCO patients reacted with an excessive PRL discharge (P less than .001). As expected, the response to both secretagogue agents was blunted in patients with idiopathic hyperprolactinemia. The present report discusses the possible implication of estrogen and the dopaminergic system in the mechanisms leading to hyperprolactinemia and enhanced PRL release in PCO.

Estrogens↗
PubMed1979

Improved sexual function in male haemodialysis patients on bromocriptine.

The effect of bromocriptine on sexual activity was studied in male haemodialysis patients in a single-blind placebo controlled trial with random cross-over. At a dose of 2.5 mg bromocriptine twice day, plasma-prolactin concentrations were consistently reduced, while sexual function as assessed by a questionnaire was markedly improved. At the doses used, side-effects, particularly hypotension, were common, but bromocriptine helped to restore sexual function in dialysed patients.

Bromocriptine↗
PubMed1979

Prolactin. I. Mechanisms of control, peripheral actions and modification by drugs.

The role of neurotransmitters in the release of prolactin (PRL) is reviewed. Special attention is paid to dopamine (DA) as the possible prolactin-inhibiting factor (PIF). Among other agents, estrogens alone can act directly on the pituitary galactotropes without involving hypothalamic factors. Peripherally, in addition to its stimulatory action on mammary tissue, PRL exerts a permissive role on ovarian steroidogenesis. A possible physiological action of this hormone on the regulation of adrenal function remains uncertain. The secretory rhythms of PRL are described and the mechanisms involved are discussed. A number of drugs can modify the secreting pattern of PRL mainly by acting on the dopaminergic control mechanisms. The usefulness of such agents in the clinical evaluation of galactotrope cell function is reviewed.

Adolescent↗
PubMed1979

Prolactin and deficient luteal function.

The possibility of prolactin-dependent subfertility was investigated in a group of 8 women, with luteal insufficiency exhibiting moderately elevated plasma prolactin (PRL) levels and/or galactorrhea. Another group of 10 normal women volunteers served as the control group. A "luteal index" was elaborated by integration of the area below the curve of plasma progesterone (P) values recorded throughout the postovulatory period. The calculated index for normal women was 177 +/- 35 (SD) expressed as [(ng/ml) x time], and the value of 107 (--2 SD) was adopted as the lower limit of normality (97.5% confidence limit). All 8 patients had luteal indexes (range 20--105) below the established limit. Therapy with bromocriptine (CB 154), 5 mg/day, suppressed PRL to normal levels and prolonged the postovulatory hyperthermic phase in 6 out of 8 women. This was accompanied by an improvement in the luteal index, and 5 women conceived. It is concluded that prolactin may interfere with normal progesterone synthesis by the corpus luteum, as demonstrated by the prompt restoration of fertility by bromocriptine treatment in women with regular cycles and inadequate luteal function.

Adult↗