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Biomedical subjects

E Del Pozo

Publications and source records attributed to E Del Pozo.

18 recordsLinked to original sources
PubMed1992

Differential potentiation by calcium antagonists of neuromuscular blockade induced by pancuronium and succinylcholine in cats in vivo.

The effects of several calcium antagonists (verapamil, nicardipine and two diltiazem isomers, d-cis and l-cis diltiazem) alone and associated to non-depolarizing (pancuronium) and depolarizing (succinylcholine) neuromuscular blockers, were evaluated on sciatic nerve-tibialis anterior muscle preparations from cats in vivo. The calcium antagonists used (at 0.1 and 0.5 mg/kg iv) did not modify the height of muscular twitches elicited indirectly. However, these agents potentiated in a dose-dependent way the neuromuscular blockade induced by iv pancuronium (2-40 micrograms/kg) and succinylcholine (6-200 micrograms/kg). The order of potency in increasing the effects of pancuronium was nicardipine much greater than d-cis diltiazem greater than or equal to verapamil, whereas the order of potency in enhancing succinylcholine effects was d-cis diltiazem greater than or equal to verapamil much greater than nicardipine. The effects of diltiazem were stereoselective, thus the potentiation induced by d-cis diltiazem was significantly greater in all cases than that induced by l-cis diltiazem, which suggests that calcium channel blockade plays a role in these interactions. However, other mechanisms such as calcium antagonists-induced nicotinic receptor desensitization may also be involved.

Animals↗
PubMed1992

Cyclosporin A. Mode of action and effects on bone and joint tissues.

Cyclosporin A is an established immunomodulatory agent with an increasing number of clinical applications. Although its precise mechanisms of action remain elusive, one of the most important known properties of CyA is its ability to inhibit the production of cytokines involved in the regulation of T-cell activation. In particular, CyA inhibits de novo synthesis of interleukin 2(IL-2), the major cytokine involved in T-cell proliferation, as well as other cytokines, probably at the level of gene transcription, as shown by the suppression of mRNA levels in activated T-cells. Although the major actions of CyA are on T-cells, there is some evidence for possible direct effects on other cell types e.g. B-cells, macrophages and, from our own work, on bone and cartilage cells. Cyclosporin A is thought to enter cells and to bind to cyclophilins, which are members of a family of high-affinity cyclosporin A-binding proteins, now known as immunophilins. The binding of cyclosporins to such proteins appears to be closely linked to the immunosuppressive action of cyclosporins. The immunophilins possess enzyme activity, ie. peptidyl-prolyl cis-trans isomerase, also known as rotamase, which can regulate protein folding, and may therefore alter the functional state of many cell proteins. Cyclosporin A blocks peptidyl-prolyl cis-trans isomerase activity but it is not clear whether this plays a part in its selective inhibition of cytokine-gene transcription. Moreover, the ubiquitous presence of cyclophilins and immunophilins raises the question of why cyclosporin A has its apparent major effects only on T-cells. Recent proposals regarding the intracellular mode of action of CyA suggest that it interacts with cyclophilin and other regulatory proteins including calmodulin and calcineurin, which is a serine/threonine phosphatase, and thereby affects the functional state of key regulators of gene transcription in its target cells. The effects of CyA on T-cells and directly or indirectly on connective tissue cells, including bone, cartilage and synovial cells, which all can produce a range of cytokines, are of interest in relation to the tissue changes that occur in inflammatory diseases, such as rheumatoid arthritis. Thus, for example, cyclosporin A inhibits in vitro the bone resorbing activity of interleukin 1, 1,25-dihydroxy-vitamin D3, parathyroid hormone and prostaglandin E2 by apparently non-T-cell effects, while in vivo protects against bone and cartilage loss in adjuvant arthritis. More needs to be known about the direct and indirect modulation of cytokine production by cyclosporin A in connective tissues, in order to understand its potential value in clinical disorders.

Arthritis, Rheumatoid↗
PubMed1990

Analgesic effects of diltiazem and verapamil after central and peripheral administration in the hot-plate test.

1. The analgesic effects of diltiazem and verapamil, both per se and together with morphine, were studied using subcutaneous (s.c.) and intracerebroventricular (i.c.v.) administrations, in the hot-plate test in mice. 2. The i.c.v. injection of verapamil (15-120 micrograms/mouse) and diltiazem (60-120 micrograms/mouse) induced dose-dependent analgesic effects. 3. The i.c.v. administration of verapamil (30-120 micrograms/mouse) and diltiazem (60-120 micrograms/mouse) significantly enhanced, in a dose-dependent way, the analgesic effects of morphine and produced a parallel displacement to the left of the morphine log dose-response line. 4. When these calcium channel blockers were administered subcutaneously at doses of 40 and 80 mg/kg, they exerted no analgesic actions, but dose-dependently potentiated the analgesic effects of morphine, producing a parallel shift to the left of the morphine log dose-response line. 5. These results suggest that inhibition of calcium entry through calcium channels induced by verapamil and diltiazem may play a role in analgesia development.

Analgesics↗
PubMed1979

Chronic dopamine receptor stimulation using bromocriptine: failure to modify thyroid function.

Administration of 2.5 mg bromocriptine (Parlodel), a dopamine agonist, on two occasions to six normal volunteers did not alter the plasma TSH response to an i.v. injection of 100 micrograms TRH, but significantly (P less than 0.01) blunted it after 200 micrograms. Chronic bromocriptine treatment (7.5--50 mg/day) of fifteen acromegalic subjects failed to influence basal plasma TSH or the response pattern to 200 micrograms TRH. The thyroxine Binding Index (TBI) and the levels of T3 and T4 were not modified by treatment. These results indicate that chronic dopaminergic therapy with bromocriptine does not alter thyroid function.

Acromegaly↗
PubMed1979

A pregnancy in an acromegalic woman during bromocriptine treatment: effects on growth hormone and prolactin in the maternal, fetal, and amniotic compartments.

An unexpected 20-week-old pregnancy was found in a young acromegalic who had been treated with 10 mg bromocriptine/day for 10 months. The drug was continued throughout the period of gestation. No growth of the pituitary adenoma was noticed. The intrauterine development of the fetus was normal. Bromocriptine therapy had no discernible effect on the expected patterns of secretion of placental hormones, but inhibited completely the increase of PRL in the serum of the mother. Maternal plasma GH concentrations were very high in spite of the treatment and progressively declined after delivery. The plasma GH level was normal in the child, but PRL was very low at birth and increased in the following days. The expected high PRL concentration was found in the amniotic fluid. This case study suggests that bromocriptine crosses the human placenta and affects the fetal pituitary, maternal GH does not influence fetal or amniotic GH, and amniotic fluid PRL correlates poorly with either maternal or fetal blood levels and is not affected by bromocriptine.

Acromegaly↗
PubMed1977

Effect of 1-5 hydroxytryptophan infusion on growth hormone and prolactin secretion in man.

The effect of a new soluble ester of 1-5 hydroxytryptophan (1-5 HTP, Ro 3-5940, 200 mg infusion) on prolactin (PRL) and growth hormone (GH) release was tested in 11 young, healthy subjects (6 men, 5 women). To minimize side-effects, peripheral decarboxylase inhibition was achieved with benserazide (Ro 4-4602.) PRL increased significantly (P less than 0.01) after benserazide alone in all subjects. A further significant increase (P less than 0.01) of PRL plasma levels occurred only in women up to 90 min after the infusion of 1-5 HTP was discontinued. Benserazide administration had no effect of basal GH levels, but a significant increase of GH release (P less than 0.01) was noticed 30-120 min after the end of 1-5 HTP infusion in both men and women. The mean peak value of GH plasma levels after 1-5 HTP administration was 32.0 +/- 8.8 ng/ml. It was postulated that benserazide penetrated at the level of the pituitary, decreasing the synthesis of dopamine and consequently reducing its known inhibitory effect on PRL release. The PRL increase (statistically significant only in women), as well as the release of GH after 1-5 HTP infusion, was considered as further evidence for stimulatory serotoninergic control of both PRL and GH secretion.

5-Hydroxytryptophan↗
PubMed1976

The influence of the prolactin inhibitor bromocriptin (CB 154) on human luteal function in vivo.

Five volunteers with normal ovarian cycles received oral doses of 2 X 2.5 mg or 3 X 2.5 mg bromocriptin (CB 154)/day respectively. The treatment started at the onset of menstruation and lasted on complete cycle. In addition to the decrease of prolactin secretion, a reduction of plasma progesterone concentrations during the corpus luteum phase was demonstrated. This fall of progesterone seemed to be preferentially due to bromocriptin-induced hypoprolactinaemia and not to direct ovarian effects of the drug.

Adult↗
PubMed1975

Successful treatment of mastodynia with the prolactin inhibitor bromocryptine (CB 154).

Mastodynia has previously been treated with gestagens or gestagen-based ovulation inhibitors with only marginal success. No other satisfactory therapy was available and in the search for a better treatment, the effectiveness of long term administration of the prolactin inhibitor bromocryptine (CB 154) to 15 patients was evaluated. Five of the subjects exhibited mammary secretion as well as mastodynia which, accorind to palpatorial, cytological and X-ray criteria, was not caused by intraductal pathology. After two to four weeks treatment with 5 mg CB 154 per day ten patients recovered fully, three showed some improvement and two were totally resistant to the treatment. Plasma prolactin levels during the follicular stage measured prior to treatment were in the normal range. All the patients continued to ovulate during the course of treatment despite the irrefutable fact that prolactin release from the pituitary was inhibited. Since there was a similar inhibition of prolactin secretion in the two patients who were resistant to treatment, it would seem that prolactin though probably very important, cannot be the only decisive factor in the hormonal control of mystodynia. Further observations showed that the premenstrual syndrome can also be successfully treated with CB 154. Upon withdrawal of treatment the possibility or relapse must be considered.

Adult↗
PubMed1975

Lack of effect of methyl-ergonovine on postpartum lactation.

There is little information about the action of ergot derivatives other than bromocriptine (CB 154) on plasma prolactin and milk secretion in human beings. In a recent report it has been suggested that ergonovine might interfere with lactation when administered post partum. The present study shows that methyl-ergonovine (Methergine), a closely related compound, has no action on prolactin or milk secretion as measured in a group of 10 breast feeding mothers in comparison with another 10 untreated puerperas.

Female↗
PubMedDate not supplied

Reversion by calcium but not by Bay K 8644 of neuromuscular blockade induced by nicardipine.

We compared the effects of nicardipine on indirectly and directly elicited twitches in phrenic-hemidiaphragm preparations from rats, and the effects of calcium and Bay K 8644 on nicardipine-induced neuromuscular blockade. Nicardipine (5-250 microM) decreased both directly and indirectly elicited muscular contractions in a concentration-dependent way. The inhibitory effect was greater when the preparation was indirectly stimulated. Nicardipine antagonism of indirectly elicited contractions was reversed in an apparently competitive way by calcium (1-4 mM). In contrast, the calcium channel agonist Bay K 8644 (0.1 and 1 microM) had no effects per se, nor did it reverse neuromuscular blockade induced by nicardipine. Interestingly, Bay K 8644, at 10 microM, decreased the height of indirectly elicited muscular contractions. These results suggest that the calcium antagonist nicardipine affects neuromuscular transmission to a greater degree than muscular contraction, this effect being antagonized by calcium. In contrast, the calcium agonist Bay K 8644 was unable to produce any effect as stimulator of calcium channels at the neuromuscular level, indicating that this drug may exhibit tissue specificity.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗