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I de Pablos

Publications and source records attributed to I de Pablos.

6 recordsLinked to original sources
PubMed1997

Study of the secretion of substance P, neurotensin and somatostatin in patients with cholelithiasis.

A comparative, case-control study on the pre- and postprandial release of three gastrointestinal peptides implicated in gallbladder motility has been carried out in humans in the attempt to determine their possible role in the pathogenesis of cholelithiasis. Fifty-seven adult patients (40 females and 17 males) with an ultrasound diagnosis of gallstones and 20 healthy subjects (9 females and 11 males) without cholelithiasis or other digestive pathology were studied. Plasma substance P, neurotensin and somatostatin were measured by means of RIA-I125 in basal fasting conditions and 30, 60 and 90 minutes after the oral intake of a semiliquid mixed meal. The levels of secretion of each hormone were compared in patients and healthy controls on an overall basis and in terms of sex, age and body weight. We found a basal and postprandial hypersecretion of substance P in patients with gallstones when compared with controls. Individuals with cholelithiasis showed a moderate decrease in neurotensin secretion after the oral meal. Somatostatin release was unchanged. In conclusion, patients with gallstones may present a functional disorder in the secretion of gastrointestinal hormones involved in gallbladder motility.

Adult↗
PubMed1988

Role of alpha 1- and alpha 2-adrenoceptors in catecholamine-induced hyperglycaemia, lipolysis and insulin secretion in conscious fasted rabbits.

1. In conscious fasted rabbits an intravenous infusion of clonidine (2 micrograms kg-1 min-1) induced hyperglycaemia. The increase in blood glucose was accompanied by an inhibition of insulin secretion and basal lipolysis. 2. Yohimbine infused at a rate of 20 micrograms kg-1 min-1 suppressed clonidine-induced hyperglycaemia and blocked the inhibitory effect on insulin secretion mediated by the alpha 2-adrenoceptor agonist. 3. The intravenous infusion of amidephrine (10 micrograms kg-1 min-1) induced an increase in insulin secretion in the absence of patent hyperglycaemia. Prazosin, 0.3 mg kg-1 s.c. selectively antagonized the effect of amidephrine on insulin secretion. 4. Isoprenaline infusion (4.4 micrograms kg-1 min-1) evoked a significant increase in blood glycerol and immunoreactive insulin plasma levels. Both responses were clearly attenuated when alpha 2-adrenoceptors were simultaneously stimulated by selective (clonidine) and less selective (phenylephrine, 20 micrograms kg-1 min-1) agonists. 5. Amidephrine infusion did not induce appreciable changes in blood glycerol nor did it modify, isoprenaline-induced lipolytic response. 6. Simultaneous infusion of isoprenaline and amidephrine induced a remarkable increase in insulin secretion. 7. It is concluded that in normal fasted rabbits stimulation of alpha 2-adrenoceptors depresses basal and beta-adrenoceptor mediated lipolysis and insulin secretion. On the other hand, selective stimulation of alpha 1-adrenoceptors does not affect lipolysis but induces insulin release. Simultaneous stimulation of alpha 1- and beta-adrenoceptors potentiates the insulin secretory response.

Animals↗
PubMed1986

Alpha-adrenoceptor involvement in catecholamine-induced hyperglycaemia in conscious fasted rabbits.

In conscious fasted rabbits an intravenous infusion of phenylephrine (20 micrograms kg-1 min-1) induced hyperglycaemia. The increase in blood glucose was accompanied by a modest increase in insulin secretion and a reduction of liver glycogen. Muscle glycogen and blood lactate levels were not altered by treatment with phenylephrine. Prazosin, 1 mg kg-1 s.c., partially attenuated phenylephrine-induced hyperglycaemia. Phenoxybenzamine infusion (16.6 micrograms kg-1 min-1) for 15 min suppressed the increase in blood glucose and the reduction in liver glycogen evoked by phenylephrine. This alpha-adrenoceptor blocker also clearly attenuated the blood glucose elevation observed on infusing adrenaline at 0.3 microgram kg-1 min-1. Blockade by phenoxybenzamine of phenylephrine- and adrenaline-induced hyperglycaemia was not accompanied by a significant increase in immunoreactive insulin plasma levels. Yohimbine infused at a rate of 20 micrograms kg-1 min-1, also completely blocked phenylephrine-induced hyperglycaemia. This suppressor effect was accompanied by a marked rebound in insulin secretion. It is concluded that in normal fasted rabbits stimulation of alpha-adrenoceptors induces hyperglycaemia. The increase in blood glucose depends mainly on liver glycogenolysis and inhibition of insulin secretion. Separate blockade of each component suffices to reduce alpha-adrenoceptor-mediated hyperglycaemia.

Adrenergic alpha-Antagonists↗
PubMed1980

[The role of hyperprolactinaemia in sterility where the cycle is anovulatory and where there is deficit of progestogen. (Investigations of the pituitary reserves of FSH, LH and prolactin) (author's transl)].

We have measured by radio-immunological assays the levels of prolactin (PRL), of FSH and of LH in the plasma in 7 cases where sterility was due to persistent anovulatory cycles and in 6 cases where there was a progesterone deficiency as the sole aetiological factor. Then we stimulated the release of these three hormones by giving 300 micrograms of TRF, PRL, and 100 micrograms of LH-RH, of FSH and of LH. The results were compared with those obtained in 7 cases of normal young women with clear-cut biphasic cycles used as controls. These results show that a rise in the reserves of prolactin in the pituitary is very common in anovulatory cycles and in progesterone deficiency. In every case where the prolactin is raised LH is significantly lowered, where as the levels of FSH do not show much variation between those found in normal women. Thus an inverse relationship between PRL and LH has been demonstrated and its significance has been commented on.

Anovulation↗