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Biomedical subjects

P Chiodera

Publications and source records attributed to P Chiodera.

At least 163 records · Page 9Linked to original sources
PubMed1986

Muscarinic cholinergic modulation of insulin response to an intravenous glucose tolerance test in normal man.

The effect of pirenzepine, a specific muscarinic cholinergic receptor antagonist, on insulin and glucagon responses to an intravenous injection of glucose was investigated in eight normal adult subjects. These volunteers received two iv glucose tolerance tests (0.33 g/kg) before and after the oral administration of 125 mg of pirenzepine (three doses of 25 mg during the day before the experiment and a fourth dose of 50 mg 2 h before glucose injection). Treatment with pirenzepine neither altered basal blood glucose levels nor affected glucose tolerance after the injection of the glucose load. In addition, it did not modify basal plasma insulin and glucagon levels and the decrement of glucagon in response to glucose injection. In contrast, pirenzepine significantly decreased insulin release induced by glucose administration. In man, during the present experimental conditions, the muscarinic cholinergic system modulates insulin, but not glucagon response to an iv glucose injection.

Adult↗
PubMed1986

Nicotinic-cholinergic involvement in arginine-vasopressin response to insulin-induced hypoglycemia in normal men.

In order to establish whether arginine-vasopressin (AVP) release in response to insulin-induced hypoglycemia is mediated by a muscarinic and/or nicotinic cholinergic pathway, 12 normal men had an insulin tolerance test (ITT) in basal conditions and after treatment with the muscarinic receptor blocker pirenzepine (40 mg IV (intravenously) ten minutes before ITT in six subjects) or the nicotinic receptor antagonist trimethaphan (0.3 mg/min X 30 min IV before ITT in six subjects). The drugs did not modify arterial blood pressure nor produce side effects capable of altering AVP secretion. Pirenzepine administration did not change AVP response to hypoglycemia, whereas trimethaphan significantly reduced AVP increase by about 50% during the ITT. These data suggest the involvement of a cholinergic-nicotinic mechanism in regulation of AVP response to hypoglycemia.

Adult↗
PubMed1986

Different effects of metoclopramide and domperidone on arginine-vasopressin secretion in man.

This study was performed in order to investigate the dopaminergic mechanism involved in the control of arginine-vasopressin (AVP) secretion in normal men. Plasma AVP concentrations were measured before and after the administration of an i.v. bolus of 10 mg metoclopramide or domperidone to twelve healthy males. Metoclopramide, a cerebral and peripheral antagonist of dopaminergic receptors, significantly stimulated AVP secretion, whereas domperidone, a dopamine antagonist which does not cross the blood-brain barrier, was without effect. These data suggest that metoclopramide stimulates the release of AVP by blocking dopaminergic receptors in structures located inside the blood-brain barrier. Alternatively, it is possible that the stimulation of AVP release induced by metoclopramide does not occur through inhibition of dopamine receptors but rather through interaction with other neuroendocrine pathways.

Adult↗
PubMed1986

Inhibition by somatostatin of LH-RH-induced LH release in normal menstruating women.

The present study was carried out in order to establish whether the concomitant treatment with somatostatin (SRIH) is capable of modifying gonadotrophin release in response to LH-RH administration in normal women during follicular, periovulatory, and luteal phases. SRIH was administered in a dose of 5.55 micrograms/min over 180 min and LH-RH (100 micrograms) was injected as a bolus at 90 min after the beginning of SRIH infusion. Within the dose used, SRIH significantly reduced LH response to LH-RH, whereas it did not alter FSH response to LH-RH. These results suggest that SRIH may play a part in the regulation of LH secretion in normal women.

Adult↗
PubMed1986

Experimental splenic regeneration.

The results of studies which indicate that splenic resection of residual parenchyma is able to regenerate are based primarily upon the weight increase of the splenic remnant at specified times after partial resection. This study was done to determine the histologic characteristics of the residual splenic tissue at 30 and 90 days after partial splenectomy in rats. The average increase in weight of the splenic polar residual after subtotal resection was 43 per cent at 30 days and 44 per cent at 90 days, and 10 per cent at 30 days and 30 per cent at 90 days for residual half spleen after hemisplenectomy. Histologic alterations, mainly present in the parenchyma near the section surface at 30 days were clearly inflammatory secondary to surgical trauma. There was no regenerative significance. At 90 days, the results of histologic study demonstrate a readjustment of the vascular net and the lymphoid tissue of the white pulp. The result is new structures which reproduces the follicular morphologic characteristics. This process requires 90 days to predominate over inflammatory postsurgical changes. Only during this phase may it have an important role in determining the increase of the residual weight. Further research into the functional capacity of the newly formed structures is necessary to confirm that the histologic modifications observed are comparable to true regeneration.

Animals↗
PubMed1986

Late modifications of residual parenchyma after splenic resections.

The increased experience in the field of splenic resections have brought up questions about the evolution of the residual parenchyma. Weight increase and the histologic structure of the splenic remnant were studied during a year following hemisplenectomy in rats. Histological studies show that the residual spleen presents a permanent compensatory hyperplasia rather than a true regeneration. This hyperplasia causes an increase in weight of the residual parenchyma which is moderate and only transitory. Indirect confirmation of findings obtained in rats comes from scintigraphic study of residual human splenic tissue after hemisplenectomy. The residual tissue keeps its original form without increase in volume, and the sectioned surface is always well identified one year after splenic resection.

Animals↗
PubMed1985

Thyrotropin-releasing hormone does not inhibit lysine vasopressin-induced growth hormone secretion in normal men.

In order to establish whether thyrotropin-releasing hormone (TRH) inhibits lysine-vasopressin (LVP)-induced growth hormone (GH) release, six normal men were tested with LVP alone or in combination with TRH. LVP strikingly increased serum GH levels; this response was not altered by TRH. These results indicate that in man TRH is not involved in the control of GH secretion in response to LVP.

Adult↗
PubMed1985

Muscarinic cholinergic mediation of LHRH-induced LH and FSH secretion in normal men.

LHRH (100 micrograms i.v. bolus) was given to six young healthy men under basal conditions and after the administration of pirenzepine (10, 20, 30 or 40 mg i.v. 10 min before LHRH), which is a selective blocker of muscarinic cholinergic receptors. Pretreatment with 10 mg of pirenzepine did not modify LH and FSH responses to LHRH, whereas larger amounts of the drug significantly reduced gonadotrophin responses to LHRH. A dose-related effect of the drug was not observed, since a maximal reduction of LHRH-induced gonadotrophin secretion was already present when 20 mg of pirenzepine were used. When the effect of pirenzepine (20 mg) on the basal concentrations of FSH and LH was studied in four additional sex and age matched subjects, no significant changes were observed for at least 120 min after the injection. These results demonstrate that LHRH-induced LH and FSH secretion involves a muscarinic cholinergic mechanism.

Adult↗
PubMed1985

Effect of naloxone on oxytocin-induced cortisol decrease in normal men.

iv administration of oxytocin decreases plasma ACTH-cortisol levels in normal men. In contrast, naloxone, a specific opioid antagonist, stimulates cortisol release, suggesting that opioid peptides exert an inhibitory control on ACTH-cortisol secretion. The present study was carried out in an attempt to determine whether an opioid pathway mediates oxytocin action; therefore, we evaluated the effect of naloxone on the decrease of cortisol induced by oxytocin. Six normal men were treated iv with oxytocin (2 IU as a bolus), naloxone (4 mg as a bolus plus 10 mg infused for 2 h) or a combination of the 2 drugs. Plasma cortisol levels were determined in samples taken before and 2 h after drug treatment. As expected, administration of oxytocin significantly decreased cortisol secretion, while naloxone had a stimulatory effect on plasma cortisol levels. When oxytocin injection was followed by administration of naloxone, cortisol levels remained unchanged; thus, naloxone abolished a cortisol decrement in response to oxytocin. These findings show that in man oxytocin requires an active opioid system in order to produce its inhibitory action on ACTH-cortisol secretion, suggesting that this effect of oxytocin could be mediated by an opioid pathway.

Adrenocorticotropic Hormone↗
PubMed1985

Inhibition by somatostatin of the release of growth hormone induced by lysine-vasopressin in normal subjects.

The effect of somatostatin (SRIH) on the release of growth hormone (GH) induced by lysine-vasopressin (LVP) was studied in six normal subjects. They were injected intravenously with 0.06 I. U./kg of LVP alone or in combination with SRIH (an intravenous bolus of 100 micrograms 10 minutes before LVP injection, followed by the constant infusion of 500 micrograms over 90 minutes). LVP strikingly increased serum concentrations of GH; this response was significantly reduced by the treatment with SRIH. This finding provides evidence that the effect of LVP on serum GH levels is sensitive to the inhibition by SRIH; it is proposed that the stimulating action of LVP on GH secretion might be mediated by the inhibition of endogenous SRIH.

Adult↗
PubMed1984

Simultaneous radioimmunoassay for plasma arginine-vasopressin and oxytocin using DEAE Sephadex A 25 extraction.

A sensitive and specific radioimmunoassay method for simultaneous measurement of plasma arginine vasopressin (AVP) and oxytocin (OT) has been developed utilizing an extraction technique on DEAE Sephadex A25. This procedure resulted in mean recoveries of 70.7% (AVP) and 65.4% (OT) in the peptide range of 5 to 100 pg/4 ml. The sensitivity of the assay is 0.5 pg/tube for AVP and 2 pg/tube for OT. The lower limit of detection for plasma extracts was 1.2 pg AVP/ml and 5 pg OT/ml plasma. Employing this method in normal human non smokers and ad libitum fluid the basal levels (mean +/- SE) of plasma AVP are 3.5 +/- 0.2 pg/ml in males and 4.6 +/- 0.4 pg/ml in females and the basal concentrations of plasma OT are 5.1 +/- 0.3 pg/ml in males and 5.4 +/- 0.3 pg/ml in females. Dehydration and water loading produced significant changes in plasma AVP and OT concentrations and a significant correlation exists between plasma AVP and plasma (r = 0.96, p less than 0.001) and urinary (r = 0.84, p less than 0.01) osmolality, but not between plasma OT concentrations and plasma (r = 0.11, NS) and urinary (r = 0.27, NS) osmolality. These results suggest that a wide range of physiological and pathophysiological changes in plasma AVP and OT can be simultaneously measured by the extraction procedure and the radioimmunoassay described.

Adult↗
PubMed1984

Evaluation of oxytocin administration on luteinizing hormone and follicle-stimulating hormone response to luteinizing hormone-releasing hormone during the menstrual cycle of normal women.

In order to determine whether oxytocin modifies luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion in response to LH-releasing hormone (LH-RH), a group of normal women, 23 to 30 years of age, was studied in the follicular, periovulatory, and luteal phases. LH and FSH response to LH-RH was evaluated in the serum under control conditions and after oxytocin infusion. Oxytocin administration failed to modify LH and FSH release induced by LH-RH. These results suggest that this neuropeptide is not involved in the control of LH and FSH at the level of the anterior pituitary.

Adult↗