Biomedical subjects

G Bertrand

Publications and source records attributed to G Bertrand.

At least 19 recordsLinked to original sources

PubMed1992

Evidence for a direct stimulatory effect of cibenzoline on insulin secretion in rats.

The effect of cibenzoline succinate, a new antiarrhythmic agent, was studied on insulin secretion in rats. Experiments were performed both in vivo and in vitro using two preparations: the isolated perfused pancreas and isolated islets. In anaesthetized rats, cibenzoline was able to increase plasma insulin levels and to reduce glycaemia. These effects were observed at 1 mg/kg i.v. in fed rats and at 3 mg/kg i.v. in fasted rats. In the isolated pancreas perfused in the presence of a slightly stimulating glucose concentration (8.3 mM), cibenzoline (2 and 6 microM) elicited a progressive and sustained insulin response in a concentration-dependent manner. In the presence of a non-stimulating glucose concentration (4.2 mM), cibenzoline was ineffective at 2 microM and slightly increased basal insulin release at 6 microM. In isolated islets incubated with 8.3 mM glucose, cibenzoline (6 and 20 microM) caused a concentration-dependent stimulation of insulin release. It is concluded that cibenzoline stimulates insulin secretion by a direct action on pancreatic B cells in rats.

Animals↗

PubMed1992

Evidence for a direct inhibitory effect of PYY on insulin secretion in rats.

Peptide YY (PYY) has been shown to inhibit stimulated insulin secretion under in vivo conditions in the mouse, the rat, and the dog. In the present study, we investigated the effects of PYY on insulin secretion from the isolated perfused rat pancreas and isolated rat islets. In isolated pancreas perfused in presence of 8.3 mM glucose, PYY at 10(-10) and 10(-9) M, but not at 10(-8) M, inhibited insulin secretion. In the presence of 5.5 mM glucose, PYY (10(-9) M) did not modify basal insulin release but reduced the biphasic insulin response to arginine (10 mM). PYY also markedly reduced the pancreatic vascular flow rate; this effect was observed at all three concentrations tested in a dose-dependent manner. In isolated islets, glucose (15 mM)-stimulated insulin secretion was inhibited by PYY at 10(-7) M. We conclude that in the perfused rat pancreas, PYY inhibits insulin secretion and induces vasoconstriction without a causal relationship. In addition, our results on isolated islets suggest that the inhibitory action of PYY on insulin secretion is exerted through a direct islet action.

Animals↗

PubMed1992

Evidence for a glutamate receptor of the AMPA subtype which mediates insulin release from rat perfused pancreas.

1. The effect of L-glutamate has been studied on insulin secretion by the isolated perfused pancreas of the rat. The glutamate receptor subtype involved has been characterized. 2. In the presence of a slightly stimulating glucose concentration (8.3 mM), L-glutamate (5 x 10(-5)-4 x 10(-3) M) induced an immediate, transient and concentration-dependent insulin response. On the other hand, in the presence of a non stimulating glucose concentration (2.8 mM), L-glutamate (10(-3) M) did not modify the basal insulin secretion. 3. The three non-NMDA receptor agonists, kainate (10(-4)-10(-3) M), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA, 5 x 10(-5)-10(-4) M) and quisqualate (5 x 10(-6)-5 x 10(-5) M) all provoked a transient and concentration-dependent insulin response from pancreas perfused with 8.3 mM glucose. Compared with glutamate, kainate exhibited a similar efficacy, whereas AMPA and quisqualate elicited only a 3 fold lower maximal insulin response. In contrast, NMDA (10(-4)-10(-3) M) was ineffective. 4. An antagonist of non-NMDA receptors, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 5 x 10(-5) M) totally prevented the stimulatory effect of L-glutamate (4 x 10(-4) M) and kainate (2 x 10(-4) M). In contrast, the NMDA receptor antagonist, (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine ((+) MK801) was without effect. 5. The insulin secretory effect of glutamate (4 x 10(-4) M) was not affected by atropine (3 x 10(-7) M) or tetrodotoxin (3 x 10(-6) M). 6. Quisqualate at a high maximally effective concentration (4 x 10(-4) M) inhibited glutamate (10(-3) M) or kainate (4 x 10(-4) M)-induced insulin release. 7. This study shows that L-glutamate stimulates insulin secretion in rat pancreas, by acting on an excitatory amino acid receptor of the AMPA subtype.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1992

Spontaneous spinal epidural hematoma causing paraplegia: resolution and recovery without surgical decompression.

Spontaneous spinal epidural hematomas are well-recognized but rare entities. The standard treatment for these hematomas has been prompt surgical evacuation. The authors report a case of a 76-year-old man who precipitously became paraplegic secondary to a spontaneous spinal epidural hematoma and then experienced the complete resolution of his neurological deficit and the hematoma. We conclude that conservative (nonoperative) management of spontaneous spinal epidural hematomas may be appropriate in those instances in which there is early and sustained neurological recovery confirmed by radiological resolution of the lesion.

Aged↗

PubMed1992

[A simplified terminology for abnormalities of the lumbar disks].

The terminology for abnormalities of the lumbar disk has always been a source of confusion. Recent advances in pathological studies have inspired the authors to propose a simple classification of common disk anomalies suitable not only for diagnostic radiologists but also for referring clinicians. Although the diagnosis of a few pathological entities will only be possible with specific imaging techniques, the proposed classification is appropriate for reporting observations from plain films, conventional tomograms, myelograms, discograms, computed tomography scans and magnetic resonance images. All lumbar disks can thus be classified into one or more of the following categories: normal, aging, scarred, ruptured and herniated. A disk herniation is defined as a localized exit of disk material beyond the limits of the original intervertebral space.

Adult↗

PubMed1992

[Bellini duct carcinoma or kidney collecting duct carcinoma].

The authors report a case of renal collecting duct carcinoma or Bellini duct carcinoma. This rare variety of renal carcinoma, which usually has a poor prognosis, is situated in the renal medulla and pyramid. It is composed of large cells similar to collecting duct cells and can be seen at a distance from the tumor. These cells are arranged in highly suggestive tubular, microcystic and papillary structures. These morphological data are compared with those reported in the literature.

Aged↗

PubMed1991

Adenosine-5'-O-(2-thiodiphosphate) is a potent agonist at P2 purinoceptors mediating insulin secretion from perfused rat pancreas.

1. The effects of a P2 purinoceptor agonist, adenosine 5'-O-(2-thiodiphosphate) (ADP-beta-S) have been studied on insulin secretion and flow rate of the isolated perfused pancreas of the rat. 2. In the presence of a moderately stimulating glucose concentration (8.3 mM), ADP-beta-S (4.95-495 nM) evoked a biphasic insulin response in a concentration-dependent manner. A comparison of relative potency between ADP-beta-S and adenosine 5'-triphosphate (ATP) showed that ADP-beta-S was 100 times more potent than ATP. On the other hand, in the presence of a non stimulatory glucose concentration (4.2 mM), ADP-beta-S (165 nM) did not modify the basal insulin secretion. 3. ADP-beta-S, at concentrations effective on insulin secretion and also at higher concentrations (1.65 and 16.5 microM), provoked an increase of the pancreatic flow rate in a concentration-dependent manner. 4. Our results show that ADP-beta-S is a potent insulin secretory P2 purinoceptor agonist. As it is resistant to hydrolysis it might be useful in studying the effect of activation of the P2 purinoceptor of beta cells on insulin secretion in vivo.

Adenosine Diphosphate↗

PubMed1991

The influence of gamma-aminobutyric acid on hormone release by the mouse and rat endocrine pancreas.

The present study was aimed at localizing gamma-aminobutyric acid (GABA) and its enzyme of synthesis, glutamic acid decarboxylase (GAD), in the mouse pancreas by immunocytochemical methods. The influence of GABA on hormone release was also studied with normal mouse and rat islets and the isolated perfused rat pancreas. Particular attention was paid to glucagon release to test a recent hypothesis suggesting that GABA mediates the still unexplained glucose-induced inhibition of glucagon release. GABA and GAD were identified only in islet cells and never in the exocrine tissue. Exogenous GABA, baclofen (agonist of GABAB receptors), muscimol (agonist of GABAA receptors), or bicuculline (antagonist of GABAA receptors) did not affect insulin and somatostatin release by isolated mouse or rat islets. GABA was also without effect on glucose-induced electrical activity in mouse B-cells. Glucagon secretion by mouse islets was only slightly inhibited (approximately 20%) by GABA. Since muscimol had a similar effect, and baclofen was ineffective, the inhibition by GABA probably involves GABAA receptor activation. Bicuculline, however, did not antagonize the inhibitory effects of GABA and muscimol, probably because the antagonist alone also decreased glucagon secretion. In contrast to GABA, low (3 mM) and high (20 mM) concentrations of glucose strongly inhibited (approximately 50-65%) glucagon release; this inhibition was not prevented by bicuculline. Similar results were obtained with the perfused rat pancreas; muscimol slightly inhibited glucagon release under various conditions, and bicuculline did not reverse the strong inhibition produced by 16.7 mM glucose. In conclusion, GABA does not affect insulin and somatostatin secretion, but inhibits A-cells, probably by acting on GABAA receptors. It is unlikely, however, that this small inhibitory effect can account for the inhibition of glucagon release produced by glucose.

Animals↗

PubMed1991

A simplified terminology for abnormalities of the lumbar disk.

The terminology for abnormalities of the lumbar disk has always been a source of confusion. Recent advances in pathological studies have inspired the authors to propose a simple classification of common disk anomalies suitable not only for diagnostic radiologists but also for referring clinicians. Although the diagnosis of a few pathological entities will only be possible with specific imaging techniques, the proposed classification is appropriate for reporting observations from plain films, conventional tomograms, myelograms, diskograms, computed tomography scans and magnetic resonance images. All lumbar disks can thus be classified into one or more of the following categories: normal, aging, scarred, ruptured and herniated. A disk herniation is defined as a localized exit of disk material beyond the limits of the original intervertebral space.

Aging↗

PubMed1990

P2 purinoceptor agonists stimulate somatostatin secretion from dog pancreas.

The effects of ATP and ADP structural analogues (2-methylthio ATP; alpha,beta-methylene ADP) on somatostatin secretion were tested in dogs. Insulin and glucagon secretion was also evaluated. Our experiments were performed in vivo and in vitro. In vivo, 2-methylthio ATP was infused directly into the pancreaticoduodenal artery of anesthetized dogs and blood was sampled from the pancreaticoduodenal vein. This ATP analogue (approximately 15 microM) immediately induced stimulation of both somatostatin and insulin secretion, which was accompanied by a slight reduction of glycemia. A delayed increase in glucagon output was observed. In vitro, using the isolated perfused dog pancreas uncinate process, alpha,beta-methylene ADP, a stable ADP analogue (16.5 microM), was infused in the presence of a substimulating glucose concentration (4.2 mM). Under these conditions, alpha,beta-methylene ADP immediately induced the stimulation of somatostatin secretion without affecting basal insulin and glucagon secretion. In conclusion our results suggest the presence of P2 purinoceptors on pancreatic somatostatin secreting cells.

Adenosine Diphosphate↗

PubMed1990

The influence of sodium omission on alpha 2-adrenergic inhibition of insulin release by mouse islets.

The mechanisms by which activation of alpha 2-adrenoceptors inhibits insulin release are still incompletely understood. This study, performed with isolated mouse islets, identifies a possible role of Na+ in this inhibition. Regardless of the stimulus used to induce insulin release, the inhibitory effect of low concentrations of clonidine (0.01-0.1 microM) was markedly smaller in the absence of Na+ (with choline or lithium as substitute) than in its presence. The effectiveness of a high concentration of clonidine (1 microM) was, however, not affected by Na+ omission. The results indicate either that Na+ omission indirectly counteracts an effect of clonidine (e.g. on a membrane permeability or on Ca2+ handling), or that Na+ is directly involved in a cellular process (e.g. a Na+ current or the Na+/H+ exchange) controlled by alpha 2-adrenoceptors.

Adrenergic alpha-Antagonists↗

PubMed1990

Spinal synovial cyst: case report using magnetic resonance imaging.

The case of a 65-year-old woman who developed a spinal synovial cyst at the L4-5 disk space is reported. Her clinical signs and symptoms are presented. A comparison among her preoperative myelogram, computed tomography scan, and magnetic resonance imaging showed magnetic resonance imaging to be more accurate in detailing both the intraoperative and pathological findings.

Aged↗

PubMed1989

Comparison of the inhibition of insulin release by activation of adenosine and alpha 2-adrenergic receptors in rat beta-cells.

Rat islets were used to compare the mechanisms whereby adenosine and adrenaline inhibit insulin release. Adenosine (1 microM-2.5 mM) and its analogue N6(-)-phenylisopropyladenosine (L-PIA) (1 nM-10 microM) caused a concentration-dependent but incomplete (45-60%) inhibition of glucose-stimulated release. L-PIA was more potent than D-PIA [the N6(+) analogue], but much less than adrenaline, which caused nearly complete inhibition (85% at 0.1 microM). 8-Phenyltheophylline prevented the inhibitory effect of L-PIA and 50 microM-adenosine, but not that of 500 microM-adenosine or of adrenaline. In contrast, yohimbine selectively prevented the inhibition by adrenaline. Adenosine and L-PIA thus appear to exert their effects by activating membrane A1 receptors, whereas adrenaline acts on alpha 2-adrenergic receptors. Adenosine, L-PIA and adrenaline slightly inhibited 45Ca2+ efflux, 86Rb+ efflux and 45Ca2+ influx in glucose-stimulated islets. The inhibition of insulin release by adenosine or L-PIA was totally prevented by dibutyryl cyclic AMP, but was only attenuated when adenylate cyclase was activated by forskolin or when protein kinase C was stimulated by a phorbol ester. Adrenaline, on the other hand, inhibited release under these conditions. It is concluded that inhibition of adenylate cyclase, rather than direct changes in membrane K+ and Ca2+ permeabilities, underlies the inhibition of insulin release induced by activation of A1-receptors. The more complete inhibition mediated by alpha 2-adrenergic receptors appears to result from a second mechanism not triggered by adenosine.

Adenosine↗

PubMed1989

An A2-purinoceptor agonist, NECA, potentiates acetylcholine-induced glucagon secretion.

The effect of a stable structural analogue of adenosine, 5'-N-ethylcarboxamidoadenosine (NECA), was studied on glucagon secretion induced by acetylcholine (ACh) in the isolated perfused pancreas of the newborn dog. The perfusion solution contained a physiological concentration of glucose (4.2 mM). In the first set of experiments, ACh (0.5 microM) infused alone for 10 min induced a significant rise of glucagon secretion (370 +/- 98%, 4 min after the beginning of infusion). In the second set, NECA (2.2 nM) infused 10 min before ACh administration, had no effect per se, but considerably increased the response to ACh (929 +/- 262% of basal value within 3 min). So, the more specific A2 purinoceptor agonist, NECA, potentiated glucagon secretion induced by the cholinoceptor agonist, ACh.

Acetylcholine↗

PubMed1989

Effects of extracellular adenine nucleotides on the electrical, ionic and secretory events in mouse pancreatic beta-cells.

1. The mechanisms whereby extracellular adenine nucleotides modulate pancreatic beta-cell function were studied with mouse islets stimulated by 15 mM glucose. 2. Adenosine 5'-triphosphate (ATP) and adenosine 5'-diphosphate (ADP) (100 microM) inhibited insulin release, 45Ca efflux and 86Rb efflux from islet cells, and decreased electrical activity in beta-cells. These changes were rapid but small and transient. 3. alpha,beta-Methylene ADP caused a rapid and sustained inhibition of insulin release, 45Ca efflux and 86Rb efflux from islet cells. It also produced a slight hyperpolarization of the beta-cell membrane, with sustained modification of the pattern but only transient decrease of the intensity of the electrical activity. In the absence of extracellular Ca2+, alpha,beta-methylene ADP increased 45Ca and 86Rb efflux without changing insulin release. Most effects of alpha,beta-methylene ATP were qualitatively similar but quantitatively smaller than those of the ADP-analogue. 4. Adenylylimido-diphosphate (AMP-PNP) slightly increased 45Ca and 86Rb efflux and potentiated insulin release in the presence of extracellular Ca2+. However, its effects on electrical activity in beta-cells were qualitatively similar to those of the alpha,beta-methylene analogues. 5. The small effects of ATP and ADP could result from their degradation into adenosine. alpha,beta-Methylene ADP appears to increase K+ permeability of the beta-cell membrane and to produce a second, intracellular, effect which largely contributes to the inhibition of insulin release. Another recognition site, with higher affinity for triphosphate derivatives, could mediate the small stimulatory effects of AMP-PNP.

Adenine Nucleotides↗

PubMed1989

Difference in the potentiating effect of adenosine triphosphate and alpha, beta-methylene ATP on the biphasic insulin response to glucose.

1. The effects of exogenous adenine nucleotides and structural analogues on the biphasic insulin response to an increase of glucose concentration in the physiological range (from 4.2 to 8.3 mM) were studied in the isolated perfused rat pancreas. Purinoceptor agonists were added either simultaneously or 15 min before increasing glucose. 2. ATP and ADP at 16.5 microM were ineffective per se in the presence of the non stimulatory glucose concentration (4.2 mM) but markedly potentiated the biphasic insulin response to glucose rise in both experimental protocols. 3. Two more stable analogues of ATP and ADP (adenylylimidodiphosphate and alpha, beta-methylene ADP (alpha, beta-MeADP)) at 16.5 microM behaved like the natural compounds: they were ineffective at a glucose concentration of 4.2 mM and potentiated both phases of insulin response to glucose rise. 4. alpha, beta-MeATP added simultaneously with the high glucose concentration, markedly potentiated the first phase of insulin response to glucose rise but did not potentiate the second one. When alpha, beta-MeATP infusion began 15 min before glucose rise, the biphasic response to glucose was not potentiated, in contrast to what occurred with ATP. 5. In the presence of alpha, beta-MeATP, the ATP potentiating effect was unaffected. 6. It is concluded that ATP and ADP, via activation of beta cell P2 gamma purinoceptors, potentiates the biphasic insulin response to an increase of glucose concentration. On the other hand, alpha, beta-MeATP did not behave like natural and other structural analogues of ATP and ADP: this difference appears not to be the consequence of desensitization of beta cell P2 gamma purinoceptors by alpha, beta-MeATP.

Adenosine Diphosphate↗

PubMed1989

Membrane and intracellular effects of adenosine in mouse pancreatic beta-cells.

Mouse islets were used to study the effects of adenosine and its stable analogue L-N6-phenylisopropyladenosine (L-PIA) on pancreatic beta-cell function. At a high concentration (500 microM), adenosine augmented glucose-induced electrical activity in beta-cells and potentiated insulin release. These effects were prevented by the inhibitor of nucleoside transport nitrobenzylthioguanosine. They probably result from the metabolism of adenosine by beta-cells. At a lower concentration (50 microM), adenosine caused a small and transient inhibition of glucose-induced electrical activity and insulin release. L-PIA (10 microM) slightly and transiently inhibited insulin release, 45Ca efflux and 86Rb efflux from islet cells, and decreased electrical activity in beta-cells. When adenylate cyclase was stimulated by forskolin in the presence of 15 mM glucose, insulin release was strongly augmented. Under these conditions, L-PIA and adenosine (with nitrobenzylthioguanosine) caused a sustained inhibition. No such inhibition was observed when insulin release was potentiated by dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP). These data are consistent with the existence of A1 purinergic receptors on mouse beta-cells. They could mainly serve to attenuate the amplification of insulin release brought about by agents acting via cAMP.

Adenosine↗

PubMed1989

Diabetes and impaired response of glucagon cells and vascular bed to adenosine in rat pancreas.

Previous studies have shown that adenosine, by activation of purinergic A2-receptors, stimulates glucagon secretion and increases vascular flow rate in isolated perfused pancreases from nondiabetic rats. Because alpha-cell function and blood flow control are known to be disturbed in diabetes, we investigated whether adenosine was still effective in streptozocin-induced diabetic (STZ-D) rats. Our experiments were performed on isolated perfused rat pancreases. Whereas, in normal rats, adenosine (1.65 microM) induced a 200% increase in glucagon output and a 25% rise in the pancreatic vascular flow rate, in rats diabetic for 5-6 wk, this nucleoside was ineffective on glucagon secretion, and its vasodilatory effect was strongly reduced. Long-term in vivo insulin treatment that reversed high glycemia levels was able to restore in large part both adenosine effects. In contrast, a short-term in vitro pretreatment with insulin was unable to restore the nucleoside effects. We conclude that STZ-D suppresses the stimulatory effect of adenosine on alpha-cells and strongly reduces its vasodilator properties; these abnormalities may be corrected in large part by long-term insulin treatment with normalization of glycemia.

Adenosine↗