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Biomedical subjects

P Joanny

Publications and source records attributed to P Joanny.

At least 19 recordsLinked to original sources
PubMed2001

Operation Everest III (Comex'97): the effect of simulated sever hypobaric hypoxia on lipid peroxidation and antioxidant defence systems in human blood at rest and after maximal exercise.

Eight subjects were placed in a decompression chamber for 31 days at pressures from sea level (SL) to 8848 m altitude equivalent. Whole blood lipid peroxidation (LP) was increased at 6000 m by a mean of 23% (P<0.05), at 8000 m by 79% (P<0.01) and at 8848 m by 94% (P<0.01). (All figures are means.) Two days after return to sea level (RSL), it remained high, by 81% (P<0.01), while corresponding erythrocyte GSH/GSSG ratios decreased by 31, 46, 49, 48%, respectively (each P<0.01). Erythrocyte SOD and plasma ascorbate did not change significantly. At sea level, maximal exercise induced a 49% increase in LP (P<0.01), and a 27% decrease in erythrocyte GSH/GSSG ratio relative to resting values (P<0.05). At 6000 m, the LP was enhanced further from 23 (P<0.05) to 66% (P<0.01), and after RSL from 81 (P<0.01) to 232% (P<0.01), while pre-exercise GSH/GSSG ratios did not change significantly. Exercise did not change plasma ascorbate relative to sea level or to 6000 m, but decreased after RSL by 32% (P<0.01). These findings suggest that oxidative stress is induced by prolonged hypobaric hypoxia, and is maintained by rapid return to sea level, similar to the post-hypoxic re-oxygenation process. It is increased by physical exercise.

Acclimatization↗
PubMed2000

The effects of ionotropic agonists of excitatory amino acids on the release of arginine vasopressin in rat hypothalamic slices.

The effects of ionotropic excitatory amino acids agonists on the release of vasopressin from rat hypothalamic slices were studied. Incubation with increasing doses of NMDA, kainate or AMPA decreased the release of vasopressin in a dose-dependent manner. The values of the IC50 were 1.0, 9.6, or 3.7 x 10-8 M, respectively. The inhibitory effect of the various excitatory amino acids tested was blocked by coincubation with their respective antagonists. Vasopressin secretion was stimulated to 140.3 +/- 7.6% of controls when the slices were obtained from chronically (7 days) salt-loaded rats. Addition of 1 x 10-7 M NMDA or 1 x 10-6 M kainate to the incubation medium antagonized the salt loading-induced increase in vasopressin release. Incubation with 1 x 10-4 M tetrodotoxin did not change basal vasopressin release, but it blocked the decrease in vasopressin secretion induced by 1 x 10-7 M NMDA or 1 x 10-6 M kainate or 1 x 10-6 M AMPA. Incubation with 1 x 10-5 M phaclophen (a GABAB antagonist) and 1 x 10-5 M bicuculline (a GABAA antagonist) was without effect on basal vasopressin secretion while it reversed the inhibition of vasopressin release induced by 1 x 10-7 M NMDA. Incubation with 1 x 10-6 M GABA alone decreased vasopressin secretion to 64.6 +/- 6.9% of control values. The inhibitory effect of GABA did not change when 1 x 10-7 M NMDA was added to the incubation medium. These findings demonstrate that ionotropic excitatory amino acids agonists inhibit vasopressin secretion from hypothalamic slices. They strongly suggest that this inhibitory effect is mediated through local GABAergic interneurones.

Animals↗
PubMed2000

Regional brain bioamine levels under hyperbaric oxygen in two unequally susceptible strains of mice.

BACKGROUND: Hyperbaric oxygen (HBO) increases monoamine deamination with related toxic products which aggravates hyperbaric oxygen (HBO) neurotoxicity. However, the possibility of some protective action of monoamines balanced by the toxicity of their metabolites have received little attention. HYPOTHESIS: To try to unmask this protective action, we compared brain monoamine levels in two strains of mice differing in HBO-sensitivity and their sensitivity to HBO after norepinephrine (NE) depletion by N-(2-chloroethyl)-N-ethyl-2-bromo benzylamine (DSP4). METHODS: Mice were exposed to 6 ATA O2 for 90 min (C57 strain) and 24 min (HBO-sensitive CD1 strain) so that 50% of mice of each strain had preconvulsive symptoms when decompressed and 50%), had one generalized convulsion. After microwave sacrifice, monoamines in the cerebral cortex, the striatum and the brainstem were analyzed. Another series studied the effect of DSP4 on the delay to symptoms of these HBO)-exposed mice. RESULTS: NE normoxic levels in the striatum were greater in the HBO-sensitive CD1 than in the C57 strain. Under HBO, NE levels in the striatum and the cortex of CD1 fell without any concomitant increase in its metabolite whereas in the C57 strain, NE decreased less and its metabolite increased. There was no strain difference and little change in the NE levels in the brainstem. The increase in toxicity induced by DSP4 was highly significant in both strains; moreover C57 strain was more affected than CD1. CONCLUSION: Monoamine depletion before HBO aggravates HBO neurotoxicity. As monoamine deamination is known to be toxic, this demonstrates that monoaminergic activation is protective. The greater toxicity of DSP4 in the C57 strain suggests the involvement of monoamines in the strain-differential susceptibility to HBO. The lower sensitivity of CD1 mice to DSP4 may be related to a combination of less NE activation under HBO that in C57 and greater activation of peroxidation and amino acids in CD1 sensitive strain.

Animals↗
PubMed1997

Effect of excitatory amino acids on rat hypothalamic somatostatin secretion in vitro.

We studied the effect of various agonists of excitatory amino acid (EAA) receptor subtypes on somatostatin (SRIF) release from incubated rat hypothalamic slices. N-Methyl-D-aspartic acid (NMDA) and L-glutamate (1 x 10(-7) to 1 x 10(-3) M) stimulated, in a dose-dependent fashion, SRIF release. The maximal effect was obtained at a concentration of 1 x 10(-4) M for both drugs. The IC50 was 3.2 x 10(-5) M and 2.1 x 10(-5) M for NMDA and L-glutamate, respectively. Incubation with 2.5 x 10(-4) M D-2-amino-5-phosphonovalerate (a NMDA receptor antagonist) or 2-amino-4-phosphonobutyrate (a metabotropic receptor antagonist) was without significant effect on basal SRIF secretion and completely blocked the increase in SRIF release induced by 5 x 10(-5) M NMDA or L-glutamate, respectively. Incubation with 1 x 10(-4) M kainate or 0.5 x 10(-4) M alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) did not change basal SRIF secretion. Incubation with 2 x 10(-4) M gamma-D-glutamylglycine (a specific antagonist of kainate and AMPA receptors) had no effect under basal conditions or during exposure to kainate or AMPA. Our data demonstrate that EAAs stimulate SRIF secretion in vitro, by an action through NMDA and metabotropic receptors but not kainate or AMPA receptors.

Animals↗
PubMed1997

Glutamate and N-methyl-D-aspartate stimulate rat hypothalamic corticotropin-releasing factor secretion in vitro.

It is known that in vivo excitatory amino acids (EAA) stimulate the hypothalamo-pituitary-adrenal axis. However their site of action is not fully understood. We investigated the possibility of a direct action of EAA on the secretion of the major adrenocorticotropin hormone (ACTH) secretagogue: corticotropin-releasing factor (CRF) from incubated rat hypothalamic slices. N-methyl-D-aspartic acid (NMDA) or L-glutamate (1 x 10(-7) to 1 x 10(-3) M) stimulated in a dose-dependent fashion CRF release. The maximal effect was obtained at a concentration of 1 x 10(-4) M for both drugs. The IC50 was 1.3 x 10(-5) M and 3.3 x 10(-5) M for NMDA and L-glutamate, respectively. Incubation with 2.5 x 10(-4) M D-2-amino-5-phosphonovalerate (a NMDA receptor antagonist) or 2-amino-4-phosphonobutyrate (a metabotropic receptor antagonist) was without significant effect on basal CRF secretion and completely blocked the increase in CRF release induced by 5 x 10(-5) M NMDA or L-glutamate, respectively. Incubation with 1 x 10(-4) M kainate or 0.5 x 10(-4) M AMPA did not change basal CRF secretion. Incubation with 2 x 10(-4) M gamma-D-glutamylglycine (a specific antagonist of kainate and AMPA receptor) had no effect under basal conditions or during exposure to kainate or AMPA. Our data demonstrate that EAA could stimulate directly CRF secretion, by an action through NMDA and metabotropic receptors, but not kainate or AMPA receptors. These findings may be relevant to the regulation of the hypothalamo-pituitary adrenal axis, both under basal conditions and during exposure to stress.

Animals↗
PubMed1997

Hyperbaric-induced enhancement of noradrenaline-evoked contraction in rat thoracic aorta.

The aim of this study was to investigate the effects of a high ambient pressure of He on vascular contraction induced by noradrenaline and to distinguish the effects of ambient pressure per se from those of increased pressure of inert gas. Rings of thoracic aorta were isolated from male Wistar rats. Isometric tension was measured in preparations exposed to 7.1 MPa (absolute pressure) of He. Dose-response curves for noradrenaline and contractions elicited by 120 mM KCl were compared with time-matched experiments performed at atmospheric pressure. The same protocol was also carried out under 7.1 MPa of N2. At the high pressure of He, the contraction elicited by noradrenaline was increased with no change in the response to K(+)-evoked depolarization. The tension developed in response to noradrenaline also increased under 7.1 MPa of N2 but the effects were less marked than during the He experiments. Moreover, the response to KCl was reduced in this circumstance. Hyperbaric conditions enhance the noradrenaline-induced contraction of rat aorta in vitro. This effect probably results from an action of pressure per se on activation of adrenoceptors. However, the hyperbaric-induced increase in vascular smooth muscle contraction is partially counteracted by high pressures of inert gases (N2, but also probably He), which impair the efficiency of the contractile machinery.

Adrenergic alpha-Agonists↗
PubMed1996

Mechanical ventilation increases substance P concentration in the vagus, sympathetic, and phrenic nerves.

Substance P (SP), a neurotransmitter localized to primary sensory neurons, is found in the vagus nerve, nodose ganglion, sympathetic chain, and phrenic nerve in various animal species. However, the changes in endogeneous SP concentration under various circumstances that involve the participation of cardiorespiratory afferent nerves are still unexplored. In the present study, attention was focused on the variations in SP content measured by radioimmunoassay (RIA) in respiratory afferent nerves (vagus nerve, cervical sympathetic chain, phrenic nerve) and respiratory muscles (diaphragm, intercostal muscles) during positive inspiratory pressure (PIP) breathing alone or PIP with an expiratory threshold load (ETL) in rabbits. SP was found in all sampled structures in spontaneously breathing control animals, prevailing in the nodose ganglion. Left-versus right-sided differences were noticed in nerves. As compared with that in control animals, the SP concentration was markedly higher in vagal and sympathetic nervous structures during PIP or PIP with ETL, and also in the phrenic nerve during ETL breathing. The SP content did not vary in respiratory muscles. These observations suggest that two very common circumstances of mechanical ventilation are associated with an increased SP concentration in nervous structures participating in the control of breathing.

Animals↗
PubMed1995

Amino acids and ammonia in the cerebral cortex, the corpus striatum and the brain stem of the mouse prior to the onset and after a seizure induced by hyperbaric oxygen.

The contents of amino acids (AA) and ammonia (NH3) were measured in corpus striatum, brain stem and cerebral cortex of two strains of mice exposed to hyperbaric oxygen (HBO). Mice of the HBO-sensitive strain (CD1) were exposed to 600 kPa O2 for 24 min versus 90 min for mice of the normal C57 strain, so that 50% of the mice in both strains developed a generalized convulsion. In the cortex of exposed but unconvulsed (EXUN) C57 mice, the contents of taurine, glutamine and NH3 increased while that of GABA decreased when compared to control mice. In the CD1 mice, NH3 content was increased while that of Asp decreased. After a convulsion, NH3 was increased in both strains, the AA contents returned to normal in C57 but Asp remained low in CD1 mice. Somewhat similar changes occurred in the striatum except that NH3 levels were less affected while GABA ones were significantly decreased in the CD1 mice exposed to HBO, whether convulsed or not. In the EXUN brain stem, Asp and Glu contents decreased. These decreases were greater in C57 on a percentage basis than in CD1 mice. GABA content was decreased in the C57 strain. After a convulsion, Asp and Glu levels remained low and NH3 accumulated in CD1 whereas in C57 only the Glu level was decreased. The cortical and striatal changes may indicate a lesser GABA supply in C57 strain and some Asp release in CD1 strain. In the brain stem of both strains, Asp and Glu release is possible in addition to GABA in C57 strain.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗
PubMed1994

Effect of streptozotocin-induced diabetes on somatostatin receptors in the anterior pituitary, hypothalamus and cerebral cortex of the male rat.

In order to better understand the mechanisms underlying the reduction in GH secretion in diabetic rats, we have characterized and measured SRIH receptors in the hypothalamus and anterior pituitary gland 5 and 9 days after induction of diabetes in the rat. Experimental diabetes was induced by an intraperitoneal injection of streptozotocin (STZ) at a dose of 65 mg/kg. Basal plasma GH was significantly reduced in diabetic rats. Chronic insulin replacement therapy partly restored plasma GH and blood glucose levels in these animals. A significant reduction in SRIH receptor concentrations was demonstrated in the hypothalamus and anterior pituitary gland, 5- and 9- days after STZ injection. These changes were not significantly corrected by insulin replacement. Cerebral cortex SRIH receptor concentrations were unaffected by experimental diabetes. We conclude that hypothalamic and pituitary SRIH receptor levels are lowered in diabetic rats. These changes may contribute to aberrant GH secretion in diabetes and they indicate that pituitary sensitivity to exogenous somatostatin should be tested in diabetic patients.

Animals↗
PubMed1993

Effect of one hyperbaric oxygen-induced convulsion on cortical polyamine content in two strains of mice.

In rat striatum, after one hyperbaric oxygen (HBO)-induced convulsion, polyamine changes are found that could promote N-methyl-D-aspartate (NMDA) activation. In the HBO-sensitive CD1 mouse, unlike in the common C57 strain, there is some support for NMDA activation after the HBO seizure. We measured PA cortical content before and after the first HBO-induced convulsion (about 608 kPa O2) in CD1 and C57 strains. Putrescine, spermidine and spermine were dansyl derived and analysed by HPLC. Exposure to HBO significantly increased putrescine content only in CD1 though a similar trend was observed in C57. No further increase was observed after convulsion whatever the strain. There were no significant changes in spermidine or spermine to support NMDA activation. Therefore, putrescine increase in CD1 cortex could reflect the free radical formation that is known to be greater in CD1 than in C57 mouse. Attempts to increase putrescine levels before HBO exposure hastened HBO-induced convulsion, less than spermidine or spermine. Because of physiological polyamine interconversion, additional experiments with indirect manipulation of putrescine levels and study of their time-course would precise these preliminary reports on putrescine and HBO.

Animals↗
PubMed1992

Effect of diabetes on in vivo and in vitro hypothalamic somatostatin release.

In order to better understand the mechanisms underlying the reduction in growth hormone (GH) secretion in diabetic rats, we studied hypothalamic somatostatin secretion both in vivo (into hypophysial portal blood) and in vitro (from hypothalamic fragments) 5, 9 and 30 days after induction of diabetes. Experimental diabetes was induced by an intraperitoneal injection of streptozotocin (STZ) at a dose of 65 mg/kg. Basal plasma GH was significantly reduced in diabetic rats at all stages. Somatostatin levels in hypophysial portal blood was unaffected in 5-day STZ-diabetic rats and significantly increased 9 days after STZ administration. Chronic insulin replacement therapy in diabetic animals partly normalized somatostatin levels as well as plasma GH and glucose levels. A good correlation was observed between in vivo and in vitro experiments. Indeed, somatostatin release from hypothalamic fragments did not change 5 days after STZ-induced diabetes and significantly increased 9 and 30 days after STZ administration. The in vitro increase in hypothalamic somatostatin secretion was observed in 10 as well as in 33 mM glucose concentration in the incubation medium. In the same experiment, the in vitro hypothalamic corticotropin-releasing factor secretion was lowered 5 and 9 days after diabetes induction. We conclude that hypothalamic somatostatin release increases in diabetic rats. These changes may contribute to the reduction in GH secretion in these animals. However, since these changes occur after the onset of plasma GH decrease, a factor(s) other(s) than somatostatin may play a causal role in the reduction in GH secretion.

Animals↗
PubMed1990

Plasma 3-methoxy-4-hydroxyphenylglycol in manic patients: relationships with clinical variables.

Plasma levels of 3-methoxy-4-hydroxyphenylglycol (MHPG) were found to be significantly higher in manic patients than in age- and sex-matched normal controls (n = 22). In 18 manic patients plasma MHPG correlated with manic symptoms but not with anxiety, depression, motor behaviour, acute psychosis, schizophrenia and severity of illness. A positive correlation between MHPG and grandiosity items on rating scales suggests a link with cognitive contents and therefore a relationship with central factors.

Adolescent↗
PubMed1988

Plasma 3,4-dihydroxyphenylethyleneglycol and 3-methoxy-4-hydroxyphenylethyleneglycol as indicators of central noradrenergic activity. A comparative study on control subjects and depressed patients.

Animal studies have suggested interspecies differences in brain norepinephrine (NE) metabolism, especially with regard to the relative proportions of 3,4-dihydroxyphenylethyleneglycol (DOPEG) compared to 3-methoxy-4-hydroxyphenylethyleneglycol (MOPEG). In order to question the value of both glycol metabolites as peripheral indices of central noradrenergic activity, a comparative study of plasma DOPEG and MOPEG (measured by HPLC) related to depression, sex, age and diagnostic categories (DSM-III) was carried out on depressed and control subjects. In addition, two groups of 8 patients were randomly submitted to a desipramine 150 mg/day, or a metapramine 450 mg/day antidepressant treatment influencing the formation of DOPEG and MOPEG in a different way. The study did not demonstrate any difference between DOPEG and MOPEG for most of the experimental factors. We found also a significant positive correlation between plasma levels of DOPEG and MOPEG. Our results support the idea that each of these two biological indices can be used in the assessment of central noradrenergic activity.

Adult↗
PubMed1987

Further studies on the effect of glucose concentrations and other oxidizable substrates upon ionic gradients and in vitro somatostatin release from rat mediobasal hypothalamus.

During in vitro incubation of rat mediobasal hypothalamus (MBH), potassium and sodium gradients were high in the presence of glucose, pyruvate, lactate or the mixture glucose and pyruvate; in the absence of substrate, the ionic gradients were markedly lowered and corresponding somatostatin release from MBH was maximal. The specific effect of glucose on somatostatin release from MBH was tested under normal tissue polarization, i.e. in the presence of pyruvate. Under these more physiological conditions, somatostatin release was submaximal and inversely related to glucose concentrations (within the range 0-7 mM).

Animals↗
PubMed1987

[In vitro release of hypothalamic corticoliberine in the rat: incubation of slices from the whole hypothalamus].

An experimental system allowing both the incubation and rapid transfert of rat hypothalamic slices has been developed in order to approach the regulation of CRF secretion. The release of CRF has been quantified by a specific radioimmunoassay. Under basal conditions, immunoreactive CRF release reached an optimum of 96.2 +/- 10.4 pg/3 hypothalami/20 min. A depolarizing concentration of KCl (56 mM) or veratridine (50 microM) applied for 20 min. induced a 222 and 257% increase, respectively, in CRF release. The in vitro CRF values released under basal and stimulated conditions are comparable to those of other hypothalamic neuropeptides. Furthermore, in vitro CRF release from the hypothalamus is in the same order of magnitude as in vivo CRF secretion estimated by hypophysial portal blood collection or median eminence push-pull cannulation.

Animals↗
PubMed1986

[Somatostatin and regulation of the secretion of growth hormone].

GH secretory bursts are due to the combination of a pulsatile GRF release and a decreased Somatostatin secretion in hypophysial portal blood. In the intermediary periods, low plasma GH levels depend on the tonic release of hypothalamic Somatostatin. Experimental studies suggest that alterations in hypothalamic Somatostatin are involved in changes of GH secretion observed under physiological (foetal life, aging, stress), pharmacological (beta-blocking agents) and physiopathological conditions (starvation, obesity, diabetes). The Somatostatin analogue SMS 201-995 induces a long-lasting inhibition of GH secretion and may be useful in the treatment of acromegalic patients.

Animals↗