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Biomedical subjects

P Joanny

Publications and source records attributed to P Joanny.

At least 19 recordsLinked to original sources

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

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

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

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

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

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

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

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

[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

[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

Brain diurnal levels of adenosine 3',5' cyclic monophosphate in C57 BL/6 and BALB/C mice.

Adenosine 3',5'-cyclic monophosphate (cAMP) was measured in whole brain of two inbred strains of mice (BALB/C and C57 BL/6) submitted to a lighting schedule consisting of 12 hr light (0700-1900) and 12 hr darkness (1900-0700). Different mean levels of cAMP were found in each strain. Furthermore, statistical analysis of diurnal brain cAMP fluctuations showed different nycthemeral rhythms in both strains. BALB/C was mainly characterized by the presence of very significant 0600 and 0800 harmonics and C57 BL/6 by an orthophase around 1700 hr. Because both strains were studied under the same experimental conditions of light, temperature and food availability, these factors cannot account for the observed differences, which were thus tentatively interpreted in terms of genetic regulatory processes.

Animals

Toxicity of some essential plant oils. Clinical and experimental study.

Commercial preparations of essences of sage, hyssop, thuja, and cedar have caused human intoxication in eight cases, from which tonico-clonic convulsions were the major symptom. The experimental study of the toxic properties of commercialized essential oils of sage and hyssop has revealed that their convulsant action was of central nervous system origin in unanesthetized rats, as proven by electrocortical records. The toxicity of the hyssop oil seems to be more powerful than that of sage, since the dose limit from which the cortical events are only subclinical is 0.08 g/kg for hyssop oil and 0.3 g/kg for sage oil. Above 0.13 g/kg for hyssop oil and 0.50 g/kg for sage oil, the convulsions appeared and became lethal above 1.25 g/kg with hyssop oil and 3.2 g/kg with sage oil. The daily repeated injection of subclinical doses revealed the cumulative toxic effect of hyssop oil, since the same low dose induced electrocortical clonic seizures. The toxicity of each oil appeared to be related to the presence of terpenic ketones, camphor in sage commercial oil, camphor and thujone in sage Dalmatian oil, thujone in thuja and cedar oils, and pinocamphone in hyssop oil. The convulsant properties of camphor are well known. The neurotoxicity of thujone and pinocamphone is demonstrated in rats for the first time.

Adolescent

[Acute phase of ventricular fibrillation in myocardial infarct. Importance of studying electrical systole by determining the QTc].

Recent reports have drawn attention to the association between long QT intervals and sudden death in myocardial infarction and certain congenital syndromes. This study was undertaken to determine the relationship between lengthening of the QT interval and primary ventricular fibrillation in acute myocardial infarction. Thirteen cases were chosen out of a total of 21 cases of primary ventricular fibrillation (5.09% of 412 cases of myocardial infarction hospitalised during this period). Ten other cases of myocardial infarction with the same features apart from the arrhythmia were used as controls. Three series of electrocardiogrammes recorded under the same technical and chronological conditions (2 before and 1 after ventricular fibrillation) were analysed. The average QT interval was corrected for heart rate (RR) with Bazett's formula. The average QTc in acute myocardial infarction was longer than the theoretical QTc (p less than 0.05). The graph showing this increase reached a peak at the 48th hour. The average QTc in patients with primary ventricular fibrillation was longer than in the control patients (p less than 0.05) and significantly longer than the theoretical value (p less than 0.001). The average QTc in survivors of ventricular fibrillation was not significantly longer than that of the control group but was longer than the theoretical value (p less than 0.01). These results justify the strict surveillance of the length of electrical systole in the first hours of the acute phase of myocardial infarction. In this series, values greater than 440 ms were associated with a high risk of ventricular fibrillation in the first week after myocardial infarction.

Acute Disease

Electroencephalographic protective action of pyridoxylate during acute hypoxia and subsequent recovery in the rat.

Pyridoxylase at a concentration of 0.6 mmol/kg body weight injected intraperitoneally in rats, increased the resistance of animals to severe hypoxia (O2:3.2%; N2; 96.,%). The electrocorticogram (ECoG) was used to indicate the effectiveness of the drug in lowering the delay of electrographic silence, in 19 control rats and 12 pretreated rats. The ECoG was also recorded period under pure oxygen. In pretreated rats, the ECoG records became flat in a mean time of 551 s, compared with 269 s in the control group. The latent periods of successive steps during cerebral anoxia were significantly delayed in pyridoxylate-pretreated rats subjected to hypoxia. During the recovery period, pyridoxylate improved the recovery of the normal ECoG, particularly when values were expressed as a function of the duration of the hypoxic period. These findings are in good agreement with the significant protection afforded by pyridoxylate on the cerebral rate of energy-rich phosphate bond utilization during hypoxia studied in a separate work.

Animals

Effect of pyridoxine, glyoxylic acid and pyridoxylate on oxidative metabolism in vitro and phosphorylated energy-rich compounds studied in rat brains during acute hypoxia and ischaemia.

Pyridoxine (1-8 mmol/l) did not change significantly the cerebral oxygen nor the hypoxic or ischaemic degradation of phosphocreatine and ATP. Glyoxylic acid (1-8 mmol/l), an inhibitor of the citric acid cycle, depressed the electrically stimulated oxygen uptake of brain slices to a lesser extent than did pyridoxylate. Moreover, at concentrations of 0.66 mmol/l, pyridoxylate predominantly delayed the hypoxic or the ischaemic breakdown of creatine phosphate and of ATP compared with glyoxylic acid (0.66 mmol/l). These findings paralleled clearly the prominent hypoxic and post-hypoxic protection afforded by pyridoxylate upon rat brain electrogenesis, reported in the preceding paper.

Adenosine Triphosphate