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Biomedical subjects

B Bonaz

Publications and source records attributed to B Bonaz.

At least 37 records · Page 2Linked to original sources
PubMed1996

Neuronal pathways involved in abdominal surgery-induced gastric ileus in rats.

The 20-min rate of gastric emptying of a noncaloric solution and c-fos expression detected by immunohistochemistry in the brain were monitored 3 h after abdominal surgery performed under 10-min enflurane anesthesia in rats. Abdominal surgery (laparotomy and 1-min manipulation of the cecum) decreased gastric emptying from 60.8 +/- 3.4 to 25.9 +/- 3.4%. Capsaicin applied to the celiac/superior mesenteric ganglia 2 wk before the experiment reduced the delay in gastric emptying induced by abdominal surgery (46.3 +/- 3.4%), whereas perivagal capsaicin application had no effect (23.6 +/- 7.9%). The corticotropin-releasing factor (CRF) antagonist [D-Phe12, Nle21,38,C alpha MeLeu37]CRF-(12--41) injected intracisternally (10-20 micrograms) prevented postoperative gastroparesis induced by surgery, while having no effect on basal gastric emptying. Abdominal surgery increased the number of Fos-positive cells in brain nuclei regulating autonomic outflow: the nucleus of the solitary tract, locus ceruleus, paraventricular nucleus, and supraoptic nucleus of the hypothalamus. These data indicate that capsaicin-sensitive splanchnic afferent fibers and activation of CRF receptors in the brain are part of the neuronal circuitry mediating gastric stasis 3 h after abdominal surgery.

Abdomen↗
PubMed1995

Brain noradrenergic systems modulate the ceco-colonic myoelectric activity in rats.

The role of the brain noradrenergic systems in the control of the ceco-colonic myoelectric activity was investigated in rats following lesions with intracerebroventricular (icv) or intracisternal (ic) injection of 6-hydroxydopamine (6-OHDA). Controls received the vehicle alone. The ceco-colonic myoelectric activity was recorded 3 weeks later in conscious rats chronically fitted with electrodes. After icv injection of 6-OHDA, lesions of rostral and caudal (spinal) noradrenergic systems were observed whereas only spinal noradrenergic systems were lesioned after ic injection. This differential pattern of lesions was followed by a differential pattern of ceco-colonic myoelectric activity. In fasted animals, a significant increase of the long spike burst (LSB) frequency (nb min-1) was observed after icv injection of 6-OHDA whereas no modification was observed after ic injection of the neurotoxic. After a 6-g pelleted rat diet, a significant increase of the LSB frequency was also observed in the icv lesioned group when compared to controls. No modification of the ceco-colonic noradrenergic innervation was observed, thus confirming the central selectivity of these lesions. Lesions of central noradrenergic systems modify the LSB frequency in rats; the rostral noradrenergic systems seem to play the major role.

Animals↗
PubMed1994

Abdominal surgery induces Fos immunoreactivity in the rat brain.

Previous neuropharmacological studies indicate that brain peptides are involved in mediating gastric stasis induced by abdominal surgery. Central pathways activated by abdominal surgery were investigated in the rat by using Fos protein as a marker of neuronal activation. Abdominal surgery (laparotomy alone or combined with cecal manipulation) was performed under brief enflurane anesthesia (7-8 minutes), and 1 hour later rats were killed and brains processed for Fos immunoreactivity. Double labeling with Fos and arginine vasopressin, oxytocin, or tyrosine hydroxylase antibodies was also performed. Abdominal surgery induced Fos staining in the nucleus tractus solitarii, paraventricular and supraoptic nuclei of the hypothalamus, locus coeruleus, and ventrolateral medulla. After abdominal surgery, 18-25% of vasopressin and 18-33% of oxytocin-labeled cells were found to be Fos positive in the paraventricular nucleus and 15% of activated cells in the nucleus tractus solitarii were positive for tyrosine hydroxylase immunoreactivity. Enflurane alone induced c-fos expression in the same brain area; however, the number of Fos-positive cells and double-labeled cells were decreased two- to fivefold and three- to eightfold, respectively, compared with the abdominal surgery groups. These data show that abdominal surgery induced activation of specific hypothalamic, pontine, and medullary neurons. These findings may have implications for the understanding of central mechanisms involved in mediating gastric ileus following abdominal surgery.

Abdomen↗
PubMed1994

Induction of Fos immunoreactivity in the rat brain after cold-restraint induced gastric lesions and fecal excretion.

Cold-restraint alters gastrointestinal function through vagal pathways. Immunohistochemical detection of the nuclear phosphoprotein Fos (Fos-IR) was used to map brain neuronal pathways activated by cold exposure for 3 h in fasted rats maintained individually in semi-cylindrical restraining cages. Gastric lesions and fecal pellet output were also monitored. In rats exposed to cold (4 degrees C) restraint for 3 h, numerous Fos-positive nuclei were observed in the dorsal motor nucleus of the vagus, raphe pallidus, locus coeruleus, and paraventricular nucleus of the hypothalamus, and, to a lesser extent, in the raphe obscurus, parapyramidal region, and medullary noradrenergic region, bed nucleus of the stria terminalis and septum. Fecal pellet output was increased by 8 fold and gastric lesions covered 19.5 +/- 1.1% of the corpus mucosa. Rats restrained at room temperature under otherwise same conditions had little or no Fos-positive cells in these brain nuclei, no gastric erosion and a low pellet output (1.3 +/- 0.5 nb/3 h). These data, in addition to previous functional studies, provide anatomic support for the involvement of neurons in the caudal raphe nuclei, dorsal motor nucleus of the vagus and paraventricular nucleus of the hypothalamus in the autonomic and endocrine responses to cold-restraint.

Animals↗
PubMed1994

Water-avoidance stress-induced c-fos expression in the rat brain and stimulation of fecal output: role of corticotropin-releasing factor.

Immunohistochemical detection of the immediate-early gene c-fos was used to determine the pattern of neuronal activity in the rat brain after exposure to water-avoidance stress known to stimulate fecal output in rats. Avoidance to water for 1 h by standing on a small platform increases pellet output and induces numerous Fos-positive cells in the parvocellular part of the paraventricular nucleus of the hypothalamus (PVN), locus coeruleus (LC) and, to a lesser extent, in the bed nucleus of the stria terminalis, lateral septum, dorsal raphe nucleus and A5 and A1 noradrenergic neurons. The corticotropin-releasing factor (CRF) antagonist, alpha-helical CRF9-41 (50 micrograms i.c.v.) reduced water-avoidance stress-induced c-fos expression mainly in the PVN and the LC (44 and 60%, respectively) and decreased by 60% the stimulated fecal output. These data indicate that water-avoidance stress activates PVN and LC neurons through CRF pathways which contribute to the stimulation of colonic motor function.

Animals↗
PubMed1993

Peripheral peptide YY induces c-fos-like immunoreactivity in the rat brain.

The influence of peripheral injection of peptide YY (PYY) on neuronal activity in the rat brain was examined by immunohistochemical detection of c-fos protein. Numerous c-fos-immunoreactive nuclei were found in the area postrema, nucleus tractus solitarius (commissural and medial subnuclei), central amygdala and thalamus (periventricular and medial) of rats injected i.p. with PYY at a dose of 300 micrograms/kg. c-fos-like immunoreactivity was found to be less when lower doses of PYY (50-200 micrograms/kg, i.p.) were injected. Either no or few cells were detected after i.p. injection of the vehicle alone. These data provide anatomical support for the centrally mediated actions of peripheral PYY on gut function.

Amygdala↗
PubMed1993

Role of CRF in stress-related alterations of gastric and colonic motor function.

Major advances have been made in the understanding of the pathophysiology of stress-related alteration of gut function. A wealth of information indicates that CRF is involved in the central mechanisms by which stress inhibits gastric emptying while stimulating colonic motor function. CRF acts in the PVN to trigger both the inhibition of gastric emptying and the stimulation of colonic motor function in response to stress, in addition to previously established endocrine and behavioral responses. Preliminary evidence exists that CRF acts in the locus coeruleus to induce a selective stimulation of colonic transit without influencing gastric emptying. The central actions of CRF to alter gastric and colonic motor function are conveyed by autonomic pathways and are unrelated to the associated stimulation of pituitary hormone secretion. The demonstration that central CRF plays a role in mediating gastric stasis resulting from surgery, peritonitis or high levels of central interleukin-1 provides new insight into the mechanisms involved in gastric ileus induced postoperatively or by infectious disease. Likewise, the demonstration that CRF in the PVN and locus coeruleus induce the anxiogenic and colonic motor responses to stress and that colonic distention activates neurons in the locus coeruleus opens new avenues for the understanding of the pathogenesis of a subset of IBS patients with colonic hypersensitivity associated with psychopathological disturbance and diarrhea-predominant symptoms.

Animals↗
PubMed1993

Peripheral bombesin induces c-fos protein in the rat brain.

Bombesin injected intraperitoneally induces c-fos protein-like immunoreactivity in the medial nucleus tractus solitarius and the parvocellular part of the paraventricular nucleus of the hypothalamus in the rat brain. C-fos expression induced by bombesin is less densely represented compared with CCK. Capsaicin pretreatment did not influence c-fos-immunoreactivity induced by bombesin and significantly reduced that induced by CCK.

Animals↗
PubMed1992

Involvement of hypothalamic noradrenergic systems in the modulation of intestinal motility in rats.

Selective lesions of the noradrenergic systems of the paraventricular nucleus (PVN) of the hypothalamus with 6-hydroxydopamine (6-OHDA) lengthen the periodicity of the migrating myoelectric complex (MMC), an index of intestinal motility, in rats. These lengthening effects resemble those obtained after lesions of the locus coeruleus (LC), thus suggesting that noradrenergic terminals from LC to the PVN are involved in this modulation.

Analysis of Variance↗
PubMed1992

Locus ceruleus modulates migrating myoelectric complex in rats.

The role of the locus ceruleus (LC) in the control of migrating myoelectric complex (MMC) was investigated in rats with lesions induced by injections of 6-hydroxydopamine (6-OHDA). Control animals received the vehicle alone. MMC was recorded in conscious rats chronically fitted with electrodes. After 6-OHDA was injected into the LC, lesions of the LC were total, partial (mostly rostral), or ineffective. The MMC period was significantly longer in animals with a total or partial lesion but was unchanged in animals with an ineffective lesion. No lesion of other brain noradrenergic nuclei was observed. The longer MMC period is comparable to that obtained after intracerebroventricular injection of 6-OHDA, which is responsible for a more diffuse destruction of brain noradrenergic systems, including LC itself. Bilateral lesions of the central tegmental tract, which carries ascending noradrenergic axons from the medullary and pontine cell groups outside the LC, do not alter the MMC cycle. Consequently, the LC is most likely the major brain noradrenergic candidate for modulating the MMC pattern in rats.

Animals↗
PubMed1991

Modulation of the migrating myoelectric complex by brain noradrenergic systems in rats.

The respective role of central and peripheral noradrenergic systems in the control of migrating myoelectric complex (MMC) was investigated in rats following lesions with 6-hydroxydopamine (6-OHDA). 6-OHDA was injected via intraperitoneal (ip), intracisternal (icis), and intracerebroventricular (icv) routes in rats. Control animals received the vehicle alone. One month later, MMC was recorded in conscious rats chronically fitted with electrodes. The MMC period was significantly lengthened after 6-OHDA ip or icv injection, and slightly shortened after 6-OHDA icis injection. No disruption of central noradrenergic systems was detected after ip lesions. Norepinephrine content was reduced in the digestive tract after ip lesions, in the spinal cord after icis lesions, and in the cortex, the hypothalamus, pons-medulla, and the spinal cord after icv lesions. After icis lesions, noradrenergic perikarya were spared in pons-medulla, whereas only pons noradrenergic perikarya were lesioned after icv lesions. We conclude that lesions of brain noradrenergic systems modify MMC periodicity in rats. The rostral noradrenergic systems may play the major modulatory role.

Animals↗
PubMed1990

Scintigraphic study of gallbladder emptying and duodenogastric reflux during non-ulcerous dyspepsia.

Cholescintigraphy with technetium 99m hydroxy imino diacetic acid (99mTc-HIDA) was used to study gallbladder emptying (GE) and duodenogastric reflux (DGR) simultaneously during the postprandial period in humans. Two groups of subjects were examined prospectively; one was a group of healthy volunteers (n = 14) and the other a group of patients with non-ulcerous dyspepsia (NUD) (n = 22). Symptoms were quantified using a clinical score (CS). GE kinetics was quantified according to two indices. DGR episodes were detected by an image-subtraction method and quantified. The group of patients with NUD showed significant early acceleration of GE (P less than 0.01). One DGR episode equivalent to 1% of the injected dose was observed in 1 of the 14 control subjects, and greater than 1% in 3 of the 22 NUD patients. However, there was no correlation between the CS, GE kinetics and DGR episodes. The physiopathological mechanism and clinical significance of these digestive motility anomalies remain to be demonstrated.

Adult↗
PubMed1990

Is there an abnormal fasting duodenogastric reflux in nonulcer dyspepsia?

A quantitatively and/or qualitatively abnormal duodenogastric reflux (DGR) could be involved in the pathogenesis of nonulcer dyspepsia (NUD). The aims of this prospective study were to look for (1) a pathological DGR profile during fasting and (2) an eventual correlation between DGR profile and clinical symptoms. Twenty-six NUD patients were investigated. Seven other operated patients with a surgical procedure facilitating DGR episodes and 27 healthy volunteers served as control groups. A clinical score was determined for each patient from a standardized questionnaire. Gastric aspiration was performed for 6 hr in fasting subjects. The aspirates were pooled into 17 samples. In each sample the concentration and the output of total bile acids was determined. If the concentration was larger than 30 mumol/liter in pooled samples, the concentrations of free bile acids and the distribution of the conjugated bile acids was determined. The percentage of aliquots with a total bile acid concentration larger than 50 mumol/liter (without upper limit), and the percentage with a concentration larger than 2500 mumol/liter was also obtained. No significant difference was demonstrated between the healthy volunteers and NUD patients, whatever the parameter considered. However, there was a significant increase in each of the quantitative parameters for the group of operated patients in comparison with the NUD patient group. No significant correlation was found between the clinical score and the DGR profile in NUD patients. Apparently, DGR episodes do not play a primary role in the pathogenesis of NUD.

Adult↗
PubMed1988

Scintigraphic study of duodenogastric reflux. Value of a computerized image-subtraction method.

Duodenogastric reflux (DGR) could be implicated in several esophageal and gastric diseases. Establishing its pathophysiological role however is difficult because of the problems in the demonstration and quantification of DGR episodes. The aim of this study was to improve a scintigraphic method of detection and quantification of DGR episodes during the postprandial period in man. The study was carried out in 14 control subjects (7 males and 7 females, median age = 25 years, range: 22-35 years). As scintigraphic recording was continuous during 150 min, all DGR episodes were revealed. In order to improve visual detection of DGR episodes, images were treated by a computerized image subtraction method. The visual detection limit of DGR episodes determined by comparison to test images was 0.6 p. 100 of the dose injected intravenously or 17 microCi. A DGR episode was demonstrated in one of the 14 control subjects. The quantity of refluxed liquid was estimated, in this case, at 30 microCi, and the duration of the reflux greater than 2 min. Continuous scintigraphic recording in association with a computer based technique of image subtraction seems to improve scintigraphic performance in the study of DGR episodes under pathological conditions.

Adult↗