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Postoperative intragastric enteral feeding in cardiac surgery patients is frequently complicated by delayed gastric emptying. The aim of the study was to evaluate how early postoperative gastric enteral nutrition affects the gastric emptying in coronary artery by-pass graft (CABG) surgery patients. In the prospective, randomized study 40 patients treated at intensive care unit after CABG surgery were studied. Patients were divided in two groups: enteral feeding group E (20 patients: age 59±8 yr.; male 70%) and control group C (20 patients: age 58±10 yr.; male 80%), respectively. Paracetamol absorption test was used to evaluate gastric emptying. In the group E postoperative gastric supply of enteral formula begun 18 hours after surgery and after 6 hours the supply was stopped and paracetamol solution was administrated by nasogastric tube. The patients in group C for.rst 24 hours received only crystalloid solutions intravenously and paracetamol solution by nasogastric tube. Blood samples were obtained at 0 (t0), 15 (t+15), 30 (t+30), 60 (t+60) and 120 (t+120) min after administration of paracetamol. The values of plasma paracetamol concentration (PPC) at 15 and 120 min were significantly higher in group E vs. group C: (t+15) 3.3±2.5 vs. 1.7±1.9 and (t+120) 5.2−2.8 vs. 3.3±1.6 (p <0.05). The PPC values at 30 and 60 min were higher, but not signi.cantly, in group E vs. group C: (t+30) 3.7±2.0 vs. 2.9±2.7 and (t+60) 5.1±3.2 vs. 3.9±3.5 (p = NS). The area under the PPC curve was 429 ± 309 in the E group vs. 293 ± 204 in the group C (p < 0.05). In conclusion an early postoperative gastric administration of nutritients after CABG surgery stimulates the gastric emptying.
Content available remote Gastric Emptying in Esophageal Substitutes
For patients undergoing esophagectomy, the stomach is the organ that is most commonly used to restore continuity in the gastrointestinal tract. As a consequence of changes in stomach shape and location, patients in the postoperative period usually experience disturbed motility of the upper gastrointestinal tract of variable intensity.The aim of the study was to assess the motility of esophageal substitutes and the emptying rate of a narrowed stomach (in particular its prepyloric portion) using scintigraphy in patients undergoing esophageal resection compared to those in healthy controls.Material and methods. Between 2000 and 2006, 297 patients (105 women, 192 men) underwent surgical treatment for esophageal cancer in the Clinic of Gastrointestinal Surgery. Ten patients (average age 59; range 54 to 67 years) who underwent an attempted curative esophageal resection were selected into the study group. Patients from this group underwent scintigraphic assessment of gastric emptying between three to 11 months after the surgical procedure (an average 7 months). Furthermore, ten healthy volunteers (average age 28; range 19 to 43 years) constituted the control group.Results. The average radiotracer retention after two hours was 44.7±6.5% in the study group and 51.1±7.4% (p>0.2) in the control group. Frequency of contractions of the whole prepyloric segment, as well as its distal fragment, in the subsequent periods of examination was comparable in both groups. Correlation among the frequency of contractions, contraction duration and duration of relaxation of the whole prepyloric segment and its distal fragment was high for the control group (correlation coefficients 0.71 p<0.001; 0.71 p=0; and 0.63 p=0, respectively). In the study group, correlation between the frequency of contractions and contraction duration was poor (coefficients of correlation 0.03 p>0.8 and -0.02 p>0.9), while correlation between duration of relaxation of the whole prepyloric segment and its distal fragment was moderate (coefficient of correlation 0.34 p>0.06).Conclusions. Formation of a gastric substitute after its narrowing and denervation (truncal vagotomy) does not abolish gastric contractility. Frequency, amplitude, duration of contraction, and relaxation duration of the prepyloric portion of the ectopic substitute do not differ significantly from the patterns of motility of the upper gastrointestinal tract in healthy volunteers.
Content available remote Central and peripheral mechanisms by which ghrelin regulates gut motility
Ghrelin is the recently discovered endogenous ligand for the growth hormone secretagogue receptor. This receptor had previously been characterized based on the stimulatory effect of synthetic peptides, enkephalin analogues, on growth hormone secretion by pituitary somatotrophs. Surprisingly, ghrelin is most abundant in the stomach, suggesting that it may have effects beyond the stimulation of growth hormone in the pituitary and that it is a new brain-gut peptide. There is now increasing evidence that ghrelin stimulates motor activity in the gastrointestinal tract. Thus ghrelin induces the migrating motor complex and accelerates gastric emptying. These are effects typical for motilin, the only peptide structurally related to ghrelin. Moreover, the receptors of both peptides are structurally related as well. The motor effects of ghrelin require rather high concentrations, while motilin at high concentrations stimulates growth hormone release. These data suggest cross-reactivity. However, in vitro binding and contractility studies in the rabbit, the classical model to study motilin agonists, show that ghrelin has very weak if any interaction with the motilin receptor. Similarly, in cell lines expressing the receptors for both peptides there is no evidence for cross-reactivity. This corresponds to the fact that the pharmacophore of both peptides is quite different. Therefore, the motor effects must be due to the stimulation of specific central or peripheral ghrelin receptors. In the guinea pig there is evidence from electrophysiology, immunohistochemistry and calcium imaging studies for ghrelin receptors on myenteric neurons. This provides the morphological basis for peripheral effects of ghrelin. In rats, ghrelin, but not motilin, enhances the response of muscle strips to electrical field stimulation by activating cholinergic pathways. In rabbits the opposite is true but some synthetic ghrelin agonists have weak effects which cannot be blocked by motilin antagonists. Apparently ghrelin is the functional equivalent of motilin in the rat, but in rabbits the motilin-ghrelin family may have yet unknown members. in vivo the effect of ghrelin can be blocked by vagotomy and there is evidence for ghrelin receptors on vagal afferents and in the nodose ganglion. Studies in the rat suggest that under physiological conditions circulating ghrelin does not activate the myenteric plexus, but is able to do so following vagotomy. Finally, centrally administered ghrelin also accelerates gastric emptying and ghrelin changes the activity of neurons of the central nuclei involved in signalling information from the gastrointestinal tract. It is concluded that ghrelin may affect gastrointestinal motility via specific ghrelin receptors located on myenteric, vagal and central neurons. Vagal and central pathways appear to be most important. The fact that ghrelin may reverse the effect of ileus on gastric emptying suggests that ghrelin agonists could find therapeutical application as prokinetics.
Diarrhea is a condition which causes malabsorption and dehydration. Recently, the anti-motility effect of several herbal compounds for the treatment of hypermotility-induced diarrhea has been studied. The root of Platycodon grandiflorum has been widely used in oriental medicine for the treatment of various chronic inflammatory diseases. The aim of the present study was to assess the effects of Platycodin D (PD), the major triterpene saponin in the root of P. grandiflorum, on gastrointestinal (GI) motility by assessing both gastric emptying (GE) and intestinal transit (IT) in mice with different treatment protocols. Mice were randomly allocated to 5 groups (n = 15/group) according to their treatment protocols (control, administered with antikinetics: atropine, dopamine, or with pro-kinetics: itoride, bethanechol) for each GE and IT test. Each group was subsequently divided into 3 subgroups (n = 5) pre-treated with different PD doses (0, 2.5, and 5 mg/kg). Pre-treatment with PD in the control treatment group of mice showed reduced GE and IT in a dose-dependent manner. At the maximum PD effect, GE and IT were reduced by 63% and 50%, respectively, compared with those in the normal control group. In the groups given atropine or dopamine, pre-treatment with PD further reduced GE and IT by 35% to 58%, respectively. The PD pre-treatment dramatically reduced the GI motility enhanced by itopride and bethanechol. On the whole, these results suggest that PD treatment might be beneficial in motility-induced diarrhea.
Pineal hormone melatonin is proposed as a potential treatment for severe sleep disturbances, and various gastrointestinal disorders. It was shown that melatonin increases intestinal motility and influences the activity of myoelectric complexes of the gut. The aim of the study was to evaluate the mechanisms of the effect of exogenous melatonin on gastric emptying rate. Male Sprague-Dawley rats were fitted with gastric cannulas under anesthesia. The rate of gastric emptying of saline was determined after instillation into the gastric fistula, from the volume and phenol red concentrations recovered after 5 min. Melatonin injected intraperitoneally (ip; 0.001-100 mg/kg) delayed gastric emptying rate of saline at 3 and 10 mg/kg doses. When administered ip 15 min before melatonin (10 mg/kg) injections, CCK2 (L-365,260, 1 mg/kg) or 5-HT3 receptor (ramosetrone, 50 µg/kg) blockers abolished melatonin-induced delay in gastric emptying rate, while the blockade of sympathetic ganglia (bretylium tosylate, 15 mg/kg) significantly reduced the delay in gastric emptying rate. CCK1 receptor blocker (L-364,718, 1 mg/kg) had no significant effect on the delaying action of melatonin. Our results indicate that pharmacological doses of melatonin delay gastric emptying via mechanisms that involve CCK2 and 5-HT3 receptors. Moreover, it appears that exogenous melatonin inhibits gastric motility in part by activating sympathetic neurons.
Delayed gastric emptying in patients with both type 1 and type 2 diabetes mellitus (DM) occurs in approximately 50% of these patients. However, the role and the action mechanism of insulin on gastrointestinal (GI) motility are still unclear. The purpose of the present study was to investigate the involvement of cyclooxygenase-2 (COX-2) and prostaglandin E2 in the effects of insulin on gastric emptying in male rats. The normal and streptozotocin (STZ)-pretreated rats were injected intraperitoneally with or without insulin, atropine and specific muscarinic receptor antagonists before examination of measurement of gastric emptying, spontaneous contractile activity of smooth muscle strips, plasma cholecystokinin (CCK), and prostaglandin E2 (PGE2) analysis. Protein expression of COX-2 and insulin receptors (IRs) were analyzed by the technique of western blot. Acute different doses of insulin accelerated gastric emptying. Atropine interrupted the insulin effect on gastric emptying, and muscarnic M1/M3 receptor antagonists interrupted the insulin-reversed gastric emptying in normal and DM rats. Besides, we observed the expression of (IRs) in GI and found that IR was changed under the insulin and DM treatment, and was also different between STZ-pretreated rats and hyperglycemic rats. Expression of COX-2 in stomach was decreased in DM rats but restored by insulin. The COX inhibitor, indomethacin, decreased the gastric emptying which was induced or reversed by insulin in normal and DM rats, respectively. PGE2 production in stomach corresponded to the COX-2 expression. The contraction of GI smooth muscle stimulated by PGE2 was increased in insulin-pretreated normal and DM rats. We conclude that insulin changed the expression of IRs in stomach in DM rats. The delayed GI motility in diabetes was at least in part due to the COX-2 and PGE2 pathway which associated with decreasing COX-2 and diminishing PGE2 production in stomach. The attenuation of PGE2 production was employed for the index of the reduction of smooth muscle contraction in stomach in diabetes. Insulin stimulated the smooth muscle contraction through the IRs and COX-2 expression plus PGE2 production in rat stomach as well as reversed the delayed gastric emptying via the nervous actions of muscarinic M1 and M3 receptors in DM rats.
The consequences of selective activation of brain somatostatin receptor-2 (sst2) were assessed using the sst2 agonist, des-AA1,4-6,11-13-[DPhe2,Aph7(Cbm),DTrP8]-Cbm-SST-Thr-NH2. Food intake (FI) was monitored in ad libitum fed rats chronically implanted with an intracerebroventricular (i.c.v.) cannula. The sst2 agonist injected i.c.v. at 0.1 and 1 µg/rat dose-dependently increased light phase FI from 2 to 6 hours post injection (2.3±0.5 and 7.5±1.2 respectively vs. vehicle: 0.2±0.2 g/300 g bw, P<0.001). Peptide action was reversed by i.c.v. injection of the sst2 antagonist, des-AA1,4-6,11-13-[pNO2-Phe2,DCys3,Tyr7,DAph(Cbm)8]-SST-2Nal-NH2 and not reproduced by intraperitoneal injection (30 µg/rat). The sst2 antagonist alone i.c.v. significantly decreased the cumulative 14-hours dark phase FI by 29.5%. Other behaviors, namely grooming, drinking and locomotor activity were also increased by the sst2 agonist (1 µg/rat, i.c.v.) as monitored during the 2nd hour post injection while gastric emptying of solid food was unaltered. Rectal temperature rose 1 hour after the sst2 agonist (1 µg/rat, i.c.v.) with a maximal response maintained from 1 to 4 hours post injection. These data show that selective activation of the brain sst2 receptor induces a feeding response in the light phase not associated with changes in gastric emptying. The food intake reduction following sst2 receptor blockade suggests a role of this receptor in the orexigenic drive during the dark phase.
In postmenopausal women various psychosomatic disorders concerning mood and appetite occur. The reason is not only estrogen deficiency, but also other hormones and neurotransmitters. The aim of the study was to estimate serotonin and melatonin levels and myoelectrical activity and gastric motor in postmenopausal women in relation to their nutritional status. The study was conducted in three 30-person groups of women: premenopausal (group I), postmenopausal with a normal body mass (group II), postmenopausal overweight (group III). Compared with group I, in group II there were no significant differences, while in group III serotonin level was lower respectively 156.5±40.2 ng/ml and 83.4±32.5 ng/ml (p<0.01), as well as the percentage of normogastria – 82.9±5.6% and 66.9±8.2 (p<0.05) and gastric emptying half-time 43.6±14.7 min and 27.4±12.2 min (p<0.01). Moreover, a negative correlation between body mass index and serotonin (r = -0.4744) and melatonin (r = -0.7146) levels was observed. The study results indicate the involvement of serotonin and melatonin in the pathogenesis of eating disorders in postmenopausal women.
U kobiet po menopauzie występują różnorodne zaburzenia psychosomatyczne, w tym dotyczące nastroju i łaknienia. Przyczyną tego jest niedobór estrogenów, ale także innych hormonów i neurotransmiterów. Celem badania było określenie stężenia serotoniny i melatoniny oraz czynności mioelektrycznej i motorycznej żołądka u kobiet po menopauzie w odniesieniu do ich stanu odżywienia. Badania przeprowadzono w trzech 30-sto osobowych grupach kobiet: przed menopauzą (grupa I), po menopauzie z prawidłową masą ciała (grupa II), po menopauzie ze współistniejącą nadwagą (grupa III). W porównaniu z grupą I, w grupie II nie stwierdzono istotnych różnic, natomiast w grupie III niższe było stężenie serotoniny, odpowiednio 156,5±40,2 ng/mL i 83,4±32,5 ng/mL (p<0,01), a także niższy był odsetek prawidłowej czynności mioelektrycznej żołądka (normogastrii) – 82,9±5,6% i 66,9±8,2 (p<0,05) oraz krótszy był czas połowicznego opróżniania żołądka (43,6±14,7 min. i 27,4±12,2 min.; p<0,01. Ponadto stwierdzono odwrotną zależność między wskaźnikiem masy ciała a stężeniem serotoniny (r = -0,4744) i melatoniny (r = -0,7146). Wyniki badań wskazują na udział serotoniny i melatoniny w patogenezie zaburzeń odżywiania u kobiet po menopauzie.
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