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Biomedical subjects

N B Ulusoy

Publications and source records attributed to N B Ulusoy.

At least 19 recordsLinked to original sources
PubMed2001

Gender influence on jejunal migrating motor complex.

The role of gender and the menstrual cycle in small bowel motility has not been clearly elucidated. Jejunal motility was recorded with a nasojejunal catheter incorporating five solid-state pressure transducers in ambulatory menstruating women and men of comparable age over 24 h. All women were studied twice, in the early follicular (early-F) and midluteal (mid-L) phases of the menstrual cycle, verified by determining serum levels of gonadal steroids and gonadotropins. The propagation velocity of phase III was slow and the contraction amplitude was high in both menstrual cycle phases compared with men, and these parameters were correlated with serum estrogen levels in the mid-L phase. In the early-F phase, migrating motor complex (MMC) cycle duration during sleep was long compared with other groups and positively correlated with estrogen concentrations, whereas in the mid-L phase MMC cycle duration during sleep was negatively correlated with serum progesterone levels. In all groups, the frequency of phase III contractions was low and the intercontractile interval measured from pressure peak to peak was long during sleep compared with the awake state. Postprandial motility did not display gender difference in any parameter examined. The results demonstrate that the majority of patterns of motility are similar in menstruating women and men, whereas certain aspects of the MMC, most conspicuously propagation velocity and phase III contraction amplitude, differ. We have also documented circadian variation of phase III contraction frequency in both women and men.

Adult↗
PubMed2001

Inhibition of gastric emptying by acarbose is correlated with GLP-1 response and accompanied by CCK release.

We investigated the effect of acarbose, an alpha-glucosidase and pancreatic alpha-amylase inhibitor, on gastric emptying of solid meals of varying nutrient composition and plasma responses of gut hormones. Gastric emptying was determined with scintigraphy in healthy subjects, and all studies were performed with and without 100 mg of acarbose, in random order, at least 1 wk apart. Acarbose did not alter the emptying of a carbohydrate-free meal, but it delayed emptying of a mixed meal and a carbohydrate-free meal given 2 h after sucrose ingestion. In meal groups with carbohydrates, acarbose attenuated responses of plasma insulin and glucose-dependent insulinotropic polypeptide (GIP) while augmenting responses of CCK, glucagon-like peptide-1 (GLP-1), and peptide YY (PYY). With mixed meal + acarbose, area under the curve (AUC) of gastric emptying was positively correlated with integrated plasma response of GLP-1 (r = 0.68, P < 0.02). With the carbohydrate-free meal after sucrose and acarbose ingestion, AUC of gastric emptying was negatively correlated with integrated plasma response of GIP, implying that prior alteration of carbohydrate absorption modifies gastric emptying of a meal. The results demonstrate that acarbose delays gastric emptying of solid meals and augments release of CCK, GLP-1, and PYY mainly by retarding/inhibiting carbohydrate absorption. Augmented GLP-1 release by acarbose appears to play a major role in the inhibition of gastric emptying of a mixed meal, whereas CCK and PYY may have contributory roles.

Acarbose↗
PubMed2000

Glucagon-like peptide (GLP-1) is involved in the central modulation of fecal output in rats.

In addition to its insulinotropic action, exogenously administered glucagon-like peptide (GLP-1) inhibits gastropancreatic motility and secretion via central pathways. The aims of the present study were to evaluate the effects of exogenous GLP-1-(7-36) amide on fecal output and to investigate the role of endogenous GLP-1 on stress-induced colonic activity. With the use of a stereotaxic instrument, adult male Sprague-Dawley rats weighing 200-250 g were fitted with stainless steel cerebroventricular guide cannulas under ketamine anesthesia. A group of rats were placed in Bollman-type cages to induce restraint stress. Fecal output monitored for 2 h was increased significantly by intracerebroventricular GLP-1 to 500, 1, 000, and 3,000 pmol/rat (P < 0.05-0.01), whereas intraperitoneal GLP-1 had no effect. Intracerebroventricular administration of the GLP-1 receptor antagonist exendin-(9-39) (10 nmol/rat) reversed the increases induced by GLP-1 (500 pmol/rat; P<0.01). Similar results were also observed with the injection of corticotropin-releasing factor receptor antagonist astressin (10 microg/rat icv). The significant increase in fecal pellet output induced by restraint stress was also decreased by both intracerebroventricular exendin (10 nmol/rat) and astressin (10 microg/rat; P<0.01-0.001). These results suggest that GLP-1 participates in the central, but not peripheral, regulation of colonic motility via its own receptor and that GLP-1 is likely to be a candidate brain-gut peptide that acts as a physiological modulator of stress-induced colonic motility.

Animals↗
PubMed1999

Distinct functional muscarinic receptors in guinea-pig gallbladder, ileum and atria.

OBJECTIVE: The contractile responses of guinea-pig gallbladder smooth muscle cells have been suggested to be mediated by M3 and M4 muscarinic receptors by different research groups. Therefore, in the present study, several pharmacological properties of cholinergic functions in guinea-pig gallbladder, guinea-pig ileum (mediated via M3 receptors), and guinea-pig and rat atria (mediated via M2 receptors) were compared. METHODS: The isometric contractions of isolated guinea-pig ileum, guinea-pig gallbladder, guinea-pig and rat atrial strips in in vitro organ bath were recorded on a polygraph and the effects of carbachol, oxotremorine, McN-A-343, and clozapine have been investigated. RESULTS: Three muscarinic receptor agonists, carbachol, oxotremorine and McN-A-343 showed different order of potencies in their negative inotropic effects and contractile actions in guinea-pig gallbladder suggesting that functional muscarinic receptors in the gallbladder are distinct from those in the atria, and similar to M4-subtypes. Clozapine which was shown to have antagonistic affinity for muscarinic M1, M2, M3 and M5, but partial agonistic affinity for muscarinic M4 receptors, contracted gallbladder concentration-dependently. On the other hand, clozapine antagonised carbachol-induced ileal and gallbladder contractions and negative inotropic effects indicating that it acts like a partial agonist in the gallbladder. CONCLUSION: It was concluded that the contractile muscarinic receptors of guinea-pig gallbladder are distinct from those of atria (M2) and ileum (M3), but seem to be of M4 subtype.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1998

Effect of intraluminal temperature on human oesophageal motor function.

Oesophageal motor activity is altered by bolus temperature. The effects of sustained cold or warm intraluminal temperature on oesophageal motility have not been documented in detail. Oesophageal manometry was performed in 11 normal subjects after intraluminal room, cold- and warm-water treatments. The intraluminal temperatures were 34.2 +/- 0.8, 30.6 +/- 1.7 and 39.7 +/- 0.9 degrees C respectively during room temperature, cold and warm applications. Low-temperature treatment prolonged the duration of lower oesophageal sphincter relaxation and the duration of oesophageal peristaltic contraction wave compared with the room temperature and warm treatments. Low temperature also attenuated the mean pressure slope of oesophageal contraction waves and resulted in an increased percentage of non-transmitted and simultaneous contractions. The effects of low-temperature application remained constant and there was no adaptation. Cooling oesophageal lumen temperature alters oesophageal motor activity, and this effect is not adaptive.

Adult↗
PubMed1998

Evidence for the presence of muscarinic M2 and M4 receptors in guinea-pig gallbladder smooth muscle.

1. The affinities of 10 selective muscarinic receptor antagonists against [3H]-quinuclidinyl benzilate (QNB) binding were determined to characterize the muscarinic receptors present in guinea-pig gallbladder smooth muscle. The highest correlation was obtained for the comparison between the pKi values for the gallbladder smooth muscle and M2 sites. Pirenzepine revealed two binding sites with affinities indicating the presence of muscarinic M2 receptors in abundance and a minor population of an additional site(s). 2. Carbachol produced gallbladder contractions, stimulated phosphoinositide (PI) hydrolysis and inhibited cAMP formation concentration-dependently with pD2 values of 6.12 +/- 0.11, 5.18 +/- 0.33 and 7.19 +/- 0.15, respectively. 3. Pirenzepine, 4-DAMP, HHSiD, pF-HHSiD, AF-DX 116, methoctramine, AQ-RA 741, guanylpirenzepine and AF-DX 384 showed competitive antagonism against carbachol-induced gallbladder contractions. There was no correlation between the pA2 values for the gallbladder and pKi values for the M2 sites, whereas significant correlations were found for the M1, M3 and M4 sites, the best correlation being between the pA2 values for the gallbladder and M4 subtypes. 4. Finally, the presence of both m2 and m4 receptor proteins were demonstrated by Western blot analysis. It is concluded that guinea-pig gallbladder smooth muscle has both muscarinic M2 and M4 receptors, which are coupled to adenylate cyclase inhibition and PI hydrolysis. 5. Although it seems likely that M2 receptors do not play a primary role in carbachol-induced guinea-pig gallbladder contraction, the characterization of the muscarinic subtypes which mediate these contractile responses needs further evidence.

Adenylyl Cyclases↗
PubMed1998

Corticosteroid therapy augments gastroduodenal permeability to sucrose.

OBJECTIVE: The aim of the present study was to investigate whether corticosteroid therapy alters gastroduodenal mucosal permeability and whether permeability alteration is associated with macroscopic mucosal damage. METHODS: Eight patients taking oral corticosteroid therapy (total prednisone-equivalent dose, 1.5+/-0.1 g; duration, approximately 30 days), nine patients with multiple sclerosis taking high-dose intravenous methyl-prednisolone therapy (total dose, 11.7+/-0.5 g; duration, approximately 9 days), and 20 age- and gender-matched controls were studied. Gastroduodenal permeability was determined using sucrose as a site-specific permeability probe. Five-hour urine was collected after ingesting 100 g of sucrose and its urinary excretion rate was measured using high-pressure liquid chromatography. Gastroduodenal endoscopy was performed before steroid therapy to exclude subjects with evidence of macroscopic mucosal lesions. The sucrose test and endoscopy were repeated after completion of corticosteroid therapy. RESULTS: The urinary sucrose excretion rates were similar in the control group and in patient groups before corticosteroid therapy. The median excretion rate of sucrose increased four (one to 28)- and eight (two to 35)-fold, respectively, as compared with pretreatment values in patients taking oral steroid and high-dose intravenous methyl-prednisolone therapy (p < 0.01). Considering all patients together, subjects who received a mean prednisone-equivalent dose of 8.4+/-1.5 g exhibited mucosal lesions, whereas patients who received 3.3+/-1.8 g did not (p = 0.06). The post-therapy increments in sucrose excretion rates were associated with neither the presence of macroscopic lesions nor with the total steroid dose received. CONCLUSIONS: Corticosteroid therapy augments gastroduodenal permeability and high doses are associated with macroscopic mucosal lesions. Steroid-induced permeability increase does not appear to be associated with the presence of macroscopic mucosal lesions.

Administration, Oral↗
PubMed1998

Interaction of omeprazole with enteric-coated salicylate tablets.

OBJECTIVE: Enteric-coated tablets are designed to resist gastric fluids and to disrupt and dissolve in the alkaline medium of the small intestine. Main objective of the present study was to investigate whether the increase in gastric pH due to omeprazole treatment alters the release rate of a drug from enteric-coated formulation. To this end, we have compared the single dose pharmacokinetics of a single-unit enteric-coated salicylate to that of uncoated acetylsalicylic acid tablets in the presence and absence of omeprazole treatment. METHODS: Study was carried out according to 4 x 4 Latin square design. Eight healthy subjects received either uncoated acetylsalicylic acid tablets or single-unit enteric-coated sodium salicylate tablets alone or following 4 days of treatment with single-dose 20 mg omeprazole, and blood samples were collected for 24 hours. Serum salicylate levels were determined by the modified spectrophotometric method of Brodie et al. [1994]. RESULTS: Salicylate was absorbed rapidly from uncoated tablets but absorption of salicylate from enteric-coated tablets was delayed, as expected. According to our results, omeprazole treatment did not influence the bioavailability from uncoated acetylsalicylic acid tablets but the absorption rate of salicylate from enteric-coated tablets was increased significantly. CONCLUSION: Findings of the present study demonstrate that omeprazole treatment significantly increases the rate of absorption of single-unit enteric-coated medication. Enhanced rate of absorption is most probably due to an early disruption of enteric coating and the intragastric release of the drug secondary to an omeprazole-mediated increase in gastric pH. The results of the present study also corroborate previous findings which have demonstrated highly variable absorption of enteric-coated single units.

Adult↗
PubMed1997

Hyperglycemia-induced attenuation of rectal perception depends upon pattern of rectal balloon inflation.

This study investigated the effects of acute hyperglycemia on conscious rectal perception in response to two different rectal distension paradigms. Eleven healthy males were studied in random order on two separate days during euglycemia and hyperglycemia with blood glucose concentrations clamped to 3.8 +/- 0.6 and 14.8 +/- 0.86 mmol/liter, respectively. In order to evoke sensory responses, rapid phasic and ramplike distensions were applied to an intrarectal balloon. Rectal sensation thresholds for initial sensation, sensation of stool and discomfort, and sensory intensities were recorded. Additionally, anorectal motor responses were investigated during phasic distension. Acute hyperglycemia did not modify rectal sensory pressure thresholds and perception scores in response to phasic distension. Neither did hyperglycemia alter the resting anal sphincter pressure, the pressure threshold for eliciting the rectoanal inhibitory reflex, or the maximal anal squeeze pressure. In contrast, hyperglycemia attenuated rectal perception in response to ramplike distension. The pressure thresholds, 10.0 +/- 1.8 and 17.0 +/- 3.6 mm Hg for initial sensation and discomfort, respectively, during hyperglycemia were significantly higher than the corresponding thresholds of 4.4 +/- 1.4 and 11.4 +/- 1.9 mm Hg observed during euglycemia (P < 0.01). Higher rectal pressures were observed at all intensities of sensation of stool and discomfort during hyperglycemia than those obtained during euglycemia (P < 0.01). Hyperglycemia did not alter the compliance of the rectum. The results of this study demonstrate that acute hyperglycemia attenuates rectal perception, and this attenuation depends upon the type of distension employed. Our findings also demonstrate that anal sphincter motor function is not appreciably modified by hyperglycemia.

Adult↗
PubMed1997

Glucagon-like peptide-1 inhibits gastric emptying via vagal afferent-mediated central mechanisms.

Exogenous administration of glucagon-like peptide-1-(7-36) amide (GLP-1), an insulinotropic hormone, inhibits gastric emptying and acid secretion in humans. The role of GLP-1 as a regulator of gastric function is elusive. In gastric fistula rats, vagal afferent denervation and peripheral administration of the GLP-1 receptor antagonist exendin-(9-39) amide enhanced emptying of a glucose meal, whereas intracerebroventricular exendin was ineffective. The rate of saline emptying was attenuated by peripheral as well as by central administration of GLP-1, and pretreatment with exendin by the respective routes reversed the inhibition by GLP-1. Vagal afferent denervation abolished the central and peripheral action of GLP-1 on gastric emptying. Neither peripheral cholinergic nor adrenergic blockade altered the delay of methyl cellulose meal emptying by intracisternal GLP-1 injection. Acid secretion in conscious pylorus-ligated rats was inhibited by intracisternal GLP-1 administration, whereas systemic GLP-1 was ineffective. These results support the notion that GLP-1 receptors participate in the central and peripheral regulation of gastric function. Furthermore, vagal afferent nerves mediate the inhibitory action of GLP-1 on gastric motor function. GLP-1 may be a candidate brain-gut peptide that acts as a physiological modulator of gastric function.

Animals↗
PubMed1996

Refractory duodenal ulcer healing and relapse: comparison of omeprazole with Helicobacter pylori eradication.

OBJECTIVE: To investigate differences between omeprazole and Helicobacter pylori eradication in patients with duodenal ulcers refractory to H2-receptor antagonists and to compare the recurrence rates after the two treatments. DESIGN AND METHODS: Forty-five patients with endoscopically proven duodenal ulcers refractory to H2-receptor antagonists and H. pylori infection were randomly assigned to 8 weeks of treatment with omeprazole 40 mg/day or 4 weeks of treatment with colloidal bismuth subcitrate 480 mg/day plus metronidazole 750 mg/day and tetracycline 1000 mg/day from day 1 to day 14. Patients were evaluated endoscopically and clinically at the end of treatment. Patients with healed ulcers were followed up for 1 year after cessation of the treatment. Endoscopy was performed at 3 and 12 months. RESULTS: Ulcer healing occurred in 100% (21/21) of patients on triple therapy and 70.5% (12/17) of those treated with omeprazole alone (P = 0.0123). The relapse rate at the 3rd month was 11.7% (2/17) in the triple therapy group and 60% (6/10) in the omeprazole group (P = 0.0248). Of the patients followed to study endpoint (relapse or endoscopy at 12 months) three of 12 (25%) receiving triple therapy, compared to six of eight (75%) receiving omeprazole, relapsed (P = 0.0648). CONCLUSION: These results show that triple therapy is more effective than omeprazole in the treatment of refractory duodenal ulcers and reduces the rate of ulcer relapse.

Adult↗
PubMed1995

Functional evidence for the involvement of GABAA receptors in cholecystokinin-induced ileal contraction.

To determine the role of GABAergic neurotransmission in cholecystokinin octapeptide (CCK-8) induced contraction of the guinea pig ileal longitudinal muscle--myenteric plexus preparation, CCKA or CCKB receptors were protected by L 364,718 and L 365,260, respectively. GABAA receptors were protected with bicuculline and the remainder of the receptors were inactivated by N-ethylmaleimide. Following the specific treatments isometric contractions in response to CCK-8 (0.1 nM - 1.0 microM) were obtained. CCKB receptor protection alone abolished responses to CCK-8. Additional GABAA receptor protection restored the responses. CCKA receptor protection alone decreased contractile responses to CCK-8, and additional protection of GABAA receptors resulted in restoration of the contractile responses at high concentrations of CCK-8. The results suggest that the CCKA and CCKB receptors that mediate the contractile action of CCK differ with regard to GABAergic neurotransmission. CCKB receptors appear to be dependent upon intact GABAergic neurotransmission, whereas CCKA receptors partially utilize this pathway.

Animals↗
PubMed1995

Modulation of gallbladder contraction by pirenzepine in humans.

OBJECTIVES: The mechanism(s) by which cholinergic innervation modulates gallbladder contraction are not fully understood. To elucidate the role of muscarinic M1 receptors in the mediation of gallbladder contraction, we investigated gallbladder volume reduction, plasma cholecystokinin (CCK), and pancreatic polypeptide (PP) responses in humans during cephalic and intestinal phases of a meal under M1 muscarinic receptor blockade with pirenzepine. METHODS: In eight healthy subjects, intraduodenal meal- and in seven subjects, sham feeding-induced gallbladder volume reduction was measured by real-time ultrasonography during saline or pirenzepine administration. Plasma CCK and PP were measured by radioimmunoassay. RESULTS: Pirenzepine partially inhibited gallbladder volume reduction in response to an intraduodenal fatty meal. The integrated gallbladder volume reduction over 120 min was 4462 +/- 445%.min compared with 6879 +/- 279%.min in the saline control group (p < 0.01). Integrated plasma CCK and PP responses were unchanged in the presence of pirenzepine. Pirenzepine abolished sham feeding-induced gallbladder contraction and plasma PP response. Sham feeding with either isotonic saline or pirenzepine infusion did not modify fasting plasma CCK levels. CONCLUSION: M1 muscarinic receptors play an important role in the intestinal and cephalic phases of gallbladder contraction. Plasma CCK response to intraduodenal meal is not influenced by M1 muscarinic receptor blockade with pirenzepine.

Adult↗
PubMed1994

The involvement of muscarinic receptors in gastric liquid emptying in the conscious rat following Roux-en-Y-antrectomy.

The gastric emptying of liquid test meals is dependent on resistance to flow at the pylorus and on pressure gradients between the duodenum and the body of the stomach. In the present study, we investigated the role and subtypes of muscarinic receptors during gastric emptying of various liquid test meals in conscious rats with gastric fistula after Roux-en-Y antrectomy. In the control rats with gastric fistula but with intact reflex pathways and pylorus, the non-selective muscarinic antagonist atropine (7 mg/kg i.p.) and M1-selective pirenzepine (7 mg/kg i.p.), acting possibly on M1 receptors, delayed saline emptying by suppressing cholinergic tone and thus relaxing the body of the stomach and contracting the pyloric sphincter. On the other hand, in Roux-rats saline and hyperosmolal saline emptying were not significantly affected, while the inhibitory effect of HCl was completely reversed. Furthermore, peptone-induced delay of gastric emptying in control rats was also reduced in Roux-rats. Pirenzepine abolished the facilitating effects of Roux-en-Y operation on acid and peptone emptying and M2-selective antagonist AF DX-116 (7 mg/kg i.p.) did not have any inhibitory effect in this regard. In conclusion, Roux-en-Y gastrectomy without vagotomy does not slow gastric emptying of liquids, and it reverses the inhibitory effects of peptone and acid through an atropine- and pirenzepine-sensitive pathway.

Anastomosis, Roux-en-Y↗