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  1. Ridzwan BH, Waton NG, Jais AM
    Gen. Pharmacol., 1989;20(2):133-6.
    PMID: 2565846
    1. Acid secretion for each dog has reached a near maximum (100%) at the 6th samples, 90 min after the intravenous infusion of histamine (10 mu ghr-1, or approximately equal to 0.3 mghr-1). 2. 0.5 mgkg-1 Cimetidine had produced a mean inhibition of 47% on the stomach. 3. 0.1 mgkg-1 Ranitidine (D 14,951) could only inhibit a maximum of 28%, and the secretion had return to normal in just 30 min. 4. 0.025 mgkg-1 Tiotidine (D 15,104) had inhibited 53% acid secretion within 15 min of exposure. Recovery was quite similar to that of Cimetidine, at 150 min. 5. At a dosage one fifth of Cimetidine (0.1 mgkg-1) D 15,144 had depressed 35% of acid secretion at the first 15 min. The inhibition is gradually increased to about 43% (at 30 min), and was maintained for the next 105 min.
    Matched MeSH terms: Gastric Acid/metabolism*
  2. Ti TK
    Ann Acad Med Singap, 1981 Apr;10(2):198-200.
    PMID: 7332283
    Paired augmented histamine tests using 40 microgram 60 microgram histamine acid phosphate (HAP) per kg body weight were conducted on each of 57 Asian subjects. The mean peak acid output (PAO) for the total series to the two different doses of HAP was 22.3 mEq/hr and 23.3 mEq/hr respectively and the difference was not statistically significant according to the paired t test. There were similarly no significant difference in PAO to the two doses of HAP in the following groups of subjects: 26 Chinese, 17 Indians, 14 Malays; 24 subjects with duodenal ulcer, 16 controls; 28 subjects with body weight below 50 kg, 19 between 50-60 kg and 10 exceeding 60 kg. These findings differ from earlier reports that for maximal gastric secretion Asians required a higher dosage of histamine compared with Caucasian subjects.
    Matched MeSH terms: Gastric Acid/metabolism*
  3. Adamu Ahmad K, Sabo Mohammed A, Abas F
    Molecules, 2016 Mar 14;21(3):256.
    PMID: 26985885 DOI: 10.3390/molecules21030256
    The use of chitosan as a delivery carrier has attracted much attention in recent years. In this study, chitosan nanoparticles (CS-NP) and chitosan-ΦKAZ14 bacteriophage-loaded nanoparticles (C-ΦKAZ14 NP) were prepared by a simple coercavation method and characterized. The objective was to achieve an effective protection of bacteriophage from gastric acids and enzymes in the chicken gastrointestinal tract. The average particle sizes for CS-NP and C-ΦKAZ14 NP were 188 ± 7.4 and 176 ± 3.2 nm, respectively. The zeta potentials for CS-NP and C-ΦKAZ14 NP were 50 and 60 mV, respectively. Differential scanning calorimetry (DSC) of C-ΦKAZ14 NP gave an onset temperature of -17.17 °C with a peak at 17.32 °C and final end set of 17.41 °C, while blank chitosan NP had an onset of -20.00 °C with a peak at -19.78 °C and final end set at -20.47. FT-IR spectroscopy data of both CS-NP and C-ΦKAZ14 NP were the same. Chitosan nanoparticles showed considerable protection of ΦKAZ14 bacteriophage against degradation by enzymes as evidenced in gel electrophoresis, whereby ΦKAZ14 bacteriophage encapsulated in chitosan nanoparticles were protected whereas the naked ΦKAZ14 bacteriophage were degraded. C-ΦKAZ14 NP was non-toxic as shown by a chorioallantoic membrane (CAM) toxicity assay. It was concluded that chitosan nanoparticles could be a potent carrier of ΦKAZ14 bacteriophage for oral therapy against colibacillosis in poultry.
    Matched MeSH terms: Gastric Acid/metabolism
  4. Azlina MF, Nafeeza MI, Khalid BA
    Asia Pac J Clin Nutr, 2005;14(4):358-65.
    PMID: 16326642
    Rats exposed to stress developed various changes in the gastrointestinal tract and hormones. The present study was designed to compare the impact of tocopherol and tocotrienol on changes that influence gastric and hormonal parameters important in maintaining gastric mucosal integrity in rats exposed to restrain stress. These include gastric acidity, gastric tissue content of parameters such as malondialdehyde, prostaglandin (PGE(2)), serum levels of gastrin and glucagon-like peptide-1 (GLP-1). Sixty male Sprague-Dawley rats (200-250 g) were randomly divided into three equal sized groups, a control group which received a normal rat diet (RC) and two treatment groups each receiving a vitamin deficient diet with oral supplementation of either tocopherol (TF) or tocotrienol (TT) at 60 mg/kg body weight. Blood samples were taken from half the number of rats (non-stressed group) after a treatment period of 28 days before they were killed. The remaining half was subjected to experimental restraint-stress, at 2 hours daily for 4 consecutive days (stressed groups), on the fourth day, blood samples were taken and the rats killed. The findings showed that the gastric acid concentration and serum gastrin level in stressed rats were significantly (P<0.05) reduced compared to the non-stressed rats in the control and TF groups. However, the gastric acidity and gastrin levels in the TT group were comparable in stressed and non-stressed rats. These findings suggest that tocotrienol is able to preserve the gastric acidity and serum gastrin level which are usually altered in stressed conditions. The PGE(2) content and the plasma GLP-1 level were, however, comparable in all stressed and non-stressed groups indicating that these parameters were not altered in stress and that supplementation with TF or TT had no effect on the gastric PGE2 content or the GLP-1 level. The malondialdehyde, an indicator of lipid peroxidation was higher from gastric tissues in the stressed groups compared to the non-stressed groups. These findings implicated that free radicals may play a role in the development of gastric injury in stress and supplementation with either TF or TT was able to reduce the lipid peroxidation levels compared to the control rats. We conclude that both tocopherol and tocotrienol are comparable in their gastro-protective ability against damage by free radicals generated in stress conditions, but only tocotrienol has the ability to block the stress-induced changes in the gastric acidity and gastrin level.
    Matched MeSH terms: Gastric Acid/metabolism
  5. Ti TK
    Ann Acad Med Singap, 1983 Oct;12(4):507-17.
    PMID: 6678134
    Basal and pentagastrin stimulated acid output was measured in 80 normal and 179 duodenal ulcer subjects of Chinese, Indian and Malay origin. Basal and maximally stimulated acid output was significantly higher in duodenal ulcer patients compared with normal subjects. There was however considerable overlap and less than one in four duodenal ulcer patients were hypersecretors. The acid output (and hence the parietal cell mass) was lower than in Caucasian subjects and this was possibly related to weight differences. The acid output did not differ significantly in the Chinese, Indian and Malay subjects, suggesting that parietal cell mass in the three racial groups is closely similar. The difference in frequency of duodenal ulcer disease in the three racial groups is thus not related to gastric secretory capacity.
    Matched MeSH terms: Gastric Acid/metabolism*
  6. Satyanarayana MN
    Crit Rev Food Sci Nutr, 2006;46(4):275-328.
    PMID: 16621751
    In recent years, infection of the stomach with the organism Helicobacter Pylori has been found to be the main cause of gastric ulcers, one of the common ailments afflicting humans. Excessive acid secretion in the stomach, reduction in gastric mucosal blood flow, constant intake of non-steroid anti-inflammatory drugs (NSAIDS), ethanol, smoking, stress etc. are also considered responsible for ulcer formation. The prevalent notion among sections of population in this country and perhaps in others is that "red pepper" popularly known as "Chilli," a common spice consumed in excessive amounts leads to "gastric ulcers" in view of its irritant and likely acid secreting nature. Persons with ulcers are advised either to limit or avoid its use. However, investigations carried out in recent years have revealed that chilli or its active principle "capsaicin" is not the cause for ulcer formation but a "benefactor." Capsaicin does not stimulate but inhibits acid secretion, stimulates alkali, mucus secretions and particularly gastric mucosal blood flow which help in prevention and healing of ulcers. Capsaicin acts by stimulating afferent neurons in the stomach and signals for protection against injury causing agents. Epidemiologic surveys in Singapore have shown that gastric ulcers are three times more common in the "Chinese" than among Malaysians and Indians who are in the habit of consuming more chillis. Ulcers are common among people who are in the habit of taking NSAIDS and are infected with the organism "Helicobacter Pylori," responsible for excessive acid secretion and erosion of the mucosal layer. Eradication of the bacteria by antibiotic treatment and avoiding the NSAIDS eliminates ulcers and restores normal acid secretion.
    Matched MeSH terms: Gastric Acid/metabolism*
  7. Deraman MA, Abdul Hafidz MI, Lawenko RM, Ma ZF, Wong MS, Coyle C, et al.
    Aliment Pharmacol Ther, 2020 06;51(11):1014-1021.
    PMID: 32343001 DOI: 10.1111/apt.15746
    BACKGROUND: Late-night supper increases the risk of postprandial reflux from the acid pocket especially in obesity. An alginate-based, raft-forming medication may be useful for obese patients with GERD.

    AIMS: To compare the efficacy of Gaviscon Advance (Reckitt Benckiser, UK) and a non-alginate antacid in post-supper suppression of the acid pocket and post-prandial reflux among obese participants.

    METHODS: Participants underwent 48 h wireless and probe-based pH-metry recording of the acid pocket and lower oesophagus, respectively, and were randomised to single post-supper (10 pm) dose of either Gaviscon Advance or a non-alginate antacid on the second night. Primary outcomes were suppression of median pH of acid pocket and lower oesophagus, measured every 10-minutes post-supper for 1 h. Secondary outcomes were suppression of % time pH acid pocket but not the lower oesophagus was suppressed with Gaviscon Advance vs antacid (all P acid pocket. (Clinical trial registration unique identifier: NCT03516188).

    Matched MeSH terms: Gastric Acid/metabolism
  8. Qodriyah HM, Asmadi AY
    Pak J Biol Sci, 2013 Dec 01;16(23):1815-8.
    PMID: 24506055
    The effect of treatment with Radix on ethanol-induced gastric lesions was investigated. The main ingredient of Radix is Eurycoma longifolia. Twenty-four rats of the Sprague-Dawley species were randomly divided into four groups. Three groups were given 0.5 mL 100% ethanol orally. Another group was used as a control and was given only distilled water orally (control). After 6 h all the rats were fed with normal diet. One group that was administered with ethanol was only given distilled water orally (no treatment). Another two groups that were administered with ethanol were treated with oral Radix 0.128 mg g(-1) b.wt. (Radix) and oral ranitidine 21.4 mg kg(-1) b.wt. (Ranitidine), respectively. After one week, all the rats were fasted overnight and sacrificed. The stomach was isolated and examined for the presence and severity of gastric lesions. Measurements for malondialdehyde content and gastric acid concentration were also done. It is found that the ulcer index was lower in the Radix and ranitidine group compared to the no treatment group whereas in the control group there was no lesion. There was no difference in ulcer index between the Radix and ranitidine group. The gastric MDA content was significantly higher in all the groups that were induced with ethanol compared to the control group but no difference between all the ethanol-induced groups. There was no difference in the gastric acid concentration in all groups. Hence it is concluded that Eurycoma longifolia in Radix is as effective as ranitidine in the treatment of ethanol-induced gastric lesions in rats.
    Matched MeSH terms: Gastric Acid/metabolism
  9. Taha MM, Salga MS, Ali HM, Abdulla MA, Abdelwahab SI, Hadi AH
    J Ethnopharmacol, 2012 May 7;141(1):273-81.
    PMID: 22374081 DOI: 10.1016/j.jep.2012.02.030
    Turnera diffusa Willd. ex Schult. has been used for the treatment of several human disorders including peptic ulcer.
    Matched MeSH terms: Gastric Acid/metabolism
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