Gastric acid secretion in streptozotocin-diabetic rats – Different responses to various secretagogues

Tashima, Kimihito; Nishijima, M.; Fujita, Akinobu; Kawauchi, Shoji; Takeuchi, Koji

doi:10.1016/s0928-4257(99)00118-7

Cited by 10 publications

(9 citation statements)

References 17 publications

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“…This finding was consistent with our previous study which was conducted on female Wistar rats using the same preparation for gastric acid measurement [13]. Interestingly, Tashima et al [14] also found an augmentation of the pentagastrin-stimulated acid output in STZ-treated rats. In contrast, long-term diabetic rats had a lower gastric acid secretion during both basal and histamine-stimulated periods [10].…”

Section: Discussionsupporting

confidence: 92%

“…It is uncertain whether their finding suggests impaired histamine H 2 receptors in diabetic rats and a changed affinity of H 2 RAs to their corresponding receptors, in turn leading to a poor acid-reducing potency of ranitidine. Third, an enhanced release of mucosal histamine is suggested to lead to an augmented pentagastrinsimulated acid output in STZ-treated rats [14]. Accordingly, the usual dose of ranitidine could not suppress the enhanced histamine release in diabetic rats, in turn leading to a poor acid-inhibitory potency as compared with controls.…”

Section: Discussionmentioning

confidence: 96%

“…Perhaps the regulation of acid output is mediated via several pathways among diabetic patients. For instance, Tashima et al [14] pointed out that vagus nerve stimulation diminished rather than increased the acid output among diabetic rats. Based on their observations, an increased mucosal histamine release after pentagastrin stimulation is suggested to be responsible for the enhanced stimulated acid output, whereas vagal neuropathy leads to a diminished acid output.…”

Section: Discussionmentioning

confidence: 99%

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Acid-Inhibitory Potency of Ranitidine in Diabetic Rats

Chang

Chen²,

Lee³

et al. 2002

Pharmacology

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The pharmacological potency of ranitidine to inhibit pentagastrin-stimulated gastric acid outputs was studied in early diabetic rats. Diabetes was induced by intravenous injection of streptozotocin 4 days before the acid study. The gastric acid output was measured every 5 min by automatic titration of collected gastric perfusates. Basal acid was collected for 45 min before a 90-min infusion of pentagastrin. Thirty minutes after onset of the pentagastrin infusion, the rats received intravenous bolus injections of ranitidine at doses of 0.03, 0.3, or 3 mg/kg. Diabetes induction obviously increased the acid-secretory ability during the pentagastrin stimulation period. Ranitidine given at the low dose to diabetic rats showed no apparent inhibitory potency (mean ± SE 106 ± 3.4 vs. 63.9 ± 3.3%, p < 0.01) with shorter duration (21.3 ± 5.4 vs. 44.4 ± 7.9 min, p < 0.05) of inhibited acid output as compared with controls. The median dose of ranitidine treatment produced less effect of an acid-inhibitory potency in diabetic rats (p < 0.05). Among the rats which received the high dose of ranitidine, the inhibitory action on the acid secretion remained diminished in diabetic rats (39.3 ± 2.1 vs. 55.1 ± 4.2%, p < 0.05). In conclusion, short-term diabetes induction in rats enhances their stimulatory acid output ability, but attenuates the pharmacologically inhibitory action of ranitidine on the stimulated acid output.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

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Acid-Inhibitory Potency of Ranitidine in Diabetic Rats

Chang

Chen²,

Lee³

et al. 2002

Pharmacology

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“…In rats with streptozotocininduced diabetes, gastric acid secretion decreases in response to vagal electrical stimulation, which suggests that a vagal neuropathy is present. 58,59 A reduction in pyloric relaxation has been noted after gastric distension if acute hyperglycemia is induced in rats; pyloric sphincter dysfunction has been suggested to be mediated by vagal damage because this effect can also be induced by subdiaphragmatic vagotomy and hexamethonium. 60 In addition, acute hyperglycemia impairs antral contractions and antropyloric coordination, which is caused, at least in part, by impaired vagal activity.…”

Section: Changes In Extrinsic Innervationmentioning

confidence: 99%

Mechanisms of Disease: the pathological basis of gastroparesis—a review of experimental and clinical studies

Vittal

Farrugia

Gómez

et al. 2007

Nat Rev Gastroenterol Hepatol

100

103

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The pathogenesis of gastroparesis is complicated and poorly understood. This lack of understanding remains a major impediment to the development of effective therapies for this condition. Most of the scientific information available on the pathogenesis of gastroparesis has been derived from experimental studies of diabetes in animals. These studies suggest that the disease process can affect nerves (particularly those producing nitric oxide, but also the vagus nerve), interstitial cells of Cajal and smooth muscle. By contrast, human data are sparse, outdated and generally inadequate for the validation of data obtained from experimental models. The available data do, however, suggest that multiple cellular targets are involved. In practice, though, symptoms seldom correlate with objective measures of gastric function and there is still a lot to learn about the pathophysiology of gastroparesis. Future studies should focus on understanding the molecular pathways that lead to gastric dysfunction, in animal models and in humans, and pave the way for the development of rational therapies.

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“…After anaesthetized with Sodium Pentobarbital (40 mg/Kg injected ip), they were randomly divided into two experimental groups (n = 12), according to the different administrations. In Group I: Gastric acid secretion was measured in a chambered stomach which prepared according to the previously described (Tashima et al, 2000). Briefly, the abdomen was incised, and both the stomach and duodemun were exposed and tied respectively; then 1.5 ml 0.9% sodium chloride (containing Alarelin, 2 Ag/Kg) was infused into the each chambered stomach.…”

Section: Effects Of Gnrh-1 Analogue On Gastric Acid Secretionmentioning

confidence: 99%