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Biomedical subjects

G B Glavin

Publications and source records attributed to G B Glavin.

112 records · Page 7Linked to original sources

The effects of environmental enrichment on voluntary ethanol consumption and stress ulcer formation in rats.

The effects of exposure to an enriched environment on subsequent voluntary ethanol intake and response to restraint stress were examined. Rats at 21 days of age were reared in an enriched environment for 90 days. Non-enriched animals were reared individually in standard laboratory cages. Following an initial 36 day ethanol exposure period, voluntary ethanol (9% v/v) preference was assessed for 10 days. In addition, at the conclusion of the ethanol test session, animals were exposed to restraint stress for a 3 hr period. Results indicate that exposure to an enriched environment produces increased voluntary ethanol consumption as compared to non-enriched controls. Furthermore, animals reared in the enriched environment demonstrated reduced gastric ulcer severity in response to restraint stress. Ethanol per se did not affect ulcer formation.

Alcohol Drinking↗

Ethanol-stress interaction: immediate versus delayed effects of ethanol and handling on stress responses of ethanol-consuming rats.

Rats screened for voluntary ethanol intake (high, medium, and low ethanol-preferring rats and non-ethanol-exposed controls) were given acute immobilization stress either immediately following the ethanol screening procedure, or after a 20 day period without access to ethanol. Among animals examined for stress responses immediately after ethanol screening, it was observed that water-only control rats developed significantly less frequent and less severe gastric stress ulcers than rats in all ethanol-exposed groups. This result suggests that ethanol, stress and routine handling may have contributed to ulcer formation in these animals. In contrast, among rats tested for stress responses after 20 days without ethanol, it was observed that the high ethanol-preferring animals showed less severe stress ulcers. These results indicate that among high ethanol-consuming animals, the presence of ethanol enhances ulcer severity, while prior experience with ethanol consumption does not appear to predispose rats to exacerbated stress gastric pathology.

Alcohol Drinking↗

Calcium modulators and the gut: an update.

Calcium is critical for stimulus-secretion coupling at the cellular level in the gut. Recent experimental evidence suggests a role for calcium modulating compounds in vivo. Specifically, calcium channel blocking drugs of the dihydropyridine class exert potent anti-secretory and anti-stress ulcer effects. However, these same compounds exacerbate ethanol-induced gastric mucosal injury. Calcium chelating compounds, including EDTA and EGTA, reduce both forms of experimental ulcer as well as gastric secretion. Mechanisms underlying the gastroprotective effects of calcium modulating agents include neural, hormonal, peptide and enzymatic activity and these compounds represent a viable avenue of research for future therapeutic development.

Animals↗

Effects of prenatal caffeine administration on offspring mortality, open-field behavior and adult gastric ulcer susceptibility.

Pregnant rats were given caffeine (0.0%, 0.017%, 0.034% or 0.05%) in their drinking water throughout gestation. Offspring were cross-fostered to non-caffeine-treated mothers at birth. A dose-related increase in offspring mortality was observed at 24 hr and at 10 days post partum. Prenatal caffeine exposure did not significantly influence open-field ambulation or defecation when tested at 48, 68, or 196 days of age. A significant dose-related increase in restraint-stress gastric ulcer susceptibility was detected at 200 days of age. Offspring from rats treated with 0.05% caffeine during pregnancy, developed significantly more frequent and significantly more severe gastric lesions than did offspring from control rats or from rats prenatally exposed to 0.017% and 0.034% caffeine. Prenatal caffeine exposure may: (1) predispose organisms to increased gastric disease susceptibility as adults and (2) interfere with neonatal feeding ability and thereby produce infant mortality.

Animals↗