Self-medication among university students in Hong Kong.

Five hundred and sixty-three university students were interviewed to survey the practice of self-medication which was found to be very prevalent (94.0%). The most commonly used items included remedies for cough and cold, antipyretics and analgesics. Topical preparations and Chinese herbal medicines were also frequently consumed. Self-medication items were mostly obtained from home medicine cabinets and pharmacy shops (not necessarily staffed by registered pharmacists) and they also relied heavily on family members and previous illness experience for information on the medications they took. The healthcare professionals only played a minor role in the provision of drug information. Nevertheless, the concept of self-medication is well-established among these university students as they recognised that minor illness could be cared for without seeing a doctor. Healthcare professionals should assume more active roles in the provision of drug information and counselling so that a good self-care programme could be established.

The gastric cytoprotective action of adenosine and prostaglandin E2 in rabbits.

The direct protective action of adenosine and prostaglandin E2 (PGE2) was examined in an isolated gastric gland preparation in rabbits. Ethanol (8%, v/v) incubation markedly increased the release of lactate dehydrogenase (LDH) and number of non-viable glands in the preparation. Both effects were prevented by PGE2 preincubation in a concentration (10(-6), 1.4 x 10(-5) or 2.8 x 10(-5) M)-dependent manner. The protective action was smaller in adenosine-treated groups, and yet the highest concentration (10(-4) M) of the compound also significantly inhibited the cytotoxic effects of ethanol. These findings indicate that both adenosine and PGE2 possess cytoprotective action on gastric glands in rabbits, but the former compound exerts its action beyond physiological concentrations. It is concluded that endogenous PGE2, but not adenosine may act as an ulcer modulator in the stomach.

Influence of chronic nicotine intake and acute ethanol challenge on gastric mucus level and blood flow in rabbits.

The effects of nicotine pretreatment on ethanol-induced gastric mucosal lesions and changes of gastric mucosal mucus levels and blood flow (GBF) were studied in anaesthetized rabbits. Nicotine treatment 25 or 50 micrograms/ml drinking water did not affect the volume of water consumption during the 10-day experimental period. It did not produce gastric mucosal lesions or affect the superficial adherent mucus content. The length of mucus-containing cells and the basal GBF were also unaffected. Intragastric administration of absolute ethanol reduced GBF, this effect was not altered by nicotine. However, the alkaloid potentiated the ulcerogenic actions of ethanol both on lesion formation and mucus depletion evoked by graded oral doses of ethanol (50 or 100%, v/v). Ultrastructurally, the mucous cells were more degenerated in the animals co-treated with nicotine and ethanol. It is concluded that reductions of mucus-containing cells and adherent mucus on the gastric mucosa are likely to be the contributory factors involved in the aggravating action of nicotine on ethanol-induced gastric mucosal lesions in rabbits.

Effect of epidermal growth factor on gastric blood flow in rats: possible role in mucosal protection.

BACKGROUND: The mechanism by which epidermal growth factor (EGF) protects the gastric mucosa against injury is unclear. Whether EGF has any effect on gastric blood flow has not been reported. METHODS: Using an ex vivo gastric chamber preparation, the effect of EGF on gastric blood flow in rats was studied by laser Doppler flowmetry. Measurements of blood flow and mucosal damage were made in both intact and sialoadenectomized rats with graded doses of EGF at basal condition and after topical application of absolute ethanol. RESULTS: Sialoadenectomy alone increased ethanol-induced gastric mucosal lesions (P < 0.05) but had no significant effect on blood flow. EGF pretreatment resulted in both a reduction in ethanol-induced gastric mucosal injury as well as a significant increase in blood flow compared with controls (both P < 0.05). Graded doses of EGF (3.12-25 micrograms) resulted in an dose-dependent increase in gastric blood flow (r = 0.68; P < 0.001), which correlated inversely with the degree of mucosal damage (r = -0.72; P < 0.001). CONCLUSIONS: Mucosal protection by EGF is accompanied by an increase in gastric blood flow; this action may contribute to its mucosal protective effect.

The cytoprotective effect of zinc L-carnosine on ethanol-induced gastric gland damage in rabbits.

The effects of zinc L-carnosine on the damaging actions of ethanol were examined in rabbit isolated gastric glands. Ethanol (8%, v/v) incubation produced a 50% viability of the gland populations and released a significant amount (38%) of the total lactate dehydrogenase (an index of membrane injury) of the glands. Zinc L-carnosine pre-incubation for 15 min markedly prevented these actions of ethanol; however, L-carnosine by itself did not have these effects. The findings indicate that zinc ion but not carnosine in the zinc L-carnosine molecule possesses cytoprotective action against ethanol-induced gastric gland damage in rabbits.

Time course study on the action of 5-hydroxytryptamine on gastric secretion and mucosal blood flow and on ethanol-induced gastric mucosal damage in rats.

The effects of 5-hydroxytryptamine (5-HT; given i.p. in doses of 1 or 10 mg/kg) on gastric secretion and mucosal blood flow (GMBF) and on ethanol-induced gastric mucosal damage were studied in rats over a period of 30-450 min. The blood pressure was also examined, in relation to the changes in GMBF. 5-HT, 10 mg/kg, given 30 min before ethanol administration markedly worsened lesion formation and this potentiating action was present for a further 90 min; a significant protective effect was seen only at 450 min after 5-HT injection. The lower dose of 5-HT, 1 mg/kg, did not affect the severity of gastric damage. 5-HT (10 mg/kg) also decreased GMBF at 30 min after injection and this lasted up to the end of 120 min, but the depressive action of ethanol on GMBF was reversed at 450 min. The basal gastric secretory volume was depressed from 30 to 120 min but acid output fell from 75 to 120 min after the higher dose of 5-HT; this reduction of acid secretion was followed by an increase from 360 to 450 min. 5-HT decreased the mean blood pressure in a dose- and time-dependent manner. The heart rate was unaffected by either dose level of 5-HT. The present study not only demonstrates the ulcerogenic action of 5-HT but also the protective nature of the amine. The reduction in secretory volume and lesion formation, but not acid secretion, seems to be related to GMBF depression, whereas the protective action depends on the maintenance of GMBF.

Effects of adenosine on gastric and cardiovascular systems, and ethanol ulceration in male and female rats.

The time course of the effects of adenosine, a vasodilator, on the ulcerogenicity of ethanol was studied in male and female rats. Gastric secretory function and mucosal blood flow (GMBF), systemic blood pressure and heart rate were monitored during the 90-min experimental period. In the male rats, adenosine 7.5 mg/kg s.c. (injected at 30 min) increased the GMBF at 45 min and depressed it at 75 min. The mean blood pressure was decreased at 45 min and steadily recovered thereafter; the heart rate was unaffected throughout the experimental period. The gastric secretory volume was elevated at 60 min, with a significant drop in gastric acid output at the same time. Ethanol administration from 45 to 90 min produced haemorrhagic lesions in the glandular mucosa. The severity of gastric damage was markedly reduced by adenosine at 45 and 60 min when the GMBF and the secretory volume were increased respectively, but severity was increased at 75 min while the GMBF was significantly reduced. In the female rats, adenosine had no effect on the secretory function but still had a depressive action on GMBF at the 75th min. In these animals, adenosine exacerbated the gastric injury at 60 and 75 min. The blood pressure was also decreased at 45 min. In conclusion, adenosine produces a different pattern of effects on the ulcerogenic action of ethanol in male and in female rats. These differential effects depend on the states of GMBF and gastric secretory volume but not on the changes of systemic blood pressure and gastric acid secretion.

Nicotine induced gastric injury. A quantitative macroscopic and microscopic analysis of the protective effects of sucralfate and feeding.

Nicotine, while an important component of cigarettes, does not cause gross gastric mucosal damage, although its microscopic effect remains unknown. We have evaluated the histology and the microvascular permeability of (a) the effect of nicotine alone or in combination with ethanol on the gastric mucosa of rats and (b) the effect of feeding and sucralfate on the mucosa of rats treated with nicotine and ethanol. Mucosal injury was assessed histologically by the depth of injury and microvascular permeability by the leakage of fluorescein isothiocyanate-labelled albumin. Our results show that nicotine induced microscopic mucosal damage and accentuated the damage induced by alcohol. The damaging effects on mucosa of nicotine and ethanol, alone or in combination, were reduced by pretreatment with sucralfate. Similarly, feeding reduced the degree of mucosal injury. Nicotine and ethanol increased leakage of albumin into the interstitium and the leakage was reduced after sucralfate pretreatment. This study substantiates the adverse effect of smoking on mucosal damage. Vascular factors are probably involved in the pathogenesis.

The membrane-stabilizing action of zinc carnosine (Z-103) in stress-induced gastric ulceration in rats.

Zinc compounds have been shown to antagonize various types of gastric ulceration in rats. Zinc carnosine (Z-103), a newly developed agent was, therefore, examined for its antiulcer effect in stress-induced ulceration and also its membrane stabilizing action in rat stomachs. Cold-restraint (restrained at 4 degrees C for 2 h) stress induced severe hemorrhagic lesions together with increased mast cell degranulation and beta-glucuronidase release in the gastric glandular mucosa. Z-103 pretreatment with a single oral dose (3, 10 or 30 mg/kg) reversed these actions in a dose-dependent manner. When the compound was incubated in concentrations of 10(-7, 10(-6), 10(-5) or 10(-4) M, with isolated hepatic lysosomes, it significantly reduced the spontaneous release of beta-glucuronidase in the medium. The present study not only demonstrates the antiulcer effect of Z-103 but also indicates that the protective action is likely to be mediated by its membrane-stabilizing action on mast cells and lysosomes in the gastric glandular mucosa.

Role of gastric mucosal blood flow in cytoprotection.

We compared the effects of graded doses of misoprostol (50-200 mg), omeprazole (12.5-50 mg), cimetidine (6.25-50 mg) and sucralfate (50-200 mg) on gastric mucosal blood flow as measured by laser Doppler flowmetry and gastric mucosal injury induced by ethanol. The results demonstrated that sucralfate, misoprostol and omeprazole, but not cimetidine, increased gastric mucosal blood flow in a dose-dependent manner and protected the mucosa against ethanol damage. The peak and summation blood flow were significantly greater with sucralfate than with misoprostol and omeprazole, but the degree of mucosal protection was similar. These results indicate that the increase in gastric mucosal blood flow, an action which is common to the three drugs, plays an important role in gastric mucosal protection, but other factors are also involved.

The effect of misoprostol, omeprazole and sucralfate on nicotine- and ethanol-induced gastric injury and gastric mucosal blood flow: a comparative study.

Nicotine, which is thought to be responsible for part of the pharmacological effect of smoking, exacerbates gastric mucosal injury in rats. The effects of misoprostol (12.5 micrograms to 100 micrograms), omeprazole (12.5 mg to 100 mg) and sucralfate (50 to 400 mg) on gastric mucosal blood flow and mucosal injury induced by nicotine were studied in an ex vivo gastric chamber preparation in rats. Rats were pretreated with nicotine (25 micrograms/mL orally) for 10 days and ethanol was added to the gastric chamber preparation. Laser Doppler flowmetry was used to measure the gastric mucosal blood flow and mucosal damage (ulcer index) was assessed by the area of haemorrhagic lesions. The ulcer index was significantly higher in rats pretreated with nicotine. Treatment with misoprostol and omeprazole lowered the ulcer index significantly compared with controls. The peak and summation blood flows were lower in nicotine-treated rats but failed to reach statistical significance. The peak blood flow (blood flow at 45 min) and the summation blood flow were significantly higher with all doses of sucralfate, misoprostol and omeprazole than in controls (P less than 0.05). The increase in gastric mucosal blood flow was significantly higher with sucralfate and misoprostol than with omeprazole. We conclude that sucralfate, misoprostol and omeprazole prevent nicotine- and ethanol-induced gastric mucosal damage and are accompanied by an increase in gastric mucosal blood flow. This indicates that smoking exacerbates gastric mucosal injury and that cytoprotective and site-protective agents can reduce injury by these noxious agents.

Endogenous prostaglandins: its role in gastric mucosal blood flow and ethanol ulceration in rats.

The involvement of endogenous prostaglandins (PGs) in modulating gastric mucosal blood flow (GMBF) is still unclear. The present study was designed to demonstrate the role of this autacoid in the basal GMBF and the restoration of blood flow after restriction of blood supply to the stomach. The ex-vivo gastric chamber was prepared and the GMBF was measured by a laser Doppler technique. 20% ethanol incubation for 10 min in the chamber increased the basal GMBF and lessened the reduction of blood flow induced by absolute ethanol. It also decreased lesion formation caused by ethanol. Indomethacin 5 mg/kg, given s.c 60 min before experimentation had the opposite effects. Ligation of the gastric artery for 20 min which reduced the GMBF by 60%, worsened ethanol ulceration. There was a marked rebound of the GMBF after the ligation was released. Indomethacin totally abolished the blood flow rebound and aggravated ethanol ulceration. However, 20% ethanol incubation significantly potentiated such a rebound in blood flow and reduced lesion formation. Indomethacin pretreatment reversed these actions, whereas misoprostol administration produced the similar effects as 20% ethanol. It is concluded that GMBF plays an important role in ethanol ulceration and both basal and rebound GMBF is probably modulated by endogenous PGs.

Effect of sucralfate on gastric mucosal blood flow in rats.

Sucralfate possesses site protective and cytoprotective actions and heals ulcers effectively, but its effect on gastric mucosal blood flow is unknown. Using an ex vivo gastric chamber preparation, we studied the effect of sucralfate on gastric mucosal blood flow in rats by laser doppler flowmetry. Under both fasting and fed states, measurements of gastric mucosal blood flow and damage were made in rats after topical application of absolute ethanol alone or after pretreatment with sucralfate. Gastric mucosal damage was assessed by measuring the total area of haemorrhagic mucosal lesions. Ethanol induced gastric mucosal lesions were significantly less with sucralfate pretreatment than without (p less than 0.008). Mucosal blood flow significantly fell after ethanol application (p less than 0.001). The fall was significantly less in fed than in fasted rats (p less than 0.05), and after pretreatment with sucralfate 100 mg or 200 mg than without in both fasted (p less than 0.0008 and 0.00001, respectively) and fed (p less than 0.002 and 0.001, respectively) rats. Graded doses of sucralfate (25-400 mg) resulted in an increase in gastric mucosal blood flow in a dose dependent manner (r = 0.731, p less than 0.001). In conclusion that sucralfate increases gastric mucosal blood flow in rats and lessens the fall in blood flow in rats treated with ethanol, and this action may contribute to its protection against the vascular damage of mucosa by ethanol.