Implications of gastric topical bioactive peptides in ammonia-induced acute gastric mucosal lesions in rats

BACKGROUND: Ammonia, one of the pathogenic factors in Helicobacter pylori-induced mucosal injury, induces acute mucosal lesions in the rat glandular stomach. METHODS: The effect of ammonia administered intragastrically on gastric peptides was investigated in urethane-anesthetized rats. RESULTS: Gastric mucosal lesions were observed 5 min after 0.3% ammonia (4 ml/kg, intragastrically). Immunoreactive endothelin-1 (ET-1) and immunoreactive thyrotropin-releasing hormone (TRH) concentrations in the gastric wall decreased significantly 2 min and 5 min after ammonia, respectively. A significant increase in gastric juice immunoreactive ET-1 and TRH levels was reciprocally observed. The severity of gastric mucosal injury and changes in gastric immunoreactive ET-1 and TRH concentrations were shown to be concentration-dependent 30 min after ammonia. Atropine (5 mg/kg, intraperitoneally, -20 min) prevented ammonia-induced injury accompanied by a block of changes in gastric immunoreactive ET-1 and TRH concentrations. BQ-485 (ET(A) receptor antagonist; 2 mg/kg, subcutaneously) also abolished ammonia-induced lesions and gastric immunoreactive TRH changes. CONCLUSIONS: These findings suggested that gastric ET-1 and TRH play a role in ammonia-induced gastric mucosal injury mediated via a muscarine and an ET(A) receptor.     

Dehydration and hydration behavior of metal-salt-modified materials for chemical heat pumps

Lithium chloride (LiCl) modified magnesium hydroxide (Mg(OH)₂) is a potential new material for chemical heat pumps. However, there is insufficient information concerning its dehydration and hydration behavior. In this study, the dehydration and hydration reactions, corresponding to the heat storage and the heat output operations, respectively, of authentic Mg(OH)₂ and LiCl-modified Mg(OH)₂ were investigated by thermogravimetric methods and near infrared spectroscopy. The dehydration of authentic Mg(OH)₂ proceeded as a one-step reaction. In contrast, the dehydration of LiCl-modified Mg(OH)₂ occurred in two steps. The dehydration reaction rates were increased by LiCl modification of the Mg(OH)₂ surface, while the activation energy for the first-order dehydration reaction was lowered. The mechanism for the hydration reaction of magnesium oxide (MgO) was different to that for the hydration of LiCl-modified MgO. This difference was explained by the effect of the LiCl on the MgO particle surface.     

A new aspect of the carotid body function controlling hypoxic ventilatory decline in humans

Ventilatory response to eucapnic sustained mild hypoxia was measured in one patient with unilateral and three patients with bilateral carotid body (CB) resection (defined UR and BR, respectively). The profile of ventilatory response in UR patient was initially augmented then gradually declined (biphasic pattern) as generally seen in normal subjects although the absolute magnitude was substantially low. On the other hand, biphasic pattern was disappeared in all three BRs. Lack of hypoxic ventilatory decline (HVD) in the late period of sustained hypoxia was in marked contrast to that reported in the anaesthetized and CB-denervated animals whose ventilation was severely depressed lower than the pre-hypoxic control level. In view of recent knowledge that the analogous mild hypoxia in normal animals and humans elicits an useful adaptation to economize energy expenditure with maintaining reversible excitability in control of respiration, BR patients were considered to have lost this ability. We conclude that in awake humans the CB not only stimulates ventilation but also controls the degree of subsequent HVD during sustained hypoxia.