Search PubMed⌕ Search

Biomedical subjects

D W Hall

Publications and source records attributed to D W Hall.

At least 37 records · Page 2Linked to original sources
PubMed1988

Morphologic evaluation of gastric mucosal protection by colloidal bismuth subcitrate (De-Nol).

The morphologic changes in the gastric mucosa of rats receiving colloidal bismuth subscitrate (CBS) at 120 mg/kg p.o. followed by intragastric instillation of 1 ml absolute ethanol have been assessed by macroscopic examination, quantitative histology and scanning electron microscopy. Macroscopically, virtually complete protection against ethanol injury was noted in CBS-pretreated animals, while control animals showed severe necrotic haemorrhagic lesions. Although light microscopy revealed disruption of the epithelium extending into the gastric pits, CBS protected deep pit cells and necrotic lesions were almost absent. By 6 h after ethanol instillation, surface epithelium was mostly restituted in the CBS group but not in the controls. Scanning electron microscopy (SEM) confirmed these findings. It is concluded that CBS protects the gastric mucosa against ethanol injury by preventing deep mucosal necrosis and that as a consequence the recovery of mucosal integrity is promoted.

Animals↗
PubMed1987

Influence of cyclandelate on in vitro red blood cell deformability.

Using filtration and viscosity techniques, cyclandelate, some of its metabolites and flunarizine were evaluated to determine their ability to maintain human red blood cell (RBC) deformability. In filtration studies, RBC suspensions were metabolically depleted, which decreased the capacity of the cells to pass through narrow filter pores. In viscosity measurements performed with whole blood, metabolic depletion resulted in an increase of blood viscosity values. The results of these experiments appeared to indicate that cyclandelate, cyclandelate alcohol and flunarizine were approximately equipotent in maintaining RBC filtration and blood viscosity values. Cyclandelate acid appeared to be less active in both studies. By measuring the adenosine triphosphate content of red blood cells it has been shown that this activity is not due to an action on red blood cell energy metabolism. Finally, experiments conducted with the calcium chelator EGTA showed that the activity of cyclandelate was reduced in the absence of Ca++ ions. The results strengthen the hypothesis that cyclandelate maintains red cell deformability by inhibiting calcium entry through the red cell membrane.

Adenosine Triphosphate↗
PubMed1987

Inhibition of human platelet functions by cyclandelate.

The effects of cyclandelate and two of its metabolites, cyclandelate alcohol and acid, on several human platelet functions in vitro were investigated. Platelet aggregation was measured turbidimetrically using platelet-rich plasma. 14C-Serotonin (5-hydroxytryptamine) release from preloaded platelets, and thromboxane B2 (TxB2) formation were evaluated simultaneously with platelet aggregation. Cyclandelate and cyclandelate alcohol, but not cyclandelate acid, in a dose-dependent fashion prevented platelet aggregation and the concomitant 14C-serotonin release and TxB2 formation induced by adenosine diphosphate, platelet activating factor and collagen. In other experiments, inhibitory synergistic activities of cyclandelate and prostacyclin (PGI2) on platelet aggregation were demonstrated; cyclandelate alcohol and PGI2 showed a somewhat less pronounced synergism. The hypothesis that the calcium modulating property of cyclandelate is responsible for the inhibition of blood platelet functions is strengthened by the inability of the drug to inhibit the calcium-independent platelet aggregation induced by ristocetin.

Blood Platelets↗
PubMed1987

Gastric mucosa protection and prostaglandin E2 generation in rats by colloidal bismuth subcitrate (DE-NOL).

The gastric protective properties of the anti-ulcer drug, colloidal bismuth subcitrate (CBS; DE-NOL) were examined in comparison with the effects of prostaglandin E2 (PGE2), sucralfate and cimetidine using an ethanol induced gastric erosion model in rats. To elucidate the mechanism of action of CBS it was studied whether it could stimulate PGE2 generation in gastric mucosa. Using a quantitative visual scoring technique of mucosal damage, CBS was shown to be less potent than PGE2, though about 4 times more potent than sucralfate at reducing ethanol induced gastric lesions. Cimetidine was only weakly active. Pretreatment of rats with CBS led to complete, partial and no protection at 0.25, 8 and 16 hr respectively. Prostaglandin generation was stimulated by vortexing biopsies of washed fundus, and the released PGE2 was measured by radio-immuno assay. PGE2 generation was dose-dependently increased by oral doses of CBS. Peak synthesis occurred at 0.25 hr. Although partial protection against ethanol lesions was found 8 hr after administration, basal levels of PGE2 had already returned at 4 hr. Indomethacin blocked control and CBS stimulation of PGE2, but only partially blocked the protection against ethanol induced lesions. These findings indicated that CBS protects the rat gastric mucosa against ethanol lesions, and that both prostaglandin and non-prostaglandin mediated mechanisms are probably involved.

Animals↗
PubMed1987

Gastric mucosa protective effects of colloidal bismuth subcitrate (DE-NOL).

We evaluated the gastric mucosal protective properties of the anti-ulcer drug, colloidal bismuth subcitrate (CBS; DE-NOL), and its ability to stimulate mucosal synthesis of PGE2 in the rat. Gastric lesions were induced by ethanol and quantified by a visual scoring procedure. CBS was about 3-4 times more protective than sucralfate at reducing lesions. PGE2 displayed potent activity in this model, though cimetidine displayed only weak activity. Increasing the concentration of a standard dose of CBS in the rat stomach enhanced the protective activity against ethanol lesions. Pretreatment of rats with CBS led to complete, partial and no protection at 0.25, 8 and 16 h respectively. PGE2 generation in gastric mucosa biopsies was dose-dependently increased by oral CBS and peak synthesis occurred at 0.25 h. Although partial protection against ethanol lesions was found 8 h after CBS, basal levels of PGE2 generation had already returned at 4 h. Indomethacin blocked CBS-stimulated generation of PGE2, but only partially blocked the protection against ethanol-induced lesions. These findings indicated that CBS protects the rat gastric mucosa against ethanol lesions and both prostaglandin- and non-prostaglandin-mediated mechanisms could contribute to this protection.

Animals↗
PubMed1986

Protective properties of colloidal bismuth subcitrate on gastric mucosa.

Colloidal bismuth subcitrate (CBS), PGE2, sucralfate, and cimetidine have been investigated for their mucosal protective effects in the ethanol-induced gastric erosion model in rats; moreover, to gain an insight into the mechanisms of action of CBS, its ability to stimulate the synthesis of gastric mucosal PGE2 was determined. Although less potent than PGE2 at inhibiting ethanol-induced gastric lesions, CBS was about 4 times more potent than sucralfate. Cimetidine displayed only very weak protective activities. CBS showed a time-dependent inhibition of ethanol-induced lesions. Complete protection was observed 15 min after treatment with CBS and partial protection was observed at 8 h, although no protection was found at 16 h. CBS increased the potential of rat gastric mucosa to synthesize PGE2 in a dose-dependent way. Up to 3-fold increases above the basal levels were found. Peak synthesis of PGE2 occurred 15 min after CBS and elevated levels were still found after 4 h. It is concluded from these studies that CBS produces potent gastric protection towards ethanol-induced injury in the rat. CBS also considerably increases the ability of rat gastric mucosa to synthesize PGE2 which may be an underlying biochemical mechanism for its protective properties on the gastric mucosa.

Animals↗
PubMed1983

Hormonal control of hamster ear sebaceous gland lipogenesis.

The sites and hormonal control of lipogenesis in hamster ear sebaceous glands are reported. Sebaceous lipogenesis was determined in ear biopsies by incubation with glucose and tracer concentrations of 14C-acetate in buffer. The 14C-labeled lipids were saponified, extracted, and determined by liquid scintillation counting. Histologically, the ears contained many sebaceous glands. The glands of male animals were much larger and more heavily lipid-stained than glands from females. Lipogenesis was almost entirely confined to the sebaceous glands in the dermal stroma. Lipogenesis was considerably higher in ear biopsies from male hamsters than from female, castrate male, or hypophysectomized male hamsters. In contrast to published data using hypophysectomized rats, where dihydrotestosterone potently and testosterone only weakly increased sebum secretion, both testosterone and dihydrotestosterone potently increased lipogenesis in the ears of hypophysectomized male hamsters. Dihydrotestosterone was somewhat more potent than testosterone in the hamster. Hypophyseal hormones do not appear to be essential for androgen stimulated lipogenesis in the hamster. In female hamsters, 5 alpha-androstane-3 alpha, 17 beta-diol, testosterone, dihydrotestosterone, 4-androstene-3,17-dione, and 5 alpha-androstane-3,17-dione produced dose-dependent increases in lipogenesis. From this and other studies, it is suggested that androgens other than dihydrotestosterone could be physiologically important in man and animals in stimulating lipogenesis in sebaceous glands.

Androgens↗