Search PubMed⌕ Search

Biomedical subjects

M Grisham

Publications and source records attributed to M Grisham.

4 recordsLinked to original sources
PubMed1996

Early albumin leakage in pulmonary endothelial monolayers exposed to varying levels of hyperoxia.

We assessed the effect of varying levels of hyperoxia on 14C-albumin flux across bovine pulmonary artery endothelial cell (BPAEC) monolayers. Endothelialized nitrocellulose filters were mounted in Ussing-type chambers which were filled with cell culture medium (M 199). Equimolar amounts of 14C-labeled and unlabeled albumin were added to the "hot" and "cold" chambers, respectively, and the monolayers were exposed to 3 hours of varying levels of oxygen (16%, 30%, 40%, 60%, and 95%). When compared to 16% O2, exposure to hyperoxic gas mixtures of 40% or greater progressively increased albumin permeability across endothelial monolayers within 3 hours to a value 2.5 times higher at 95% O2 compared to 16% O2 (p < 0.001). Hyperoxia-induced permeability increases were prevented by catalase, superoxide dismutase, desferrioxamine, and allopurinol. Our data indicate that hyperoxia induces endothelial permeability changes more rapidly than previously reported even at O2 concentrations as low as 40%.

Albumins↗
PubMed1994

A diclofenac derivative without ulcerogenic properties.

In this study, we assessed the effects of addition of a nitroxybutyl moiety to diclofenac on its ulcerogenic properties. The diclofenac derivative, 'nitrofenac', was examined in terms of its ability to induce acute gastric erosions and chronic-type gastric ulcers in rats and rabbits, respectively. The effects of these compounds on prostaglandin synthesis in the stomach and at a site of peripheral inflammation were also assessed, as were their anti-inflammatory properties in a model of acute inflammation. Diclofenac dose-dependently caused acute gastric mucosal injury in the rat at all doses tested (10-40 mg/kg), that was significantly greater in severity than that observed with the same doses of nitrofenac. In rabbits, twice-daily administration of diclofenac induced penetrating antral ulcers and small intestinal damage. No damage was observed in the stomach or small intestine of rabbits receiving nitrofenac. Diclofenac and nitrofenac exerted similar inhibitory effects on prostaglandin E2 synthesis in the stomach and in a carrageenan-sponge model of peripheral inflammation. These compounds exerted similar inhibitory effects on carrageenan-induced paw edema. Nitrofenac, but not diclofenac, caused a significant increase in plasma levels of nitrate/nitrite. These results suggest that the addition of a nitroxybutyl moiety to diclofenac markedly reduces the ulcerogenic properties of this compound without interfering with its ability to inhibit cyclo-oxygenase activity or to reduce acute inflammation.

Animals↗
PubMed1989

Endotoxin induces bacterial translocation and increases xanthine oxidase activity.

Previously, we documented that endotoxin induces bacterial translocation from the gut and that inhibition or inactivation of xanthine oxidase activity reduces endotoxin-induced bacterial translocation. Consequently, experiments were performed to correlate endotoxin-induced bacterial translocation with changes in intestinal mucosal structure and xanthine dehydrogenase and oxidase activity. Segments of the jejunum, ileum, cecum, proximal colon, distal colon, and liver were harvested from ICR mice 24 hr after IP administration of E. coli 0111:B4 endotoxin (0.1 mg). Xanthine dehydrogenase and oxidase activities were measured in these samples and correlated with intestinal morphology. Bacteria translocated from the intestines to extraintestinal organs in 70% of the mice receiving endotoxin, while the organs of control mice were sterile (p less than 0.01). Endotoxin injured primarily the ileal and cecal mucosa and increased ileal and hepatic xanthine dehydrogenase and cecal oxidase activities (p less than 0.05). These results suggest that xanthine oxidase-induced mucosal damage plays a role in endotoxin-induced bacterial translocation.

Animals↗