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Biomedical subjects

S H Burstein

Publications and source records attributed to S H Burstein.

32 records · Page 2Linked to original sources
PubMed1988

Cannabinoids and pain responses: a possible role for prostaglandins.

The principal metabolite of delta 1-THC, delta 1-THC-7-oic acid exhibits significant analgesic action in the mouse hot plate test. The parent delta 1-THC has a similar effect when measured at later time points; however, 10 min after drug administration, a pronounced hyperalgesia is seen. This hyperalgesia can be inhibited by prior administration of either indomethacin or delta 1-THC-7-oic acid, presumably because of their ability to inhibit eicosanoid synthesis. Administration of prostaglandin E2 (PGE2), at doses that were a small fraction of the delta 1-THC given, resulted in a strong hyperalgesic response. Unlike delta 1-THC, the metabolite does not produce a cataleptic state in the mouse, which eliminates this as a basis for the hot plate response. The evidence presented is consistent with a mechanism in which the metabolite inhibits eicosanoid synthesis whereas the parent drug elevates tissue levels of prostaglandins.

Analgesia↗
PubMed1986

Active smoking depresses prostaglandin synthesis in human gastric mucosa.

To determine the effect of smoking on gastroduodenal mucosal prostaglandin synthesis, endoscopies were done after an overnight fast on 10 nonsmokers, 12 active smokers who smoked four cigarettes in the hour before endoscopy, and then 11 of the smokers who refrained from smoking for 12 hours. Biopsy samples of fundic, antral, and duodenal mucosae were incubated, and the accumulation of prostaglandin E2 and 6-keto-prostaglandin F1 alpha in the incubation medium was measured by radioimmunoassay. We assumed that accumulation of prostaglandins in the medium reflected mucosal synthesis. Comparison of active and inactive smoking showed that active smoking significantly depressed 6-keto-prostaglandin F1 alpha synthesis in antral and fundic mucosa and prostaglandin E2 synthesis in antral mucosa. Comparison of nonsmokers and inactive smokers showed no difference in prostaglandin synthesis. Active smoking causes a transient decrease in prostaglandin synthesis in fundic and antral mucosae. This depression of prostaglandin synthesis may help explain slower ulcer healing and predisposition to ulcer recurrence in smokers.

6-Ketoprostaglandin F1 alpha↗
PubMed1980

The nature of the inhibition of cholesterol esterase by delta 1-tetrahydrocannabinol.

An improved assay for cholesterol esterase based on the use of fatty acid radiolabelled cholesterol esters has been developed. The method was used to demonstrate the effects of delta 1-tetrahydrocannabinol on a crude Leydig cell esterase preparation and on crystalline pancreatic esterase. Both enzymes were inhibited and the Km values determined (6.6 mumol/1 for the Leydig cell esterase and 6.25 mumol/1 for the pancreatic enzyme). While the former exhibited a mixed type of inhibition, the latter clearly was competitive.

Animals↗