[Evaluation of the biosynthesis of mono-HETES and leukotrienes in diseased periodontal tissues].

Many arachidonic metabolites have been shown to have marked potent biological effects in animals. The cyclooxygenase and lipoxygenase products of arachidonate metabolism are known to play a key role in the development of inflammatory symptoms and signs. Reports published during past decades indicate that cyclooxygenase products of arachidonic acid metabolism are present in much higher concentrations in inflamed than in healthy periodontal tissues. Since information about the role of lipoxygenase products of arachidonic acid metabolism in human periodontal disease is lacking, the objective of this study was to determine the ability of diseased and non-diseased gingival tissue to synthesize lipoxygenase products from the precursor arachidonic acid. Twenty-six samples of diseased tissue and nine samples of non-diseased tissue were included in our data analysis. After incubation of the tissue with 100,000 cpm [3H]-arachidonic acid, lipoxygenase products were separated by high performance liquid chromatography (HPLC) and identified by comparison with cochromatographed standards. Our results showed that inflamed gingival tissue synthesized significantly larger amounts, of LTB4(p < 0.01), LTC4(p < 0.01), LTD4(p < 0.01), LTE4(p < 0.01), 5-HETE(p < 0.05), 12-HETE(p < 0.01), and 15-HETE(p < 0.01), compared to non-diseased tissue. The lipoxygenases are more active in inflamed gingival tissue than in non-diseased gingival tissue. 12-HETE and 15-HETE were the the major metabolites formed by lipoxygenases in diseased and non-diseased human gingiva. Since we did not functionally determine the fractions separated by HPLC, our present data may only provided indirect evidence for the existence of lipoxygenase products in periodontal tissue. However, our study did establish a research model for the investigation of arachidonic acid metabolism in the pathogenesis of periodontal disease.

Neuromuscular interactions between succinylcholine and esmolol in the rat.

To study the neuromuscular interactions between succinylcholine (Sch) and esmolol, we determined the dose-response relationship of Sch and the neuromuscular actions of the 3xED90 dose of Sch, both prior to and following esmolol pretreatment. Twenty rats were anaesthetized with urethane. Train-of-four stimulation was applied every 12 s to the sciatic nerve, and the electromyogram (EMG) of the tibialis anterior muscle was measured. The results showed that the potency of Sch decreased with esmolol pretreatment. The ED50 of Sch increased significantly, from 191 ug/kg to 227 ug/kg after esmolol infusion, p < 0.05. The duration of EMG depression achieved by the 3xED90 dose of Sch decreased significantly with esmolol pretreatment (12 min vs 14 min p < 0.05), and also the onset time was significantly longer (43 sec vs 28 sec, p < 0.05). There were no significant difference between groups with regard to the maximal block or recovery index. The results of two methods of study demonstrated that the pharmacological interaction between Sch and esmolol is antagonistic instead of potentiating.