九州歯科学会雑誌

Essential oils, volatile oils made of aromatic vegetables, have been used for foods, cosmetics, sanitary goods from the far past, and also for medical drugs for more than 4 centuries. Especially in formulae of dental drugs, essential oils have played more important roles rather than as aromatic elements. The purpose of this study was to demonstrate usefulness of their oils and thymol, a main constituent of some kinds of them. Local irritation and systemic toxicity of 3 essential oils employed frequently in dental drugs were examined first. All of the 3 oils caused much weaker irritation than Liquefied phenol. Clove oil, eucalyptus oil and peppermint oil were in descending order in irritation strength. Clove oil was the only one of the three oils showing skin cauterization, which did not appear by 2 time dilution. Then pharmacological actions were observed on thymol, which have been more frequently used in dental formulary rather than as essential oils. Thymol-drugs, dental drugs with thymol, showed more excellent effect on various kinds of the tested microbials than nonthymol-drugs. The vapor of thymol-drugs as well as drugs themselves gave very clear inhibitory zone under the culture condition of approximate body temperature. Antimicrobial efficacy of thymol against 5 microbials was 2-15 times stronger than that of phenol. Vapor of thymol showed distinguished inhibition, whereas the one of phenol hardly any effect. Both in vivo irritation and cauterization caused by thymol were milder than that by phenol, while toxicity to growth of culture cells was more serious by the former than by the latter. Systemic toxicity estimated through acute toxicity test of thymol was at so low level that use of thymol-drugs in dental practice was considered to be safe enough insofar as they were applied in normal way. Furthermore, thymol showed inhibition of neutrophil chemotaxis and it is expected that thymol has an inflammatory action of free radical scavenger.

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It has been well known that intracellular increase in Ca^<++> induced by massive release of excitatory amino acid and by increased phospholipid metabolism during and after ischemia that plays an important role in brain damage. Furthermore, recent studies revealed that mild hypothermia (only 2-5℃ reduction of brain temperature below normothermia) provided protective effect, though the mechanism of this effect is still unclear. The present study was designed to gain further insight into the mechanism for neuroprotective effect of mild hypothermia especially focussing on the changes of intracellular signal transduction system in a model of progressive forebrain ischemia in the rats. Two series of study were performed in male Wistar rats in which the brain temperature was kept either at normothermia (37℃) or at a mild hypothermia (33℃) during the ischemic period. Forebrain ischemia (10 and 30 min duration) was producted by bilateral occlusion of the carotid artery combined with hemorrhagic hypotension (mean BP=50mmHg). In the first series of experiment, neuropathological damages were assessed by the immunohisto-chemical reactivity for microtubule-associated protein (MAP2) in the cerebral cortex, striatum, hippocampus, and thalamus. In the second series, the changes in binding for ^3H-PDBu were measured to evaluate the functional changes of protein kinase C. The progressive decrease in MAP2 immunoreactivity was observed, the order of severity being striatum>hippocampus>cerebral cortex>thalamus. The binding for ^3H-PDBu decreased by 33%, 25% in the hippocampus, cerebral cortex after 30 min of ischemia, respectively. In the mild hypothermia group, the decrease in MAP2 immunoreactivity was attenuated in the striatum and hippocampus after 30 min of ischemia. This decrease in ^3H-PDBu binding was significantly less in hippocampus. These results suggest that, in progressive ischemia, mild hypothermia may ameliorate the cytoskeletal damages possibly by inhibiting the perturbation of intracellular signal transduction system.

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Spinally delivered adenosine receptor agonists and its analogs have recently been shown to have antinociceptive effects. However, the mechanisms by which adenosine produces antinociception are not clear. Therefore, the present study evaluated the modulating effect of adenosine A_1 receptor agonist, KF24345, R-PIA injected intrathecally (I.T.) on the tactile-allodynia, associated with cerebrospinal fluid (CSF)-glutamate release induced by injection of GABA_A receptor antagonist, bicuculine (BIC). The microdialysis probe and polyethylene tube (PE-10) were intrathecally implanted into lumbar segment under halothane anesthesia in fourty-five Sprague-Dawley rats. After three days, rats were divided into six groups ; i) Control (saline), ii) and iii) KF24345 at doses of 10μg and 100μg, iv) R-PIA at doses of 10nM, v) 10nM R-PIA plus 300nM aminophylline, and vi) 100μg KF24345 plus 300nM aminophylline. The tactile-allodynia was evaluated by touch-evoked agitation (TEA) which scored 0 (no response to hair touching at lumbar level) to 3 (strong agitation appeared). Using an intrathecal microdialysis, glutamate concentration in cerebrospinal fluid (CSF-Glu) was periodically (10 min intervals) determined simultaneously by a HPLC-ECD. Intrathecal BIC injection evoked a transient strong agitation (TEA score : 4.7 at 10 min, 1.0 at 30 min), associated with increased CSF-Glu (70% at 10 min.). KF24345 and R-PIA attenuated such increases of TEA and CSF-Glu dose-dependently. Such action of KF24345 (100nM) was reversed by codelivery of aminophylline (300nM). Base on the present study, it is clearly demonstrated that KF24345, R-PIA can prevent allodynia in a dose-dependent manner. This attenuating effect was reversed by adenosine A_1 receptor antagonist, suggesting R-PIA has a potent anti-allodynic effect via inhibiting adenosine A_1 receptor activity at spinal cord. In addition, the microdialysis study demonstrated that R-PIA attenuates increased spinal glutamate release evoked by allodynia through presynaptic inhibition of primary afferent input.

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