Biomedical subjects

Reizo Inoki

Publications and source records attributed to Reizo Inoki.

3 recordsLinked to original sources

PubMed1989

Modified formalin test: characteristic biphasic pain response.

A modified formalin test in mice was investigated. The pain response curve induced by 0.5% formalin was biphasic, having 2 peaks, from 0 to 5 min (first phase) and from 15 to 20 min (second phase). A low concentration of formalin was used, allowing the effects of weak analgesics to be detected. Centrally acting drugs such as narcotics inhibited both phases equally. Peripherally acting drugs such as aspirin, oxyphenbutazone, hydrocortisone and dexamethasone only inhibited the second phase. Aminopyrine and mefenamic acid which acted on both central and peripheral sites inhibited both phases, but the second phase was inhibited by lower doses. Thus, this method enables one to easily distinguish the site of action of analgesics. Furthermore, pain response in the first phase was inhibited by capsaicin-treated desensitization and Des-Arg9-(Leu8)-bradykinin (bradykinin inhibitor). The second phase was inhibited by compound 48/80 pretreatment, indomethacin and bradykinin inhibitor. Therefore, it is suggested that substance P and bradykinin participate in the manifestation of the first phase response, and histamine, serotonin, prostaglandin and bradykinin are involved in the second phase. These results indicate that the first and second phase responses induced by formalin have distinct characteristic properties, and it is a very useful method for examining pain, nociception and its modulation by pharmacological or other means.

Analgesics↗

PubMed1983

A possible involvement of the central endorphin system in the autoanalgesia induced by chronic administration of Freund's adjuvant solution in rats.

Chronic pain was induced in rats by daily injections of complete Freund's adjuvant into hind paws. Daily changes of pain threshold and endorphin (ED) content and their receptors in 4 divided parts: cortex, diencephalon-mesencephalon containing striatum (D-M), pons-medulla (P-M) and spinal cord, were measured. Decrease in pain responsiveness was observed in the adjuvant-injected group with concomitant increase of ED content in P-M and spinal cord. This decrease in pain responsiveness in the adjuvant-injected group was significantly different from that in the non-treated control group being partially reversed by naloxone. Furthermore, [3H]met-enkephalin binding sites increase in number in P-M of the adjuvant-injected group when maximal decrease of pain responsiveness was observed, returning to control level thereafter. Scatchard analysis revealed the increase of the low affinity binding site in P-M of the adjuvant-injected group. In cortex and D-M, on the other hand, ED content tended to decrease and no change was observed in number of [3H]met-enkephalin binding sites. These results indicate that the ED system in P-M and spinal cord may be more substantially involved in autoanalgesia than in cortex and D-M.

Animals↗

PubMed1978

Effects of aspirin and morphine on the release of a bradykinin-like substance into the subcutaneous perfusate of the rat paw.

The effects of aspirin and morphine on the release of bradykinin-like substance into the substaneous perfusate following various noxious stimuli were investigated in rat paw preparation. Subcutaneous perfusion was performed with saline or with saline containing o-phenanthroline or soy bean trypsin inhibitor at a rate of 3--4 drops/min. Ten drops per fraction were assayed for bradykinin activity. Pressure on the instep, application of heat to the foot and stimulation of the sciatic nerve were employed as noxious stimuli. Aspirin (200 mg/kg i.p.) inhibited the release of bradykinin due to heat, pressure and sciatic nerve stimulation, while morphine (5 mg/kg i.m.) inhibited only the release of bradykinin due to sciatic nerve stimulation. Results suggest that analgesics, such as aspirin and morphine, have a depressant action on pain by inhibiting the release of bradykinin locally. They also suggest that aspirin inhibits the release of bradykinin regardless of the type of noxious stimuli, while morphine inhibits the release of bradykinin which is mediated by neural mechanisms.

Animals↗