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Biomedical subjects

R Inoki

Publications and source records attributed to R Inoki.

At least 73 records · Page 4Linked to original sources
PubMed1983

Changes of the Met-enkephalin-like peptide content induced by noxious stimuli in the rat incisor pulp.

It was examined what mechanism involved in an increase of met-enkephalin (met-EK)-like peptide content in the pulp induced by noxious stimuli. The increased content of the peptides by cavity formation as noxious stimulation was not influenced by cycloheximide, but attenuated by FOY-305 [N,N-dimethyl carbamoyl-methyl 4-(4-guanidinobenzoyloxy) phenyl acetate methanesulfonate], a trypsin-like enzyme inhibitor, and enhanced by captopril, and attenuated by infusion of saline in the pulp cavity. From these results, it was suggested that noxious stimuli on the pulp led to activation of trypsin-like enzymes followed by an increased content of met-EK-like peptides, and thereafter, the peptides, such as met-EK, might be degraded by angiotensin converting enzyme (ACE). Furthermore, an immunohistochemical study demonstrated that met-EK-like immunoreactivity (met-EK-IR) of cells in the rat incisor pulp was clearly increased following tryptic digestion of the pulp section, supporting a suggestion mentioned above.

Animals↗
PubMed1983

A possible relationship between processing from precursor proteins to opioid peptides and noxious stimulation in the rat incisor pulp.

The content of met-enkephalin (met-EK)-like peptides in a crude extract from intact pulp of the rat markedly increased with tryptic digestion but not with carboxypeptidase B(CPase B) digestion, while the content of leu-enkephalin (leu-EK)-like peptides more markedly with CPase B- than with tryptic digestion. On the other hand, results by High Performance Liquid Chromatography (HPLC) showed that the contents of both met-EK-Arg-Phe and leu-EK in cavity formed pulp increased 6 times as much as those contents in intact pulp, while the met-EK content in cavity formed pulp increased 2 times as much as that in intact pulp. Furthermore, results by gel filtration of crude extract from intact pulp showed that one peak of met-EK-like immunoreactivity (met-EK-IR) appeared at position of approximately 30,000 of molecular weight and a broad peak of leu-EK-IR appeared at position of approximately 60,000 of molecular weight following tryptic digestion. From these results, it was suggested that noxious stimuli might cause activation of trypsin-like enzymes followed by processing from one precursor protein to met-EK-like peptides as well as from another to leu-EK-like peptides in the rat incisor pulps.

Animals↗
PubMed1981

Algesiogenic and analgesic activities of synthetic substance P.

The objective of our study was to determine whether the pure synthetic substance P(SP) is algesiogenic or analgesic when administered centrally or peripherally. The relationships between SP-induced analgesia and the content of morphine-like factor (MLF) in the brain were also studied. Intracarotid arterial administration of SP (20-200 microgram) produced no pseudoaffective responses to pain in six out of nine rats, but in the remaining three, there was an exhibition of these responses. Chlorpheniramine pretreatment antagonized these responses. On cantharidin blister base experiments in humans, SP (10(-3) g/ml) produced slight pain and an itchy sensation. SP given intracerebroventricularly produced an analgesia in mice in a dose of 5 ng/mouse, as determined by the acetic acid-induced writhing and hot plate methods. These SP-induced analgesia were antagonized by naloxone pretreatment. SP did not alter the content of MLF in the mouse whole brain. However, SP5-11 not only produced an analgesia but also increased the content of MLF. These results suggest that SP has a slight algesiogenic activity which might be mediated by histamine and a slight analgesic activity which might be mediated by MLF.

Analgesics↗
PubMed1979

Significance of adrenergic alpha-effect on salivary kallikrein secretion in the submandibular gland of the dog.

The effects of the sympathetic nerve stimulation and the administrations of sympathomimetics on the secretion of salivary kallikrein induced by the chorda tympani stimulation were examined quantitatively and qualitatively in the submandibular gland of the dog. The secretion of salivary kallikrein may be mediated through both adrenergic alpha- and beta-receptors. The activities of salivary kallikrein secreted by either the chorda tympani stimulation or isoproterenol were not inhibited by soy bean trypsin inhibitor in vitro, but those secreted by the sympathetic nerve stimulation and noradrenaline or adrenaline were markedly inhibited in vitro. These results suggested that secretion of glandular kallikrein was induced by the chorda tympani stimulation and the sympathetic beta-stimulation, and secretion of plasma kallikrein was induced by the sympathetic alpha-stimulation.

Animals↗
PubMed1979

Bradykinin as an algesic (pain producing) substance in the pulp.

A rat uterine smooth muscle contracting substance was released into the superfusate of the dog's exposed canine pulp after noxious stimulation of the pulp by pricking, heat and electrical stimulation. This active substance was acid- and heat-resistant and was decomposed by carboxypeptidase B and alpha-chymotrypsin, but not by carboxypeptidase A and trypsin. This substance was also tested on several types of smooth muscle. Electrical activity of nerve cells in the reticular formation, which were sensitive to stimulation of the instep of the foot by pinching, was activated by the intrafemoral administration of the active substance. The algesic activity of this substance was examined in cantharidin blister base in man. This study conclusively demonstrated that the active substance of the pulp released by noxious stimulation produced pain and it was identified as bradykinin.

Animals↗
PubMed1979

A test for analgesics as an indicator of locomotor activity in writhing mice.

Marked depression of locomotor activity was observed in writhing mice given acetic acid i.p. This depression of the activity was evidenced by a squatting posture in reaction to pain. The hypoactivity was reversed dose-dependently by nonnarcotic analgesics such as acetyl-salicylic acid, aminopyrine and mefenamic acid in smaller dosages than those obtained by the conventional writhing syndrome test, and was also reversed dose-dependently by narcotic analgesics such as morphine, pethidine and codeine. Consequently, this hypoactivity test proved to be useful for analgesics screening.

Acetates↗
PubMed1977

Effects of morphine and acetylsalicylic acid on kinin forming enzyme in rat paw.

Coaxial perfusion was carried out in the rat paw; pinching the instep of the foot and electrical stimulation of the sciatic nerve caused an increase in the release of a bradykinin-like substance and kinin forming enzyme into the perfusate. Release of the latter was noted with pinching even independently of the release of the bradykinin-like substance. Acetylsalicylic acid (200 mg/kg i.p.) inhibited the release of kinin forming enzyme due to pinching or to sciatic nerve stimulation, while morphine (5 mg/kg i.m.) inhibited only the release of the enzyme due to sciatic nerve stimulation. Our results suggest that production of localized pain may be largely due to the activity of the released kinin forming enzyme and the bradykinin-like substance. In addition, the mechanism of inhibition by morphine on release of kinin forming enzyme appears to differ from that of acetylsalicylic acid.

Animals↗
PubMed1976

Effects of morphine and barbiturate on the SI and SII potentials evoked by tooth pulp stimulation of rats.

The effects of morphine and barbiturate on the evoked potentials recorded from the primary and secondary somatic sensory areas of rats were investigated. The electric stimulation of contra- and ipsilateral tooth pulp (CTP and ITP) was used. The afferent impulse from dental pulp projected to the sensory face areas I and II (SI and SII). Morphine in doses of 2.5-10 mg/kg definitely inhibited SI and SII potentials evoked by CTP stimulation. Morphine also inhibited SII potentials evoked by ITP stimulation, while it rather enhanced SI potentials evoked by ITP stimulation. Pentobarbital sodium in doses of 4-16 mg/kg tended to inhibit SI potentials, but showed no effect or rather an enhancement on SII potentials evoked by CTP stimulation. Pentobarbital sodium enhanced SI and SII potentials evoked by ITP stimulation. In a large dose of 32 mg/kg, pentobarbital sodium inhibited SI and SII potentials evoked by ITP and CTP stimulations. The results suggest that SII is more closely related to the analgesia due to morphine than is SI.

Animals↗
PubMed1976

[Pharmacological comparison between enflurane and halothane].

General pharmacological properties of enflurane (E) and halothane (H) were investigated. Maximum blood concentrations of both drugs reached 30 min after inhalation. E showed lower maximum blood concentration, initial velocity of uptake and shorter half life than H. Neither drug had any effect on neuromuscular junction, but E increased N-M effect of succinylcholine. Both drugs decreased tension of uterine and intestine muscles. Poly- and monosynaptic reflexes were inhibited more by H. ED50's of E and H for intestine muscles. Poly- and monosynaptic reflexes were inhibited more by H. ED50's of E and H for righting reflux were 1.25 and 1.40%, respectively. Tonic and clonic convulsions and death induced by electric shock were inhibited more by E. Almost equal anticonvulsive potency was observed for chemoshocks. Death due to electric and chemoshock was remarkably inhibited by both drugs. Spontaneous EEG was altered in a different manner, although flattened with spikes at 4% concentration of both drugs. E altered rhythmicity of recruiting response and both drugs inhibited this response. H inhibited more remarkably the augmenting response and E inhibited the arousal response. E increased negative potentials of the primary response evoked by sensory stimulation, while H decreased these potentials. Both drugs completely inhibited the secondary response.

Animals↗
PubMed1976

[Analgesics and the kallikrein-kinin system].

The mechanism of analgesic actions of aspirin, aminopyrine and morphine was investigated in reference to the kallikrein-kinin system and the results suggested that the analgesic actions of these agents are definitely related with the peripheral kallikrein-kinin activity. The central action of kinin appears to differ from the peripheral action.

Aminopyrine↗