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Biomedical subjects

R Inoki

Publications and source records attributed to R Inoki.

At least 91 records · Page 5Linked to original sources
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↗
PubMed1975

[Effects of adrenergic agents on secretion of salivary kallikrein in the submandibular gland of the dog].

The effects of sympathetic nerve stimulation and administrations of sympathomimetics on the secretion of salivary kallikrein induced by stimulation of Chorda tympani were examined quantitatively and qualitatively in the dog submandibular gland. Both sympathetic stimulation and administrations of sympathomimetics such as norepinephrine, epinephrine, and isoproterenol caused increased secretion of salivary kallikrein. Among these effects, those of the sympathetic stimulation, norepinephrine, and epinephrine were not completely abolished by pretreatment with phenoxybenzamine or propranolol, but the effect of isoproterenol was abolished by pretreatment with propranolol, and was hardly influenced by pretreatment with phenoxybenzamine. From these results, it would appear that secretion of salivary kallikrein may be mediated through adrenergic alpha- and beta-receptors. On the other hand, in contrast with the activities of the salivary kallikrein secreted by Chorda tympani stimulation or administration of isoproterenol which were not inhibited by SBTI, the activities of the salivary kallikrein secreted by sympathetic stimulation as well as administration of norepinephrine or epinephrine were markedly inhibited by SBTI. From these results, it is concluded that secretion of glandular kallikrein is due either to Chorda tympani stimulation or is mediated through adrenergic beta-receptor, while secretion of plasma kallikrein is mediated through adrenergic alpha-receptor.

Animals↗
PubMed1971

Effects of nicotine on salivary amylase secretion from rabbit parotid gland.

1. The effects of nicotine on amylase secretion induced by auriculo-temporal nerve stimulation were studied.2. Nicotine caused a transient increase in secretion as well as flow rate of amylase.3. No difference in nicotine action was found between acute sympathetic decentralization of the gland and acute denervation.4. The increase in amylase secretion due to nicotine was not inhibited by phenoxybenzamine, bretylium and chronic denervation, but was prevented by hexamethonium, propranolol and adrenalectomy.5. The increase in flow rate due to nicotine was not inhibited by propranolol, chronic denervation and adrenalectomy, but was prevented by hexamethonium, phenoxybenzamine and bretylium.6. These results show that the action of nicotine in increasing amylase secretion is neither a direct action on the ganglion nor on the nerve terminal of the cervical sympathetic nerve, but is an indirect action of catecholamines released from the adrenal medulla on the post-junctional receptors.7. The study also suggests that the initial acceleration of salivary flow due to nicotine is characterized by a mechanism different from that of amylase secretion.

Adrenal Medulla↗