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Biomedical subjects

K Sugaya

Publications and source records attributed to K Sugaya.

At least 145 records · Page 8Linked to original sources
PubMed1988

Effects of cimetidine on prostanoid production in the gastric corpus specimens from rats.

In order to examine the effect of cimetidine on the production of prostanoids in the stomach mucosa, the amounts of prostaglandin (PG) E2, F1 alpha and thromboxane (TX) B2 were determined after the specimens from the rat stomach corpus were incubated in the presence of cimetidine. Cimetidine significantly stimulated the production of PGE2 in the specimens at a concentration of 10 microM, but did not significantly affect the production of PGF1 alpha and TXB2 at concentrations of 1 to 100 microM.

Animals↗
PubMed1988

[Effect of oxybutynin on lower urinary tract function].

The effect of oxybutynin on lower urinary tract function was studied by combined recording of cystometry and sphincter electromyogram (EMG) in 7 decerebrate dogs. Micturition was induced by bladder filling before and after oxybutynin. The statistical analysis was carried out on the urodynamic parameters. Oxybutynin at a dose of 30, 100, and 300 micrograms/kg significantly increased the threshold volume during the collecting phase in a dose dependent manner. In the urodynamic parameters of the emptying phase considered to be influenced by cholinergic activity there was a small but significant decrease in maximum pressure only at 300 micrograms/kg. Therefore, oxybutynin is probably acting as a strong antispasmodic agent. Oxybutynin seems to be useful for the relief of symptoms associated with detrusor instability and hyperreflexia.

Animals↗
PubMed1987

Electrical and chemical stimulations of the pontine micturition center.

In an acute decerebrate cat, electrical stimulation of the pontine micturition center (PMC) resulted in micturition. Carbachol injection into the PMC also resulted in micturition. The pattern of changes in bladder pressure and the sphincter activity observed during carbachol-induced micturition was almost identical to that observed during reflex micturition. The injection site corresponded to the nucleus locus coeruleus alpha (LC alpha). These results suggest that activation of cholinoceptive neurons in the LC alpha presumably becomes a trigger to recruit any one of a number of neuronal circuits involved in micturition.

Animals↗
PubMed1987

Possible involvement of the CCK receptor in the benzodiazepine antagonism to CCK in the mouse brain.

In mice, intraperitoneally injected chlordiazepoxide and proglumide, both of which are regarded as cholecystokinin (CCK) receptor antagonists in the peripheral tissues, dose-dependently inhibited the satiety induced by 200 ng of intracisternally administered CCK octapeptide (CCK8). Intraperitoneally administered diazepam (1 mg/kg) and/or Ro 15-1788 (5 mg/kg), a benzodiazepine antagonist, both prevented the elevation in the pain threshold induced by 1 microgram of CCK8. However, Ro 15-1788 did not antagonize the effect of diazepam that reversed the CCK-induced antinociception. Ro 15-1788 also inhibited the satiety induced by CCK8. From these results, it was considered that the antagonism, which was observed in the present work, of benzodiazepines and proglumide to CCK8 seemed to occur at the CCK receptor and not at the benzodiazepine receptor in the brain.

Animals↗
PubMed1987

Pontine urine storage center in the dog.

Electrical stimulation of the presumptive pontine urine storage center, areas ventral to and/or lateral to the pontine micturition center, elicited an increase in threshold volume at which reflex micturition occurred in response to bladder filling with physiological saline, suggesting a facilitatory effect on the urine storage function. The electrolytic lesions made in the stimulated areas were histologically identified to distribute at the nucleus reticularis pontis oralis, Kölliker-Fuse nucleus and subcoeruleus. These nucleus seemed to work as a pontine urine storage center and to perform a reciprocal action with the pontine micturition center.

Animals↗
PubMed1986

Cholecystokinin antagonism by benzodiazepines in the food intake in mice.

Three benzodiazepines, chlordiazepoxide, diazepam and flurazepam, were demonstrated to reverse the suppressed food intake in mice in response to cholecystokinin octapeptide (CCK8). CCK8 (200 ng) was administered intracisternally, and the benzodiazepines intraperitoneally at doses of 0.1 to 1 mg/kg. The three benzodiazepines slightly depressed the feeding by themselves, but significantly reversed the satiety effects of CCK8. Naloxone (2 mg/kg) decreased the food intake but failed to reverse the CCK8 satiety action. The benzodiazepines were considered to antagonize the satiety action of CCK8 in the central nervous system through unknown mechanisms.

Animals↗
PubMed1986

Reversal of antinociceptive effect of caerulein by benzodiazepine.

Benzodiazepines, chlordiazepoxide and diazepam reversed the antinociceptive action of caerulein in mice. Benzodiazepines (1-5 mg/kg) were administered intraperitoneally and 100 ng of caerulein was injected intracisternally to mice. Benzodiazepines did not change the basal pain threshold of mice but significantly antagonized the antinociceptive effect of caerulein. Proglumide (200 mg/kg, i.p.), which has been claimed to be a specific cholecystokinin receptor antagonist, could also antagonize the antinociceptive effects of caerulein. Naloxone (5 mg/kg) partially but significantly antagonized the antinociceptive effect of caerulein, suggesting that one of the mechanisms of antinociceptive action of caerulein is related to endogenous opioid peptides since benzodiazepines do not act on opioid receptors. Benzodiazepines may decrease the antinociceptive effect of caerulein through acting on cholecystokinin receptors in the central nervous system.

Analgesics↗