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Biomedical subjects

K Sugaya

Publications and source records attributed to K Sugaya.

At least 163 records · Page 9Linked to original sources
PubMed1985

Cholecystokinin antagonism by benzodiazepines in the contractile response of the isolated guinea-pig gallbladder.

Three benzodiazepines, chlordiazepoxide (CDP), diazepam (DZP) and medazepam (MZP), inhibited the contractile response of circular muscle strips from the isolated guinea-pig gallbladder to sulfated cholecystokinin octapeptide (CCK8) in the presence of atropine. The dose-response curves for CCK8 were shifted in parallel to the right by 10(-6) to 10(-5) M of the three benzodiazepines, although the maximum response to CCK8 was depressed by higher concentrations. Schild plot analysis of the antagonism gave pA2 values of 6.70 for CDP and 7.33 for DZP and slopes of the regression lines close to 1.0, suggesting that the antagonism was competitive in nature. The responses to acetylcholine, histamine and bradykinin were also depressed by 10(-5) M of DZP, but no parallel shift of their dose-response curves was observed. The non-specific inhibitory action of the benzodiazepines on these agonists was presumed to be due to the calcium antagonist-like action of the benzodiazepines. The antagonism between CCK8 and the benzodiazepines in the gallbladder was unaffected by GABA.

Acetylcholine↗
PubMed1985

Reversal of antinociceptive effect of cholecystokinin by benzodiazepines and a benzodiazepine antagonist, Ro 15-1788.

Intraperitoneally administered benzodiazepines, chlordiazepoxide (2-5 mg/kg), diazepam (1 mg/kg), flurazepam (1 mg/kg) and a benzodiazepine antagonist, Ro 15-1788 (0.5 mg/kg), reversed the antinociceptive effect in mice which was induced by intracisternal administration of 1 microgram of sulfated cholecystokinin octapeptide. The antinociceptive effect of cholecystokinin was reversed by naloxone, suggesting that the antinociceptive action involves endogenous opioid peptides in its production. On the other hand, morphine-induced analgesia was not reversed by diazepam and Ro 15-1788. These facts rule out opioid receptors as the site of the antagonism between the benzodiazepines or Ro 15-1788 and cholecystokinin on the antinociceptive effect. Benzodiazepines and Ro 15-1788 seem to inhibit the release of opioid peptides induced by cholecystokinin.

Analgesics↗
PubMed1985

Caerulein antagonism by benzodiazepines in the food intake in mice.

Intracisternal administration of caerulein inhibited the food intake in mice, but the caerulein action was antagonized by benzodiazepines such as chlordiazepoxide, diazepam and flurazepam which were administered intraperitoneally in low doses (0.2 to 2 mg/kg). The antagonism mechanism between caerulein and benzodiazepines remains unclear, but the characteristics of the antagonism were similar to those which had been observed with cholecystokinin and benzodiazepines.

Animals↗
PubMed1985

Inhibition of cholecystokinin response in the gallbladder by dibenamine and its protection by benzodiazepines.

The contractile response of the guinea-pig gallbladder to cholecystokinin (CCK) and acetylcholine (ACh) was irreversibly inhibited by 5 X 10(-5) M dibenamine, and the dibenamine-induced inhibition in the CCK response was prevented by 10(-4) M chlordiazepoxide (CDP) and diazepam (DZP), but not by 10(-2) M proglumide or 10(-6) M atropine. The dibenamine-induced inhibition in the ACh response was prevented by 10(-6) M atropine, but not by 10(-4) M CDP. These findings suggest that the binding of CCK to the CCK receptor can be inhibited by benzodiazepines.

Animals↗
PubMed1985

Inhibition of hypothermic effect of cholecystokinin by benzodiazepines and a benzodiazepine antagonist, Ro 15-1788, in mice.

Intracisternally administered cholecystokinin produced long lasting hypothermia in mice, and the hypothermic effect was significantly antagonized by benzodiazepines like chlordiazepoxide and diazepam and by a benzodiazepine antagonist, Ro 15-1788, that were administered intraperitoneally. Proglumide, a cholecystokinin antagonist, failed to prevent the hypothermia induced by cholecystokinin at a dose of 200 mg/kg. Benzodiazepines and Ro 15-1788 revealed a considerably strong hypothermic effect, but they still prevented the hypothermic effect of cholecystokinin. The precise mechanism of the antagonism between cholecystokinin and benzodiazepines remains unclear at present.

Animals↗
PubMed1983

[Postoperative complications and followup in cystectomy].

Clinical studies on postoperative complications and prognosis were done on 27 patients who had undergone cystectomy at our hospital. Thirty one postoperative complications were seen in 16 patients. Early complications which developed within 3 months of operation were more frequent (25 cases). They included pyelonephritis (5 cases), wound infection (4 cases), pulmonary complications (2 cases), cardiovascular complications (2 cases), ileus (2 cases) and delayed ambulance (2 cases) in decreasing order of frequency. Complications related to urinary diversion were observed in 4 out of 6 late complications. Reoperation secondary to surgical complications were done in 6 cases. Four of the 6 reoperations were related to gastrointestinal complications, all of which would be fatal if left untreated. Postoperative followup period ranged from 3 weeks to 49 months with a mean period of 12.8 months. The present status of the patients is as follows: 16 patients alive, 10 patients dead and 1 patient lost to followup. So far we cannot draw a definite conclusion regarding the relationship between surgery and the prognosis of the patients because the followup period is too short in many patients. In our experience: 1) The fewest cancer deaths occurred in patients who had undergone radical surgery; 2) the largest percentage of living patients was seen in the group of patients who had undergone radical cystectomy; and, 3) almost all patients with low stage tumors are living more than 6 months after operation.

Adult↗
PubMed1983

A case of amelanotic malignant melanoma of the female urethra.

We report a case of amelanotic malignant melanoma of the female urethra. The clinical course was unusually long and complicated by asynchronous resectable metastases to the lung and the brain. The patient died of generalized metastasis in spite of successful resection of the metastatic lesions and post-operative chemotherapy, two years and five months after the first presentation. To the best of our knowledge this is the second reported case of amelanotic melanoma in the female urethra.

Female↗