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Biomedical subjects

K Shima

Publications and source records attributed to K Shima.

At least 469 records · Page 26Linked to original sources
PubMed1980

Excitatory effects of dihydrocapsaicin on nociceptive neurons in the medial thalamus.

Effects of capsaicin and dihydrocapsaicin, which are pungent substances contained in Capsicum annuum L., were studied in 32 gallamine triethiodide immobilized cats. Single units were recorded from the medial thalamus using stainless steel microelectrodes. Of the 56 neurons recorded, 28 were responsive to both noxious (pinching) and non-noxious (hair and/or tapping) stimuli, while 16 were activated only by non-noxious stimuli. The remaining 12 neurons did not respond to any natural stimulus. Somatic receptive fields of nociceptive and non-nociceptive neurons were found to be widely distributed over the whole body. Twenty-six of 28 nociceptive neurons were activated by an intra-arterial administration of bradykinin, capsaicin and dihydrocapsaicin. Fourteen of 16 non-nociceptive neurons were not activated by these substances. The mean latency and duration of bradykinin were 8.7 and 12.5 sec, those of capsaicin were 1.2 and 6.1 sec and those of dihydrocapsaicin were 1.3 and 5.0 sec, respectively. The increase of firing frequency produced by capsaicin and dihydrocapsaicin was inhibited by morphine and this inhibition was antagonized by naloxone. However, the activity of medial thalamic neurons with non-noxious stimuli was not affected by these drugs. These results suggest that the pain-conducting fibers were selectively activated by capsaicinoids as well as by bradykinin.

Action Potentials↗
PubMed1980

Failure of exogenous insulin to inhibit C-peptide release from the perfused rat pancreas.

In order to ascertain whether insulin secretion is inhibited by insulin per se, the effect of exogenous rat insulin on basal and stimulated rat C-peptide reactivity (CPR) release was studied in the isolated perfused rat pancreas. The pancreas was perfused with a medium containing 20 or 200 ng/ml of rat insulin for a 20 min equilibration period and successively for a 25 to 30 min test period during which time glucose (300 mg/100 ml), tolbutamide (500 micrograms/ml), glucagon (500 ng/ml) or arginine (10 mM) was added as a secretagogue. The concentration of glucose in the basal medium was 60 mg/100 ml. Exogenous insulin did not significantly suppress the basal CPR secretion, nor did it cause a suppression of the peak value or incremental area of CPR while the pancreas was stimulated, but it rather augmented them. No inhibitory effect of exogenous insulin on the basal or stimulated CPR release was noticed in the present study.

Animals↗
PubMed1980

A study of the physiological role of glucagon. Passive immunization with antiserum specific for pancreatic glucagon in rats.

To investigate the physiological role of glucagon in the maintenance of euglycemia, the effect of the neutralization of glucagon by an antiserum specific for glucagon on blood glucose and C-peptide immunoreactivity (CPR) levels was studied in the basal as well as in the hyperglucagonemic states caused by hypoglycemia or an intravenous infusion of arginine in rats. The antiserum employed in this study was raised in rabbits by subcutaneous injection as a conjugate of BSA and the C-terminal fragment of glucagon. Since the antiserum was found to contain 896 ng/ml of antibody-bound glucagon, the antigen-stripped glucagon antibody was prepared. Its affinity constant and binding capacity were 2.57 x 10(10) M-1 and 147 nM, respectively. After the administration of 1 ml of the antiserum in 24-hr-fasted rats, no free immuno reactive glucagon (IRG) was detected during the experiment for 60 min. Likewise, antiserum treatment prevented a rise in the plasma IRG level following an arginine infusion and insulin-induced hypoglycemia. Plasma CPR levels tended to be lower in antiserum-treated rats than in the control in any conditions covered by the present study. However, changes in blood glucose levels the both groups were comparable. These results demonstrate that in the presence of glucagon antibodies euglycemia can be maintained with a reduced supply of insulin.

Animals↗
PubMed1980

Decrease in blood glucose and release of gut glucagon-like immunoreactive materials by bombesin infusion in the dog.

Synthetic bombesin (100 ng/min) was infused under pentobarbital anesthesia in normal dogs and in insulin deprived depancreatized dogs 4 days after surgery. The release of gut glucagon-like immunoreactive materials (gut GLI) calculated as the difference between the values measured using cross-reacting antiserum and a so-called pancreatic glucagon specific antiserum was markedly stimulated by bombesin infusion. Plasma glucagon immunoreactivity (GI) measured by pancreatic glucagon specific antiserum also showed a small increase, whereas plasma glucose decreased significantly with a transient rise in insulin. The plasma glucose level did not decrease in depancreatized dogs. Gut GLI response in the regional mesenteric vein to 5% glucose administered into the loop of the ileum was strongly augmented by bombesin infusion. It is concluded that (1) bombesin infusion decreased blood glucose level in normal dogs but not in depancreatized dogs. (2) Bombesin infusion markedly augmented the release of GLI from the intestine. (3) Bombesin also stimulated the release of glucagon which was probably of gastrointestinal origin. (4) Insulin release was stimulated transiently by bombesin infusion. Thus, a competition of gut GLI with glucagon at the glucagon receptor site may be an explanation of the reduction in blood glucose.

Animals↗
PubMed1980

[Dependence of scattered Mn K alpha / K beta X-ray intensity ratio on the scatterer materials].

The K alpha / K beta ratio of Mn KX-rays scattered by metallic samples changed remarkably with the geometry between the sample and the (55)Fe source-Si(Li) detector system. On the contrary, this intensity ratio changed little in the cases of non-metallic scatterer samples such as lucite or mylar. This difference is interpreted as due to the occurrence of strong or weak interference in the coherent scattering photons.

Elementary Particles↗
PubMed1980

[Contribution of 210Bi beta-ray induced bremsstrahlung to the emission of Pb-KX-rays observed in the lead shielded gamma-ray background spectrum (author's transl)].

Observation of gamma-ray background has been done by using a Ge(Li) semiconductor detector when it was placed inside the lead shielding material. With the aid of a very simple model calculation, the concentration of 210Pb radioisotope embedded in the lead material has been estimated to be 0.1-0.4 (Bq/Pb-g) (3-12 (pCi/Pb-g). The origin of Pb-KX-ray emission, the highest peak in the background spectrum, has been investigated by comparing the 210Pb-47 keV gamma-ray and Pb-KX-ray peak counts. As the results, about 50 +/- 30% of Pb-KX-ray production is estimated to be due to the Pb-K shell photoionization which is induced by the bremsstrahlung of 210Bi beta-ray.

Background Radiation↗
PubMed1979

Anomeric specificity in the response of gut glucagon-like immunoreactive materials to glucose.

An anomeric specificity of the glucose sensors of A cells and B cells of the pancreas has been reported. In this context the present authors investigated, using the canine intestinal loop prepared from the terminal portion of the ileum, how glucagon-like immunoreactive materials (GLI) of the gut would respond to glucose anomers in an attempt to explore a possible anomeric specificity of glucose-stimulated gut GLI secretion. As a result GLI was found to be more readily released into the blood stream after an intestinal alpha-glucose load than following beta-gluocse during a 15-minute observation period. It is thus suggested that gut GLI-secreting cells have glucose sensors similar to those of pancreatic A or B cells which are specific for the alpha-glucose anomer.

Animals↗
PubMed1979

Half life of gastrointestinal glucagon-like immunoreactive materials.

The composition, half life and hyperglycemic action of the porcine gastrointestinal glucagon-like immunoreactive materials were examined. Glucagon immunoreactivity (GI) measured using specific antiglucagon serum was more abundunt in the extract from the gastric fundus than in the one from the small intestine. When the extract from the gastric fundus was injected in dogs, the half life (T1/2) of total glucagon-like immunoreactivity (total GLI) measured using nonspecific antiglucagon serum was 9.5 +/- 1.1 min (mean +/- SEM), which was longer than that of crystalline pancreatic glucagon, 3.4 +/- 0.2 min, but shorter than that of the extract from the small intestine, 15.9 +/- 1.3 min. On the other hand, T1/2 for GI from the gastric fundus was 5.1 +/- 0.9 min, which was not significantly different from that of crystalline pancreatic glucagon. Blood sugar levels were significantly increased from the basal by 25 +/- 4 mg/100 ml at 10 min and 19 +/- 4 mg/100 ml at 15 min following an injection of the extract from the gastric fundus, but such a change in blood sugar levels was not demonstrated when the extract from the small intestine was injected. These results suggest that GI of the gastric fundus is close to pancreatic glucagon in respect of its metabolism and hyperglycemic activity.

Animals↗