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Biomedical subjects

T Mine

Publications and source records attributed to T Mine.

At least 109 records · Page 6Linked to original sources
PubMed1988

Effects of secretin on content of PGE2 and 6-keto PGF1 alpha in gastric mucosa.

To determine the involvement of prostaglandins in the action of secretin on the promotion of the healing process in injured gastric mucosa, the effect of secretin infusion on the content of PGE2 and 6-keto PGF1 alpha (a major metabolite of PGI2) in human gastric mucosa was investigated. Specimens of both normal and injured mucosa were obtained from each of the patients who underwent polypectomy a week prior to the study. The specimens were obtained before and 20 min after intravenous infusion of secretin [2 Crick, Harper and Raper (CHR) units/kg] or saline. The basal content of PGE2 in injured mucosa was three times higher than that in normal gastric mucosa. Secretin did not increase the PGE2 content of normal gastric mucosa. However, secretin induced a sevenfold increase in the PGE2 content of injured mucosa. The content of 6-keto PGF1 alpha was not affected by secretin. These results suggest that, in injured mucosa, PGE2 is involved in the healing process and in the action of secretin as well.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Sources of calcium mobilized by glucagon in isolated rat hepatocytes.

Effects of glucagon on cytoplasmic concentration of free calcium, [Ca2+]c, were studied in aequorin-loaded hepatocytes. Addition of 5 nmol/l glucagon resulted in a prompt, but transient increase in aequorin bioluminescence. Glucagon, at 5 nmol/l, induced an increase in [Ca2+]c even in medium containing 1 mumol/l calcium, although the response was considerably smaller than that observed in medium containing 1.0 mmol/l calcium. When hepatocytes incubated in the presence of 1 mumol/l extracellular calcium were first stimulated by phenylephrine and subsequently by either glucagon or angiotensin II, there was a response of [Ca2+]c to glucagon, but not to angiotensin II. Dantrolene (50 mumol/l), which inhibits an increase in [Ca2+]c induced by phenylephrine, did not inhibit the increase in [Ca2+]c induced by glucagon. In contrast, dinitrophenol (50 mumol/l) abolished [Ca2+]c response to glucagon without abolishing the increase in [Ca2+]c induced by angiotensin II. These results suggest that glucagon mobilizes calcium from both intracellular and extracellular pools and that the intracellular calcium pool involved in glucagon action may be different from that mobilized by either phenylephrine or angiotensin II.

Angiotensin II↗
PubMed1988

[Acute epidural hematoma of the posterior fossa in a case of von Willebrand's disease].

A rare case of acute epidural hematoma of the posterior fossa associated with von Willebrand's disease is reported. A 9-year-old boy fell down and hit his occipital region against a floor. Soon after he came home and slept, but three hours later he began to vomit and became drowsiness. He visited our hospital and his Glasgow Coma Scale showed 13 points. CT scan on admission showed acute epidural hematoma of left posterior fossa and contusional hematoma in the right temporal lobe. The bleeding time was over 18 minutes. He had been suspected to be suffering from von Willebrand's disease two years ago. Then fresh blood, fresh frozen plasma and anti-hemophilic globulin were prepared. Ten hours after injury, the operation was begun. Fresh epidural hematoma existed as a clot beyond transverse sinus. During the procedure of dural tenting suture, diffuse bleeding from bone, muscle, subcutaneous tissue and dura occurred and it was difficult to stop the bleeding. By using fresh blood and anti-hemophilic globulin, the bleeding was controlled, and then the operation was achieved. In the postoperative course a new epidural hematoma was found in the left temporal region and a new but asymptomatic retinal hemorrhage was found in his right eye. He was discharged without any neurological deficits 25 days after operation.

Acute Disease↗
PubMed1988

[Clinicophysiological study of multimodality evoked potentials and computed tomographic findings in persistent vegetative state].

The auditory brainstem response (ABR), short latency somatosensory evoked potential (SSEP) and visual evoked potential (VEP) of patients in the persistent vegetative state (PVS) are reported, and the correlations between the electrophysiological findings and the CT scan findings with the three clinical grades of the PVS (transitional, incomplete and complete vegetative syndromes) are discussed. Twenty two patients in a vegetative state caused by subarachnoid hemorrhage (3), hypertensive intracerebral hemorrhage (5), cerebral infarction (6), head injury (3), cerebral anoxia (4) and brain tumor (1). Each evoked response was evaluated for the presence or absence of abnormalities and assigned a grade ranked I to III. Briefly an evoked response was assigned a grade I, II, III if it satisfied the respective criteria of normal, moderately abnormal and severely abnormal or absent electrical activity. On the other hand CT scan findings in the PVS were evaluated for abnormal low density areas, ventricular dilatation and enlargement of the sulci and cisterns indicative of atrophy of the brain parenchyma. SSEP and VEP were better correlated with the clinical grade than ABR, and upper brainstem atrophy and abnormal low density area in CT scan findings were more valuable as an index to expresses the clinical features than ventricular dilatation. On the basis of these results, it is concluded that studies of ABR, SSEP and VEP associated with CT scan findings in the PVS could be a useful diagnostic aid to evaluate the lesions of these patients.

Adult↗
PubMed1987

Assessment of the role of Ca2+ mobilization from intracellular pool(s), using dantrolene, in the glycogenolytic action of alpha-adrenergic stimulation in perfused rat liver.

To identify the role of Ca2+ mobilization from intracellular pool(s) in the action of alpha-adrenergic agonist, the effects of dantrolene on phenylephrine-induced glycogenolysis were investigated in perfused rat liver. Dantrolene (5 X 10(-5) M) inhibited both glycogenolysis and 45Ca efflux induced by 5 X 10(-7) M phenylephrine. The inhibition by dantrolene was observed in the presence and absence of perfusate calcium. In contrast, dantrolene did not inhibit glycogenolysis induced by glucagon. To confirm the specificity of dantrolene action on calcium release in liver, experiments were also carried out using isolated hepatocytes. Dantrolene did not affect phenylephrine-induced production of inositol 1,4,5-trisphosphate. The compound did inhibit a rise in cytoplasmic Ca2+ concentration induced by phenylephrine both in the presence and absence of extracellular Ca2+. Thus, these results suggest that calcium release from an intracellular pool is essential for the initiation of alpha-adrenergic stimulation of glycogenolysis in the perfused rat liver.

Animals↗
PubMed1986

Comparison of the changes in cytoplasmic free calcium concentration induced by phenylephrine, vasopressin and angiotensin II in hepatocytes.

Effects of phenylephrine, vasopressin and angiotensin II on cytoplasmic free calcium concentration, [Ca2+]c, were examined by monitoring aequorin bioluminescence in isolated hepatocytes preloaded with aequorin. In the presence of 0.5 mM calcium in the medium, the pattern of changes in aequorin bioluminescence induced by phenylephrine was different from that induced by vasopressin or angiotensin II. When extracellular calcium concentration was reduced to 1 microM, however, these three agents induced identical changes in aequorin bioluminescence. These results suggest that the mode of action of phenylephrine on cytoplasmic free calcium concentration differs from that of either vasopressin or angiotensin II and that the difference in ability to increase calcium influx may account for the distinct patterns induced by these agents.

Aequorin↗
PubMed1986

Evidence for direct effect of tolbutamide on hepatic glycogenolysis induced by Ca2+-dependent hormones.

The effects of tolbutamide and glibenclamide on hepatic glycogenolysis in perfused rat liver were investigated. Tolbutamide per se did not influence glucose output from the liver, but at therapeutic concentrations (about 350 microM) it significantly inhibited the glycogenolysis induced by phenylephrine, vasopressin and angiotensin II, while glibenclamide did not. Neither tolbutamide nor glibenclamide inhibited the glycogenolysis induced by glucagon. Tolbutamide potentiated the inhibitory effect of submaximal concentrations of insulin on glycogenolysis induced by phenylephrine. This effect of tolbutamide was elicitable even in the absence of calcium in the perfusate, and was additive to that of trifluoperazine. However, tolbutamide did not potentiate the inhibitory effect of insulin on glucagon-induced glycogenolysis. Tolbutamide inhibited the glycogenolysis induced by A23187, a calcium ionophore. These results indicate that, in addition to its known effect on insulin secretion, tolbutamide has a direct effect on the liver to inhibit glycogenolysis induced by Ca2+-dependent hormones (catecholamines, vasopressin and angiotensin II) and A23187. Thus, it is likely that tolbutamide inhibits the effect of Ca2+ mobilized by Ca2+-dependent hormones to stimulate glycogenolysis.

Angiotensin II↗
PubMed1986

Inhibition of the glycogenolytic effects of alpha-adrenergic stimulation and glucagon by cobalt ions in perfused rat liver.

Cobalt ions (2 mM) inhibited the glycogenolysis induced by phenylephrine and glucagon in perfused rat liver. Cobalt ions also inhibited 45Ca++ efflux from prelabelled livers induced by phenylephrine and glucagon. In addition, they inhibited the rise in tissue levels of cyclic AMP caused by glucagon, but did not inhibit the stimulation of 45Ca++ efflux or glycogenolysis by cyclic AMP or dibutyryl cyclic AMP. The specific binding of glucagon and alpha-agonist to hepatocytes was not inhibited by cobalt ions. These data suggest that cobalt ions, presumably through their high affinity for calcium binding sites on membranes inhibit the stimulation of glycogenolysis by phenylephrine and glucagon in distinct ways; one by inhibiting calcium mobilization and the other by inhibiting cyclic AMP production. Therefore, it is conceivable that membrane-bound calcium plays an important role in stimulating Ca++ mobilization by phenylephrine, and cyclic AMP production by glucagon.

Animals↗
PubMed1986

Echocardiographic detection and treatment of intraoperative air embolism.

A real-time two-dimensional echocardiogram was used to detect the presence of an air embolism in patients undergoing neurosurgical procedures in the sitting position. The technique could with good sensitivity detect the appearance of a single air bubble intraoperatively, thus allowing early intervention to prevent development of further air emboli. Two types of air embolism could be differentiated; the single-bubble type and the "stormy-bubble" type. The single-bubble type was observed during skin and muscle incisions, craniotomy, and brain lesion excision. Further embolism development was prevented by electrocoagulation and application of bone wax. The stormy-bubble type occurred during dura and muscle incisions and was prevented by electrocoagulation, reflection of the dura, or suturing the affected muscle. The routine use of a Swan-Ganz catheter for removal of air embolism by suction proved effective for the treatment of the stormy-bubble type of air embolism. Masking the operative field with saline-soaked cotton strips was of moderate benefit in the stabilization of the single-bubble type of air influx, but proved to be of little value in controlling the entrance of the stormy-bubble type.

Echocardiography↗
PubMed1985

A case of biliary cystadenocarcinoma with recurrent jaundice. Diagnostic evaluation of computed tomography.

A 73-year-old male patient with biliary cystadenocarcinoma and episodes of recurrent jaundice is reported. This very rare tumor was suggested as a possible diagnosis by the computed tomographic findings showing intrahepatic cystic masses with septations and papillary projections. The diagnosis of the mucin-producing tumor was supported by aspiration of mucinous bile with a cannule inserted endoscopically via the major duodenal papilla. The computed tomographic findings and the diagnosis were verified by pathologic studies made on the material obtained surgically. The mucinous bile is assumed to have been responsible for the recurrent jaundice.

Aged↗
PubMed1985

Influence of extracellular phosphate concentrations on the regulation of hepatic glucose output.

Experiments were carried out to investigate the role of extracellular phosphate in the hormonal regulation of glycogenolysis in perfused fed-rat liver. Omission of phosphate from the perfusate did not affect the ATP, ADP and AMP contents of the tissue and the basal glucose output from the perfused liver. However, it inhibited significantly the glycogenolysis induced by glucagon, cyclic AMP, phenylephrine and vasopressin but not that induced by 2,4-dinitrophenol. In the absence of perfusate phosphate, the increase in phosphorylase a activity caused by the addition of glucagon, phenylephrine and vasopressin was significantly less than that observed in the presence of perfusate phosphate. Insulin inhibition of the glucagon- or cyclic AMP-induced glycogenolysis was abolished when the perfusion was carried out with the phosphate-free buffer. However, the inhibitory effect of insulin on phenylephrine-induced glycogenolysis was clearly demonstrated even when the perfusate contained no phosphate. These data indicate that in the phosphate-depleted liver, the hormonal control of phosphorylation and dephosphorylation of phosphorylase is impaired. The difference in the phosphate dependency of insulin action on glucagon-and alpha-adrenergic agonist-induced glycogenolysis suggests that the mechanism or site of insulin action on glucagon and phenylephrine is different.

Adenine Nucleotides↗
PubMed1985

Transpetrosal approach for aneurysms of the lower basilar artery.

Extradural subtemporal access to the petrosal ridge and a resection of the anterior pyramidal bone produced direct observation of the lower basilar artery, with minimum retraction of the temporal lobe and preservation of the temporal bridging veins. Two patients with lower basilar trunk aneurysms facing toward the brain stem, were operated on by the "transpetrosal approach," with successful clipping of the aneurysms. Auditory function was preserved in one case. This approach decreases the possibility of retraction damage to the temporal lobe, brain stem, or cranial nerves, and may be helpful for surgery of aneurysms arising around the vertebrobasilar junction or at the origin of the anterior inferior cerebellar artery.

Adult↗
PubMed1983

Inhibitory effect of [Asu1 . 7]-eel calcitonin on glucagon-induced glycogenolysis in perfused rat liver.

In an attempt to elucidate the mechanism by which calcitonin modulates glucose metabolism, the effect of elcatonin ([Asu1 . 7]-eel calcitonin), a potent synthetic eel calcitonin analogue, on hepatic glycogenolysis was investigated by use of perfused liver from fed rats. Elcatonin, as infused into the portal vein at concentrations between 10 mU/ml and 200 mU/ml did not affect glucose output into the hepatic venous effluent. At concentrations higher than 100 mU/ml, it inhibited the glycogenolysis stimulated by submaximal concentrations of glucagon which was perfused concurrently. This aspect of elcatonin effect was reproduced by synthetic salmon calcitonin. Though elcatonin showed a marked inhibition of the glycogenolytic activity induced by glucagon at or less than 5.7 X 10(-11) M, the inhibitory effect became undetectable when higher concentrations of glucagon were employed. Elcatonin did not inhibit the glycogenolysis induced by dibutyryl cyclic AMP at near (0.5 microM) or less than half-maximally effective (0.2 microM) concentrations. In addition, it did not inhibit the glycogenolytic activity half-maximally stimulated by alpha-adrenergic agonist (phenylephrine, 0.4 microM) or vasopressin (0.2 mU/ml). Elcatonin inhibited the cyclic AMP production of the tissue induced by glucagon infusion. These data indicate that elcatonin modulates hepatic glycogenolysis by preventing the glucagon effect at a step before cyclic AMP production and with an apparently competitive kinetics. In view of the concept that Ca++ is involved in the glycogenolytic effect of alpha-adrenergic agonist and vasopressin, the fact that elcatonin did not influence the action of these agents suggests that Ca++ fluxes are not involved in the elcatonin effect on liver.

Animals↗