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Biomedical subjects

K Tsuda

Publications and source records attributed to K Tsuda.

At least 325 records · Page 18Linked to original sources
PubMed1987

Release of cholecystokinin and gallbladder contraction before and after gastrectomy.

The contraction of the gallbladder by ultrasonography and release of cholecystokinin (CCK) by specific radioimmunoassay in response to the ingestion of oral fatty meal before and 1 month after gastrectomy in five patients with early gastric cancer was studied. Before gastrectomy, basal concentrations of CCK (13.4 +/- 2.3 pmol/L) rose significantly to a maximum of 23.3 +/- 3.6 pmol/L at 20 minutes after ingestion of oral fatty meal, and remained significantly elevated during the study. Gallbladder contraction began as CCK concentrations rose, demonstrating significant correlation with plasma CCK. One month after gastrectomy, CCK showed a rapid and greater response to the ingestion of fatty meal, attaining a maximum of 53.7 +/- 7.3 pmol/L at 10 minutes, then gradually falling to basal level. The maximal contraction of the gallbladder after gastrectomy was almost the same as before gastrectomy (62.7 +/- 4.0% of original area), showing a significant correlation with plasma CCK, but refilling of the gallbladder was induced earlier with corresponding reduction of plasma CCK. Simultaneous measurement of plasma concentrations of pancreatic polypeptide revealed a fairly similar response to plasma CCK before and after gastrectomy. The release of CCK is the chief mechanism by which the ingestion of a fatty meal causes contraction of the gallbladder even after gastrectomy as well as before gastrectomy.

Aged↗
PubMed1986

Effects of oral glucose administration on preproinsulin mRNA in rats in vivo.

An experiment was performed to examine whether the acute increase in insulin release induced by oral glucose ingestion is associated with alterations in pancreatic preproinsulin mRNA (PImRNA) levels. Rats either fed ad libitum or after overnight fast were used. Fasted rats were administered glucose orally in a conscious, unrestrained state. Pancreatic RNA was extracted and the relative level of PImRNA was determined by dot blot analysis with a cloned rat preproinsulin I cDNA probe. In fasted animals PImRNA levels decreased compared with those of fed animals and showed no significant changes after acute glucose administration, while blood glucose and plasma insulin increased rapidly to maximum values at 15 min after glucose administration. Although the transcription rate was not directly measured in this experiment, it is possible that the rapid increase in insulin release from the beta cell under physiological conditions is controlled by post-transcriptional regulations.

Animals↗
PubMed1986

Clinical analysis of 33 patients with adult T-cell leukemia (ATL)-diagnostic criteria and significance of high- and low-risk ATL.

The clinical characteristics of 33 patients with adult T-cell leukemia (ATL) are described. All patients were born and have lived in Miyazaki Prefecture (southwest of Japan). Because of a wide range of clinical presentations and courses, they were subdivided into 2 groups. In the high-risk group, patients presented with high white-cell counts (WBC greater than or equal to 20,000/microliter) and over 30% of abnormal lymphoid cells (18 patients) and hypercalcemia with a low percentage of leukemic cells (5 patients). In this group the median survival time was only 3 months despite various modes of treatment. In contrast, patients of the second group exhibited a low percentage of abnormal lymphoid cells (WBC less than 20,000/microliter and/or leukemic cells less than 30%) and had no hypercalcemia (8 patients). Their clinical course was chronic with a median survival of 8 months, regardless of modalities of treatment. Two patients went through a period when the number of circulating leukemic cells was low (less than or equal to 5%) before overt leukemia appeared. Other clinical features, signs, symptoms, routine laboratory data, serum anti-ATL-associated antibody, cell membrane markers and cytogenetic studies were similar to those observed in other districts of Kyushu island.

Adult↗
PubMed1986

Enhanced calcium-sensitivity of erythrocytes in hypertension--calcium-induced changes of erythrocyte osmotic fragility in essential hypertension.

To investigate the Ca-sensitivity of the erythrocyte membrane in hypertension, the changes of the osmotic fragility of erythrocytes by Ca-loading and the effects of Ca-channel blockers or calmodulin-antagonist were observed in patients with essential hypertension. Erythrocytes were obtained from untreated patients with essential hypertension and age-matched normotensive subjects. Treatment of erythrocytes with Ca-ionophore A23187 and Ca in bathing medium caused the reduction of the osmotic fragility of erythrocytes dose-dependently on Ca-concentration. The degree in alteration of the osmotic fragility of erythrocytes was greater in essential hypertension than that in normotensive controls. In addition, Ca-induced changes of erythrocyte osmotic fragility was inversely correlated with the plasma renin activity in essential hypertension. In the presence of Ca-antagonists (verapamil, diltiazem) or calmodulin-antagonist (trifluoperazine), the reduction of the osmotic fragility of erythrocytes by Ca-loading was inhibited, and the differences of the osmotic fragility of erythrocytes between the hypertensives and the normotensive controls were abolished by these drugs. These results suggest that the greater changes of the osmotic fragility of the erythrocytes by Ca-loading in essential hypertension might be due to the abnormality of Ca-handling of the cell membranes causing an increase in the intracellular Ca concentration, contributing at least partially to the pathogenesis of hypertension.

Adult↗
PubMed1986

Effects of calcium-antagonists on norepinephrine release from sympathetic nerve endings in rat mesenteric vasculature.

The present study was designed to investigate whether Ca-antagonists influence norepinephrine release from the sympathetic nerve endings in resistance vessels. Isolated mesenteric vascular preparations of rats, perfused with Ringer-Locke solution, were used to determine the effects of verapamil or diltiazem on norepinephrine release from sympathetic nerve terminals. Pressor responses to exogenous norepinephrine and electrical nerve stimulation were recorded, and the norepinephrine contents of the perfusate were measured before and after the electrical nerve stimulation, using high pressure liquid chromatography with an electrochemical detector. Pressor responses to exogenous norepinephrine and electrical nerve stimulation were depressed dose-dependently by verapamil and diltiazem. The inhibition of the pressor responses for nerve stimulation was greater than exogenous norepinephrine. Both verapamil and diltiazem reduced norepinephrine release from the mesenteric arterial beds after the electrical nerve stimulation. These results indicate that Ca++-antagonists, such as verapamil and diltiazem, have inhibitory effects on norepinephrine release from the sympathetic nerve endings, in addition to their direct actions on the vascular smooth muscle. It is also suggested that the presynaptic inhibitory action of Ca++-antagonists could be due to the blockade of Ca++-channels in nerve cell terminals, which may be important in the clinical use of Ca-antagonists.

Animals↗
PubMed1986

Neurotransmitter release, vascular responsiveness and their suppression by Ca-antagonist in perfused mesenteric vasculature of DOCA-salt hypertensive rats.

To investigate the role of norepinephrine release from the sympathetic nerve endings and vascular responsiveness in the pathogenesis of hypertension, the perfused mesenteric preparations were used in DOCA-salt hypertensive rats (acute phase: 10 days after operation, chronic phase: 7-8 weeks). In addition, the effects of a Ca-antagonist (verapamil) on the norepinephrine release and vascular responsiveness were also examined. Vasoconstrictor responses to the electrical nerve stimulation were significantly greater in DOCA-salt hypertension in the chronic phase than the age-matched normotensive controls. The pressor responses to exogenous norepinephrine were significantly enhanced in DOCA-salt hypertension both in acute and chronic phases. Endogenous norepinephrine overflow from the sympathetic nerve endings during the electrical nerve stimulation was enhanced in the chronic phase of DOCA-salt hypertension, but not in the acute phase, compared with the age-matched normotensive controls. After infusion of verapamil, the pressor responses and norepinephrine overflow by the electrical nerve stimulation were significantly inhibited, and the suppression was greater in chronic DOCA-salt hypertension than in the normotensive controls. These results demonstrate that the vascular responsiveness was increased in both acute and chronic phases of DOCA-salt hypertensive rats, while the norepinephrine overflow from the adrenergic nerve terminals was enhanced only in the chronic phase. More marked inhibition of the vasoconstrictor responses and norepinephrine overflow in the presence of a Ca-antagonist in chronic DOCA-salt hypertension might represent the higher Ca-dependency in the neurotransmission of the peripheral resistance vessels, especially in the mechanism of presynaptic norepinephrine release, than their normotensive controls, and it could partly contribute to the development and maintenance of DOCA-salt hypertension.

Animals↗
PubMed1986

Peripheral neural mechanism of hypertension in rat models--peripheral sympathetic neurotransmission in hypertension.

To investigate the peripheral neural mechanism of hypertension, norepinephrine release from sympathetic nerve endings was evaluated in various hypertensive rat models. The isolated mesenteric vasculatures were prepared in 7-9-week-old and 20-22-week-old spontaneously hypertensive rats (SHR), DOCA-salt hypertensive rats (DOCA-HT), two-kidney, one clip renal hypertensive rats (2K1C-HT) and their age-matched normotensive controls. The vasoconstrictor responses to exogenous norepinephrine (EN) were significantly enhanced in all hypertensive rat models compared with their age-matched normotensive controls. The pressor responses to electrical nerve stimulation (NS) were greater in SHR than age-matched Wistar-Kyoto (WKY) rats, and were also increased in DOCA-HT. The norepinephrine overflow during NS was significantly greater in young SHR and chronic DOCA-HT than in the normotensive controls. In 2K1C-HT, the norepinephrine overflow by NS was somewhat reduced compared with sham-operated normotensive controls. Inhibition by calcium-antagonist (verapamil) of the pressor responses and norepinephrine overflow during NS was significantly greater in young SHR and chronic DOCA-HT than in their controls. The facilitatory effect on the norepinephrine overflow exerted by the alpha 2-adrenoceptor antagonist, yohimbine, during NS was significantly less in young SHR and chronic DOCA-HT.

Animals↗
PubMed1986

Effects of alpha-human atrial natriuretic peptides on neurosecretion and vascular responsiveness in spontaneously hypertensive rats.

Effects of alpha-human atrial natriuretic peptides (alpha-hANP) on the norepinephrine overflow from the sympathetic nerve endings and vascular responsiveness were investigated in the perfused mesenteric intestinal loop preparations from 7- to 9-week-old spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto rats (WKY). Pressor responses to electrical nerve stimulation or exogenous norepinephrine were inhibited by alpha-hANP (3.4 X 10(-7) to 1.0 X 10(-6) mol/l), and norepinephrine overflow during the nerve stimulation was concomitantly suppressed by alpha-hANP. The pressor responses and norepinephrine overflow by nerve stimulation were greater in SHR than the age-matched WKY, while the inhibition of these responses by alpha-hANP was significantly less in SHR than in WKY. These results demonstrate that alpha-hANP could affect both pre- and post-synaptic sites of the resistance vessels, and less reduction in the pressor responses and norepinephrine overflow by alpha-hANP in SHR suggests insufficient regulation of adrenergic neurotransmission by cardiac peptide in hypertension.

Animals↗
PubMed1986

Effects of epinephrine and dopamine on norepinephrine release from the sympathetic nerve endings in hypertension.

The purpose of the present study was to analyse the regulatory mechanisms of epinephrine and dopamine on norepinephrine release from the sympathetic nerve endings in the resistance vessels in hypertension. The perfused mesenteric arteries were used for the experiment in spontaneously hypertensive rats (SHR; 7-10 weeks old) and age-matched normotensive Wistar-Kyoto (WKY) rats. Norepinephrine overflow during electrical nerve stimulation was significantly greater in SHR than in WKY rats. A low concentration of epinephrine (5.5 X 10(-9) mol/l) potentiated norepinephrine overflow from the nerve endings in SHR, and this was antagonized by propranolol, while this overflow was reduced by the same concentration of epinephrine in WKY rats. Higher concentrations of epinephrine decreased the norepinephrine overflow both in SHR and WKY rats, and this was antagonized by yohimbine. Dopamine reduced the norepinephrine overflow during electrical nerve stimulation, suppression being significantly less in SHR than in WKY rats. These results suggest that in SHR the increased norepinephrine overflow from sympathetic nerve endings may be partly caused by the facilitatory effect of epinephrine (through presynaptic beta-adrenoceptors) and impaired dopamine-mediated inhibition on the nerve terminals, which might contribute to the enhanced adrenergic activity in hypertension.

Animals↗
PubMed1986

Absolute configuration at C-24 of 5 beta-ranol, a principal bile alcohol of the bullfrog.

The stereochemistry of the hydroxyl group at C-24 in 5 beta-ranol (27-nor-5 beta-cholestane-3 alpha,7 alpha,12 alpha,24,26-pentol) a principal bile alcohol of the bullfrog which is structurally related to the major human urinary bile alcohol, 27-nor-5 beta-cholestane-3 alpha,7 alpha,12 alpha,24,25-pentol, is described. Two isomers (IIIa and IIIb) at C-24 of 27-nor-5 beta-cholest-25-ene-3 alpha,7 alpha,12 alpha, 24-tetrol were synthesized from cholic acid (I) by the conversion to 3 alpha, 7 alpha, 12 alpha-triacetoxy-5 beta-cholan-24-al (II) followed by a Grignard reaction with vinylmagnesium bromide. The absolute configurations at C-24 of the unsaturated tetrols (IIIa and IIIb) were elucidated as S and R, respectively, by means of the difference of the reactivity to Sharpless oxidation, a stereoselective epoxidation. Catalytic hydrogenation of each delta 25-tetrol (IIIa or IIIb) gave (24R)- or (24S)-27-nor-5 beta-cholestane-3 alpha,7 alpha,12 alpha, 24-tetrol (IVa or IVb). The configurations at C-24 of two isomeric 3 alpha,7 alpha,12 alpha,24-tetrahydroxy-27-nor-5 beta-cholestan-26-oic acids (Va and Vb) were determined as S and R, respectively, by means of their conversion into the saturated tetrols (IVa and IVb) of known absolute configurations by a Kolbe electrolytic coupling with acetic acid. The lithium aluminum hydride reduction product of the 24R-acid (Vb) was identical with the naturally occurring 5 beta-ranol, hence 5 beta-ranol has the 24R configuration.

Animals↗
PubMed1986

[Experimental and clinical studies on the effects of supplemental administration of bile salts after relief of biliary obstruction].

Changes of hepatic bile production and hepatocellular function such as bile acid and bilirubin excretion, BSP transfer rate constant, hepatic clearance of bile acid and ultrastructure of bile secretory apparatus after relief of biliary obstruction were investigated in both experimental rat model and clinical cases. The results were as follows: Increase in bile acid excretion after total bile fistula was significantly delayed in the jaundiced rats as compared with that of the control rats. In the jaundiced rats, bile salt-induced choleretic effect was significantly augmented and sodium taurocholate infusion caused a marked decrease in bilirubin excretion. Biliary transport of BSP was significantly decreased after biliary decompression, but showed remarkable restoration by simultaneous injection of sodium taurocholate. Hepatic clearance of 14C-taurocholic acid was disturbed in a group with long-term obstruction. The most remarkable morphological alterations were found in the bile canaliculus in the rat with relieved obstruction. Studies on clinical cases showed correlation between bile acid clearance and bilirubin excretion. In conclusion, effective elimination of plasma bilirubin after biliary decompression might be achieved by supplemental administration of bile salts, provided that bile acid clearance remains intact.

Adult↗
PubMed1985

Effect of truncal vagotomy on intestinal phase of pancreatic polypeptide release in dogs.

In order to elucidate the role of the vagus nerve in the intestinal phase of pancreatic polypeptide (PP) release, mongrel dogs were given a 4-min intraduodenal infusion of saline, 20% glucose, or 10% soybean oil solution (50 ml each), before and one month after truncal vagotomy including pyloroplasty (TV). The saline infusion did not change the basal PP level, while the glucose infusion elicited a monophasic transient PP release, and the soybean oil infusion elicited a monophasic prolonged PP release in the intact dogs. The PP response following glucose infusion was almost abolished after TV, while the PP response to fat was attenuated, but a significant increase was nevertheless observed after TV. These results suggest that the vagus nerve has an important role in the intestinal phase of PP release and that other factors, e.g. hormonal, might also be involved in the regulatory mechanism, especially after fat loading.

Animals↗
PubMed1985

Total actual speaking time in infants and children with otitis media with effusion.

For the purpose of supporting the premise that remarkable improvements in the child's attitude and performance rendered by improving the hearing impairment after aspiration of effusion and insertion of ventilating tubes in infants and children causes the increase in actual speaking time, an apparatus for measuring the time of vibration of the vocal cords was newly devised. Using this instrument, the duration of speaking time of children with otitis media with effusion was measured preoperatively and postoperatively. Preoperative and postoperative mean speaking times (speaking minutes/measured hours) were found to be 8 min 24 s per hour and 10 min per hour, respectively (number of patients: 30). These variable means were significant when examined by a Student's t-test. Pre- and postoperative speaking times showed no significant differences (10 min 24 s preoperatively and 10 min 54 s postoperatively) in the control group for surgery, consisting of 5 children having adenoidectomy and/or tonsillectomy.

Adenoidectomy↗
PubMed1985

Measurement of young children's total actual speaking time by a newly devised accumulator as an assessment of otitis media with effusion.

Aspiration of effusion and insertion of ventilating tubes in children with persistent effusion are effective ways of treating otitis media with effusion. In consequence, an increase in actual speaking time rendered by improving the hearing impairment must surely enrich the lives of children afflicted with this disease. To assess the increase in speaking time following aspiration of effusion and insertion of ventilating tubes, we devised a speech accumulator (RYU et al., 1983) which records the vibration time of the vocal cords by a small contact microphone attached to the neck. Total actual speaking time was measured with this device in children with effusion, and preoperative and postoperative speaking times were compared. Furthermore, an increase in actual speaking time invariably coincided with gain of hearing by middle ear ventilation. Children in whom insertion of the tube and adenoidectomy and/or tonsillectomy were performed were recruited for the study. The placebo group for surgery was made up of children selected at random who underwent adenoidectomy and/or tonsillectomy and suffered no hearing impairment, hence, there was no insertion of the tube. There was no significant difference between preoperative and postoperative total speaking times in patients of the placebo group.

Child↗
PubMed1985

Effects of diltiazem (a calcium antagonist) on neurosecretion and vascular responsiveness in hypertension.

The purpose of the present study was to analyse the mechanisms of the vasodepressive action of diltiazem (one of the Ca antagonists) in hypertension. The perfused mesenteric preparation was used in spontaneously hypertensive rats (SHR, Okamoto and Aoki, 7-9 weeks old) and age-matched Wistar-Kyoto rats (WKY). The effects of diltiazem on norepinephrine overflow from the sympathetic nerve endings and vascular responsiveness were investigated. Pressor responses to electrical nerve stimulation were inhibited dose-dependently by diltiazem. Norepinephrine overflow during periarterial nerve stimulation was also inhibited by diltiazem, and its suppression was significantly greater in SHR than in the age-matched WKY rats. Vasoconstrictor responses to exogenous norepinephrine were also reduced by diltiazem in both SHR and WKY rats. The inhibitory effects of diltiazem were more evident in SHR than in WKY rats. These results demonstrate that diltiazem could affect both pre- and postsynaptic sites of the resistance vessels and cause a decrease in electrically stimulated norepinephrine overflow from the sympathetic nerve endings, in addition to the direct effects on the responsiveness of the vascular smooth muscles. The marked reduction of the pressor responses and norepinephrine overflow by diltiazem in SHR might explain the Ca-dependency in the pathogenesis of hypertension.

Animals↗