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Biomedical subjects

K Shimamura

Publications and source records attributed to K Shimamura.

280 records · Page 16Linked to original sources

Reflex changes in sympatho-adrenal medullary functions in response to baroreceptor stimulation in anesthetized rats.

Effects of increased and decreased blood pressure on adrenal sympathetic nerve activity and catecholamine secretion were examined in anesthetized Wistar rats. Efferent nerve impulses were counted and adrenal venous plasma was collected just before and 30 s after the onset of hypotensive stimulation induced by bleeding (average decrease in systolic blood pressure over the stimulation period was 38 mm Hg) or a hypertensive stimulation induced by phenylephrine administration (average increase in systolic blood pressure over the stimulation period was 41 mm Hg). While nerve activity and epinephrine and norepinephrine secretion were not significantly altered by the change in blood pressure in baroreceptor denervated animals, there were increases in these variables (131.1% of control levels for epinephrine, 117.5% for norepinephrine, and 127.1% for nerve activity) in response to bleeding and a marked decrease (to 63.0% of control levels for epinephrine, 53.9% for norepinephrine, and 54.0% for nerve activity) in response to phenylephrine administration with baroreceptors intact. These changes were significant both with respect to control blood pressure levels and with regard to the effect of stimulation in the baroreceptor-denervated animals. The reflex responses in adrenal nerve and catecholamine secretion were generally proportional in magnitude. The present results are discussed with regard to the effects of somatic stimulation on nerve activity and catecholamine secretion.

Adrenal Medulla↗

Spontaneous and agonist-induced contractions and endothelium-dependent relaxation in aortae from SHRSP and WKY rats under various levels of passive force.

1. The influence of the passive force on the contraction and endothelium-dependent relaxation in aortae of normotensive Wistar Kyoto (WKY) rats and stroke-prone spontaneously hypertensive rats (SHRSP) were compared. 2. Force changes of endothelium-intact and -removed preparations were measured isometrically by a force-displacement transducer. Endothelium-dependent relaxation was observed by applying acetylcholine to the preparation precontracted in the presence of 5 x 10(-7) mol/L noradrenaline. 3. The preparations showed spontaneously developed tension (tone) that increased with the increase in the passive force. The effect of passive force was greater in preparations from SHRSP. Contraction initiated by noradrenaline was also increased by passive force up to 30 mN, then showed a tendency to decrease. 4. Endothelium-dependent relaxation was depressed as the passive force was increased. Preparations from SHRSP showed impaired endothelium-dependent relaxation and were influenced by passive force to a lesser degree when compared with preparations from WKY rats. 5. Relaxation by sodium nitroprusside was influenced by passive force to a much lesser extent than that by acetylcholine. 6. Indomethacin potentiated endothelium-dependent relaxation and blocked the effect of passive force in both preparations. 7. The difference in relaxation and the effect of passive force is primarily caused by the difference in the release of endothelium-derived contracting factor, which is thought to be a product of the cyclo-oxygenase pathway of the arachidonic acid cascade.

Acetylcholine↗

Detection of allele loss on chromosome 16q in DNA isolated from fine needle aspiration specimens of breast tumors. A simulation study using surgically resected specimens.

OBJECTIVE: To clarify whether analysis of loss of heterozygosity (LOH) on chromosome 16q is possible using DNA isolated from fine needle aspiration specimens, a simulation study was performed using resected biopsy or mastectomy specimens of 37 breast carcinomas and 3 fibroadenomas. STUDY DESIGN: A highly polymorphic (AC)n repeat region on the D16S305 locus on chromosome 16q24 was amplified in the DNA samples by the polymerase chain reaction (PCR) using 32P-labeled oligonucleotide primers, and the PCR products were electrophoresed in denaturing gel for detection of LOH by autoradiography. RESULTS: PCR was successful in 34 cases, and LOH was detected in 10 (71%) of 14 carcinomas but not in the 3 fibroadenomas. These results were almost always compatible with the data obtained by restriction fragment length polymorphism analysis on chromosome 16q using Southern blotting. CONCLUSION: Examination of LOH on 16q by (AC)n polymorphism analysis using fine needle aspiration specimens is suggested as a supportive tool for preoperative diagnosis of breast tumors.

Adult↗

Influences of endothelium on the time course of noradrenaline-, 5-HT-, prostaglandin F2alpha- and high-K+-induced contractions in aortae of WKY and SHRSP.

Influences of endothelium on contraction of aortic smooth muscle by various agents were studied and those in the preparations from Wistar Kyoto rat (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) were compared. Endothelium depressed the contractions induced by noradrenaline and 5-hydroxytryptamine (5-HT). The time course of the contraction was bi- or tri-phasic in the former and slow rising monophasic in the latter. On the other hand, the depression was weaker in the contraction by prostaglandin F2alpha- and high K+. The depression was blocked by the removal of endothelium or in the presence of Nomega-nitro-L-arginine (L-NNA), indicating that nitric oxide (NO) released from endothelium was responsible for the inhibition. The inhibition was weaker in the preparation from SHRSP when compared to that in the preparation from WKY. Relaxation by acetylcholine (ACh) of the preparation precontracted in the presence of respective contractile agent was impaired in the preparation from SHRSP. It is concluded that mode of inhibition of the contraction varies depending on the agents used to initiate the contraction, i.e. depending on the mode of the release of NO. In the preparation from SHRSP, the influence of endothelium is impaired due to the reduced release of NO.

Acetylcholine↗

Involvement of endothelium-derived factors in controlling the active tone of smooth muscle in aorta from hypertensive rats.

Control of the active tone by endothelium in aortae from various strains of spontaneously hypertensive rats was studied. The active tone was negligibly observed in endothelium-intact preparation. The application of N(G)-nitro-L-arginine (L-NNA, 10(-4) M) induced slowly developed active tone in the preparations from hypertensive rats but no active tone was induced in the preparation from normotensive Wistar Kyoto rats (WKY). The developed tension was stronger in preparations from rats with higher blood pressure as observed in endothelium denuded preparations. The developed active tone in the presence of L-NNA was greater than that observed in endothelium denuded preparations. The active tone was abolished by the removal of extracellular Ca2+ or by the application of Ca-antagonists. L-arginine counteracted the effects of L-NNA and depressed the developed active tone in the presence of the latter drug. The application of indomethacin (10(-5) M) depressed the active tone of the preparations from SHRSP by 25.5+/-5.2%. Increasing extracellular K+ concentration or application of tetraethylammonium (TEA) could not be used to observe the effect of endothelium-derived factors on the active tone, because of their strong contractile effect. Simultaneous application of apamin and charybdotoxin induced an elevation of tension which was often associated with spontaneous tension oscillation. It is concluded that the active tone, which is smooth muscle origin, is depressed by endothelium-derived nitric oxide (NO) strongly and potentiated by a product of arachidonic acid cascade through cyclooxygenase pathway. The involvement of endothelium-derived hyperpolarizing factor (EDHF) in the depressing effect of endothelium is thought to be small.

Animals↗

Decreased modulation by endothelium of noradrenaline-induced contractions in aorta from stroke-prone spontaneously hypertensive rats.

Influences of endothelium on contractions of aortic ring preparations from 15 to 17 weeks old stroke-prone spontaneously hypertensive rats (SHRSP) and age-matched Wistar-Kyoto rats (WKY) were compared. Noradrenaline-induced contraction was potentiated by endothelium removal; the potentiation was greater in the WKY aorta. Noradrenaline (10(-5) M) induced a biphasic contraction in endothelium-intact WKY aorta, while endothelium-intact SHRSP aorta or endothelium-removed preparations of both strains showed a monophasic sustained contraction. The tension changes in high-K-induced contracture of the endothelium-intact preparation was less pronounced in both WKY and SHRSP aortae. The relaxation by acetylcholine (10(-5) M) of endothelium-intact aortae, precontracted with noradrenaline (5 X 10(-7) M), amounted to 78% in the WKY and to 44% in the SHRSP preparation. In endothelium-removed aortae, sodium nitroprusside induced a comparable relaxation in both WKY and SHRSP preparations. These results indicate that the endothelium plays an important role in controlling the noradrenaline-induced contraction and that the lower influence of endothelium in the SHRSP aorta is most likely due to a decreased activity of this endothelium.

Acetylcholine↗

Influences of sodium on the contractile action of vanadate in depolarized vas deferens and ureter of the guinea-pig.

Effects of extracellular Na+ on the contractile action of vanadate were studied using depolarized smooth muscles of the guinea-pig vas deferens and ureter. Both sodium vanadate and ammonium vanadate induced tension development of the preparations in K-Tyrode's solution containing 12.3 mM Na+. The tension developments were enhanced greatly in K-60 mM solution with 89.3 mM Na+ and diminished in Na+-free K-Tyrode's or Na+-free K-60 mM Tyrode's solution, and slight relaxations were observed in the vas deferens soaked in the latter two Na+-free solutions. The addition of Na+ to Na+-free solution in the presence of vanadate induced a marked increase in tension. Vanadate induced slight tension development of depolarized preparations in the absence of Ca which was less affected by Na+. Ca-induced contraction of depolarized preparations was also markedly potentiated by vanadate. The potentiation was more prominent in the presence of Na+ and less prominent in the absence of Na+; the maximum tension was less affected by Na+ than the vanadate-induced contraction of depolarized preparation, but the tension decay was greatly accelerated in the absence of Na+. It was suggested that Na+ enhances the contractile action of vanadate through Ca extrusion mechanism of cell membrane.

Animals↗

Pharmacokinetics of platinum in cancer patients following intravenous infusion of cis-diammine(glycolato)platinum, 254-S.

The pharmacokinetics of platinum in cancer patients were examined following an intravenous infusion of cis-diammine(glycolato) platinum, 254-S. The plasma concentrations of total platinum, which decreased biexponentially after the infusion, were proportional to the dose over the range of 10 to 120 mg/m2, suggesting linearity of the pharmacokinetics. The plasma concentrations of ultrafilterable platinum were similar to those of total platinum and there was little difference in the pharmacokinetic parameters between total platinum and ultrafilterable platinum. These findings show that almost all of the platinum derivative is unbound, which is thought to be the active form, in plasma after administration of 254-S. Platinum was eliminated from blood faster when given as 254-S rather than as cisplatin because of the low protein binding. The urinary recovery within 24 hours was about half of the dose, suggesting that platinum given as 254-S was distributed to various tissues and organs in an active form.

Adolescent↗