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Biomedical subjects

K Terada

Publications and source records attributed to K Terada.

At least 289 records · Page 16Linked to original sources
PubMed1987

Actions of flunarizine, a Ca++ antagonist, on ionic currents in fragmented smooth muscle cells of the rabbit small intestine.

Actions of flunarizine on the Ca++ inward and K+ outward currents were investigated using fragmented smooth muscle cells (smooth muscle ball) prepared from the longitudinal muscle layer of the rabbit ileum. Flunarizine dose dependently inhibited the Ca++ inward current (ID50 = 1.4 microM). The decay of the inward current consisted of two exponentials and flunarizine had no effect on these time constants. When command pulses (100 msec; stepped up to 0 mV from -60 mV) were applied every 20 sec, the peak amplitude of the inward current remained unchanged. Flunarizine above 0.3 microM slowly inhibited the peak amplitude of inward current, in a voltage- and use-dependent manner. Intracellular perfusion of flunarizine, up to 100 microM, did not modify the peak amplitude of the inward current. This Ca++ antagonist also inhibited the K+ outward current, in a dose-dependent manner (ID50 = 5.8 microM) and accelerated inactivations of this current. When the command pulses (300 msec; stepped up to +20 mV from -60 mV) were applied repetitively every 20 sec, amplitudes of the K+ outward current were not affected. However, flunarizine, above 1 microM, reduced the peak amplitude of the K+ outward current slowly. These results indicate that although flunarizine possesses the property of a Ca++ antagonist, it also inhibits the K+ outward current, in a manner different from that observed on the Ca++ inward current.

Animals↗
PubMed1987

Selective and long-lasting inhibitory actions of the dihydropyridine derivative, CV-4093, on calcium currents in smooth muscle cells of the rabbit pulmonary artery.

Effects of CV-4093, a newly synthesized dihydropiridine type of Ca antagonist, on membrane currents in enzymatically dispersed single smooth muscle cells of the rabbit main pulmonary artery were investigated using the single electrode voltage clamp method. Three types of membrane currents were evident, i.e., Ca and Na inward and K outward currents. CV-4093 potently inhibited the Ca inward current, as compared to findings with other currents. When the potential was at -60 mV, CV-4093 consistently inhibited the Ca current evoked by depolarization to 0 mV. However, a low concentration of CV-4093 (1-3 nM) enhanced the Ca current evoked by the depolarizing pulse of -20 mV, when the membrane potential was held at -80 mV. Inhibition of the Ca current induced by CV-4093 developed slowly and over 10 min was required to reach the maximum inhibition. Changes in the frequency of the depolarizing pulse did not modify the rate of inhibition induced by CV-4093. The inhibition was not restored by washout of the drug for over 40 min, and hyperpolarizations of the membrane did not accelerate the recovery. The IC50 of CV-4093 obtained for the K outward current was 3000 times larger than that obtained for the Ca inward current. CV-4093 apparently has highly selective and long-lasting inhibitory actions on the Ca current in smooth muscle cells of the rabbit main pulmonary artery.

Animals↗
PubMed1987

Radical hysterectomy as surgical salvage therapy for gynecologic malignancy.

Fourteen patients with recurrent or second primary gynecologic malignancies after pelvic irradiation underwent radical hysterectomy as surgical salvage therapy. Six patients had microscopic regional metastatic disease at the time of surgery. All of these patients died of recurrent tumor. Overall disease-free actuarial survival at five years was 27%; excluding patients with regional metastatic disease, five-year survival was 54%. Complications requiring subsequent major surgical intervention occurred in 29% of patients. There appears to be a limited role for radical hysterectomy as surgical salvage therapy in patients with centrally limited invasive disease after pelvic irradiation.

Adult↗
PubMed1986

Hypophagia induced by endogenous or liposome-encapsulated 3,4-dihydroxybutanoic acid.

Hypophagia induced by 3,4-dihydroxybutanoic acid (2-deoxytetronic acid, 2-DTA), an endogenous short-chain polyhydroxymonocarboxylic acid, was investigated in rats. Intraperitoneal injection of 2500 mumol 2-DTA did not suppress feeding, but 2.5 mumol 2-DTA injected into the third cerebroventricle did. To efficiently transport exogenous 2-DTA into the brain, its encapsulation and delivery in specially made sulfatide liposomes was attempted. Feeding was suppressed dose-dependently by intraperitoneally injected 2-DTA in liposomes. Injection of 2500 mumol 2-DTA into the common carotid artery also suppressed feeding. Administration by either route prolonged postprandial intermeal interval with no change in meal size, as was observed after central administration of 2-DTA. Injection of 2.5 mumol 2-DTA into the third cerebroventricle elevated plasma glucose level, leaving insulin and free fatty acids unaffected. These findings, together with previous results, indicate that at least one site for the physiological action of 2-DTA is in the hypothalamic centers for food intake.

Animals↗
PubMed1986

Interstitial pneumonitis in autoimmune MRL/lpr mice and its treatment with cyclosporin A.

Age-associated changes of anti-double-stranded (ds) DNA antibodies, anti-single-stranded (ss) DNA antibodies, and serum immune complex concentrations were studied in MRL/lpr mice. All anti-ds DNA antibodies, anti-ss DNA antibodies, and immune complexes began to be detected in the sera of MRL/lpr mice aged 8 to 13 weeks and increased remarkably after 17 weeks of age. Almost no pathological findings were observed histologically in the lungs of MRL/lpr mice aged 8 weeks but interstitial pneumonitis became evident at 14 weeks of age. Peribronchial and perivascular lymphocyte infiltrations were seen in the lungs of 14-week-old MRL/lpr mice and became more severe at 21 weeks of age. Oral administration of cyclosporin A to 15-week-old MRL/lpr mice markedly prolonged their life span. The lungs of 44-week-old MRL/lpr mice given cyclosporin A showed few pathological findings except for minimal perivascular lymphocyte infiltration.

Animals↗
PubMed1986

Membrane currents recorded from a fragment of rabbit intestinal smooth muscle cell.

Properties of ionic currents in smooth muscle membranes of the longitudinal muscle layer of the rabbit ileum were investigated using the single electrode voltage clamp method. In the present experiments, this method was applicable only to the smooth muscle ball (fragment) and not for the dispersed whole cell, because of incompleteness of the voltage clamping. A voltage step elicited a transient inward current followed by an outward current. This outward current was partly inhibited by Mn2+ or nisoldipine or by a reduction in the extracellular [Ca2+] ([Ca2+]o). Tetraethylammonium (TEA) reduced the delayed outward current in a dose-dependent manner, but 50 mM TEA did not produce a complete block of a residual current. When the pipette contained K+-free (Cs+ with TEA+) solution, the residual outward current was abolished. The inward current was elicited at -30 mV (holding potential of -60 mV) and reached the maximal value at +10 mV; the polarity was reversed at +60 mV. This inward current depended on the [Ca2+]o and was blocked by Mn2+ or nisoldipine. Ba2+ also permeated the membrane, and the inward current evoked by Ba2+ was also blocked by Mn2+ or nisoldipine. Reduction of [Na+]o in a solution containing 2.4 mM Ca2+ neither modified the current-voltage relation nor the decay of the inward current, but when [Ca2+]o was reduced to below 1 microM, Na+ permeated the membrane and was blocked by nisoldipine. In conclusion, ionic currents were recordable from the fragmented ball of the longitudinal muscle of rabbit ileum. There were at least two K+ currents as the outward current (Ca2+-dependent K+ and delayed K+ currents) and a Ca2+ current as the inward current. The property of the Ca2+ channel was similar to that observed with other preparations.

Animals↗
PubMed1986

Anorexia induced in rat by D-glucosamine deoxidized at C-1.

The effects of D-glucosamine (2-amino-2-deoxy-D-glucose), an endogenous glucose analogue, and 1-deoxy-D-glucosamine on feeding behavior were clarified. Test solutions (24 mumol) were infused into the third cerebroventricle of the rat. Glucosamine induced a feeding episode within 30 min after infusion and then prolonged the ensuing postprandial intermeal interval for the first 4 h of the dark period, while glucose suppressed feeding by decreasing meal size. Ventricular injection of 1-deoxyglucosamine potently suppressed feeding in a dose-related manner by affecting all meal parameters, and oral administration of 2,400 mumol also induced anorexia. Changes in activity of glucose-sensitive neurons in the lateral hypothalamus and glucoreceptor neurons in the ventromedial hypothalamus after electrophoretic application of glucosamine and 1-deoxyglucosamine were compatible with behavior changes. The results indicate that replacement of a hydroxyl group by an amino group at C-2 of the glucose molecule affects feeding behavior and deoxidation of C-1 potently induces anorexia.

Administration, Oral↗
PubMed1986

Cyclosporin A-induced suppression of ongoing IgE antibody formation in the mouse.

Persistent anti-ovalbumin (OA) IgE antibody formation in the mouse was suppressed by oral administration of cyclosporin A (Cy A). Spontaneous anti-OA IgE antibody formation in vitro was also suppressed by Cy A added to the culture. Anti-OA IgG antibody responses in vivo and in vitro were less affected by Cy A. Cy A-induced immunosuppression was T cell-dependent since removal of T cells from the immune spleen cell suspension abolished the Cy A-induced suppression of antibody formation. Supplementing normal spleen T cells resulted in recovery of Cy A-induced suppression of spontaneous antibody formation in vitro. Cy A-induced suppressor T cells carried both Lyt 1 and Lyt 2 surface markers.

Animals↗
PubMed1986

Present status of thromboembolic complications in patients with prosthetic heart valves.

When the incidence of thromboembolism (TE) as a complication was investigated in 171 patients with prosthetic heart valves using pyrolytic carbon, 10 cases were identified in a mean follow-up period of 2.43 years. Of these 10, two patients had died. The incidence of TE as a percentage per patient--year was 2.41 on the whole, 2.15 in patients with aortic valve replacement (AVR), 2.48 in patients with mitral valve replacement (MVR) and 2.52 in patients with double valve replacement (DVR). It is evident that TE is still an important complication following prosthetic heart valve surgery and the patient's return to society. TE tended to occur somewhat more often in cases of MVR and DVR than in those of AVR. TE was apt to appear early in the postoperative period, often within a year, and was often seen in the brain. To prevent TE, it is necessary to carefully control blood coagulation by the administration of anticoagulants.

Adult↗