Biomedical subjects
Publications and source records attributed to S Shibata.
A highly potent cardiotonic polypeptide, anthopleurin-A, was isolated from the sea anemone, Anthopleura xanthogrammica (Brandt), using solvent partition, gel permeation chromatography, and cation-exchange chromatography. It is a pure basic polypeptide wtih a molecular weight of about 5500.
Both reserpine and 6-hydroxydopamine (6-OHDA) pretreatment potentiated the sensitivity of guinea pig aortic strips to norepinephrine (NE), barium, methoxamine and potassium indicating postjunctional supersensitivity. However, cocaine treatmetn only potentiated the NE response indicating prejunctional supersensitivity. 6-OHDA and reserpine-induced supersensitivity but not cocaine-induced supersensitivity was accompanied by an increase in 45Ca influx.
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Morphologic changes of extracapillary and chronic progressive glomerulonephritis with contracted kidneys, resembling those of adult human chronic glomerulonephritis, were induced in rats by a single injection of the purified glycopeptide and Freund's incomplete adjuvant into the hind footpads. The purified glycopeptide was prepared by TCA treatment or DEAE-cellulose chromatography from the nephritogenic glycopeptide which is known to have the ability to induce typical morphologic changes of membranous glomerulonephritis. As demonstrated in this report, the purification procedures result in complete elimination of contaminating free amino acids from the nephritogenic glycopeptide. The basic pathogenesis of the new experimental model of proliferative glomerulonephritis (including typical chronic glomerulonephritis) appears to have other than immune complex mechanisms.
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Anthopleurin-A (AP-A), a polypeptide with MW ca. 5500 (53 amino acids), isolated from the sea anemone, Anthopleura xanthogrammica (Brandt), elicited a potent positive inotropic effect but without an accompanying chronotropic effect on the isolated cardiac muscles of rat, rabbit, guinea pig and cat. Similarly in dogs and cats in situ, i.p. injections of AP-A increased the contractile force without effect on heart rate or blood pressure. The cardiotonic potency for AP-A was equivalent to that of isoproterenol but much greater than that for ouabain or glucagon on the isolated cardiac muscle. AP-A increased the contractile force (cardiac output) and decreased atrial pressure in dog heart during pentobarbital-induced failure. This inotropic effect was not inhibited by propranolol pretreatment. The Ca++ requirement to restore the contractile force was less in AP-A-treated than in ouabain or isoproterenol-treated tissues. After AP-A treatment, the cardiac contractility was more resistant to hypoxia and to low or high temperature stress than ouabain-treated or control preparations. AP-A at 5 10(-9) M increased the duration of the action potential, its mean rate of rise and conduction in the guinea-pig atria and ventricles. At the maximum effective concentration, AP-A did not inhibit Na+, K+-activated adenosine triphosphatase, phosphodiesterase (high Km and low Km) and cyclic 3',5'-adenosine monophosphate content of guinea-pig heart. AP-A (5 X 10(-8) to 5 X 10(-7) M) neither contracted nor relaxed the isolated vascular smooth muscle. The results suggest that AP-A may be useful in the clinical management of cardiac failure and as an experimental tool to study the pharmacology and physiology of cardiac muscle.
Dopamine caused relaxation in young rat but not old rat aortae contracted with prostaglandin F2 alpha. The antagonizing action of propranolol was less effective on the relaxing effect of dopamine than that of isoproterenol or norepinephrine. Chlorpromazine or haloperidol abolished the relaxing effect of dopamine but only reduced the effect of norepinephrine and isoproterenol. The relaxing effect of dopamine is mainly mediated by the activation of dopamine sensitive receptors.
The effect of chemical sympathectomy by 6-hydroxydopamine (6-OHDA) treatment was studied on guinea-pig atria. 6-OHDA treatment significantly reduced the positive inotropic effect of nicotine and tyramine on the left atrium, while similar treatment on the intact atria and the right atrium showed a decreased response to tyramine but not to nicotine. After 6-OHDA treatment the left atrium but not the right atrium showed supersensitivity to noradrenaline. The 6-OHDA induced reduction of catecholamine content and noradrenaline uptake was less effective on the right atrium in comparison to the left atrium and ventricles. After 6-OHDA treatment, tissue catecholamine fluorescence disappeared from all tissue layers of the left atrium but the number of specific fluorescent nerve terminals of the right atrium was only slightly decreased. These results indicate that adrenergic mechanisms of the right atrium exhibit higher resistance to sympathectomy by 6-OHDA than the left atrium.
Nephritogenic tubular epithelial antigen (Tub-Ag), which had been found in immune complexes deposited along the glomerular capillary walls of some patients with idiopathic membranous glomerulonephritis, was solubilized from renal tubuli of humans by Pronase digestion. Soluble Tub-Ag was then purified by gel filtration and ion exchange chromatography on DEAE-Sephadex. Three DEAE fractions, designated as 0.07 M, 0.13M, and 0.23 M fractions, raised antibodies in rabbits and fluoresceinated antibodies against any of these fractions reacted exclusively with luminal layer of proximal tubular epithelia. Among three fluoresceinated antibodies, however, only the one directed to 0.07 M fraction bound with immune complexes which were deposited along the glomerular capilary walls of the patients with Tub-Ag (DEAE 0.07 M fraction) was physicochemically homogenous with a S20 value of 8.2. Utilizing 125I-labeled Tub-Ag, a sensitive and quantitave radioimmunoassay of Tub-Ag was developed. Tub-Ag was demonstrated to occur naturally in serum and urine, as well as in all the organs tested including kidney, intestine, liver, spleen, stomach, heart, and lung. Tub-Ag was detected even in the sera of anephric patients on maintenance hemodialysis (60.8 +/- 7.8 radioimmunoassay units/ml), although at slightly lower levels than in those of normal individuals (69.9 +/- 10.6 units/ml). The size of serum Tub-Ag was identical to that of molecules bearing Tub-Ag activity solubilized by Pronase from all the organs tested, indicating that circulating Tub-Ag was maintained mainly by organs other than kidneys.
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Fluorescein angiography was carried out by modification of method as described by Feindel et al. The hemisphere was widely exposed to allow visualization of surface blood vessels. In the experimental room, the dye was injected rapidly either through a fine polyethylen catheter placed in the lingual artery or thorough the cannula in the femoral vein. For "lingual" angiography 1.6 ml of 1% sodium fluorescein were used, while for "femoral" angiography, 4 ml of 10% solution were injected. In the operating room 4 ml of 1% sodium fluorescein are rapidly injected into an internal carotid catheter. Serial photographs of the passage of the dye through the surface vessels of the hemisphere were taken with a motor-drive Nikon camera at interval of 0.4 seconds, or longer when indicated, starting at the time of the injection. The shutter was synchronized with the discharge of a rapid re-charging stroboscopic light. A wratten gelatin filter 47A (Kodak) was used over the light and a Nikon filter Y52 over the camera lens for Kodak high speed ektachrome film to obtain color photographs. The timing of the interval between photographs was measured to within in 0.4 seconds by recording from a ink written oscillography synchronized with the shutter. Thus the velocity of flow in individual vessels could be calculated from the serial photographs.
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The radioactive adenosine 3',5'-monophosphate (cyclic AMP) level derived from 8-14C adenine in intact rabbit platelets decreased in the presence of mitochondrial inhibitor (potassium cyanide) or uncoupler (sodium azide), and markedly increased by the addition of NaF, monoiodoacetic acid (MIA), or 2-deoxy-D-glucose. The stimulative effect of the glycolytic inhibitors was distinctly enhanced by the simultaneous addition of sodium succinate. MIA did neither directly stimulate the adenyl cyclase activity nor inhibit the phosphodiesterase activity. These results suggest that cyclic AMP synthesis in platelets is closely linked to mitochondrial oxidative phosphorylation.
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