[Olivo-ponto-cerebellar atrophy with olivary hypertrophy, binucleated neurons and fibrous gliosis in the cerebral white matter (author's transl)].
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Biomedical subjects
Publications and source records attributed to I Ohmura.
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Decarboxylation of L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS) by the higher speed supernatant of the rat heart homogenate and the regional distribution of L-threo-DOPS decarboxylase activity were examined. Decarboxylation was demonstrated to occur specifically with L-isomer but not with D-isomer. Addition of pyrogallol was necessary for maximal recovery of norepinephrine. The optimal condition for decarboxylation of L-threo-DOPS by the rat heart enzyme was similar to conditions required with the enzymes from brain and kidney. Under the optimal conditions, Km and Vmax for L-threo-DOPS were 2.1 mM and 6.4 nmoles/mg protein/15 min, respectively. Decarboxylation of L-threo-DOPS was markedly inhibited by D-threo-DOPS and D-DOPA. The L-aromatic amino acid decarboxylase activity was highest in the right auricle followed by the atrial body, the left auricle, the right ventricle and the left ventricle.
Shapes of the contractions induced by K, acetylcholine (AHc), histamine and Ba consisted of the phasic contraction (PC) and the subsequent tonic contraction (TC). PCs by K, ACh and histamine are initiated by the release and the passive influx of Ca, whereas that by Ba is only initiated by the release of Ca. TCs by K, ACh and histamine are maintained by the active influx of Ca, whereas that by Ba is maintained by the active influx and the release of Ca. Storage sites of Ca in the cell membrane of this preparation can be divided into three; the first, the second and the third, which contain the loosely, the less loosely-, and the tightly-bound Ca, respectively. K releases Ca to elicit contraction from the first division, ACh or histamine does so from the first and second divisions, and Ba does so from all of the three divisions. Based on the influence of high K-depolarizing bath solution on the relaxations by isoproterenol (Iso) and papaverine (Pap) and the effects of Iso and Pap on the shapes of contractions by K, ACh, Ba and exogenous Ca, the following assumptions were made: antispasmodic action of Iso is produced by inhibition of cell membrane (inhibition of release and influx of Ca), whereas that by Pap is due to this inhibition followed by inhibition of the muscle contractile system with the increase of concentrations. The effects of Iso and Pap on the concentration-action curves of the contractions by K, ACh, Ba and exogenous Ca(Table II) suggest that the parallel shift to the right of the curves of K, ACh and Ba is due to the functional antagonism between the antispasmodics and the mobilization of Ca produced by the contracting agents.
Dibenamine (DB) produced contraction due to influx and release of Ca in normal medium, whereas it produced relaxation of the K-induced contraction due to depression of the activity of the muscle cell membrane. DB inhibited active influx, passive influx and release of Ca induced by ACh in this order as the concentrations were increased and also inhibited the contraction by histamine selectively as compared with the contractions by ACh, K and Ba, the inhibition of the ACh-, K- and Ba-contractions being almost to the same degree. In addition, DB inhibited to much the same degree the phasic contraction(PC) and tonic contraction(TC) by histamine, whereas it inhibited TC in preference to PC induced by ACh, K and Ba. Irreversible inhibition by DB of ACh-, K- and Ba-induced contractions were protected by Ca, whereas those of histamine-induced contraction were selectively protected by histamine and antihistamine, but not by Ca. These results indicate that the antagonism of DB and its irreversibility against histamine may be due to blockade of the histaminergic receptor, whereas those against ACh, K and Ba may be due to inhibition of the Ca-site. Evidence has been obtained suggesting that the irreversible parallel shift to the right of the log concentration-action curve of histamine after washout of DB may be due to spare receptors, whereas that of ACh, K or Ba may be due to inhibition of the Ca-site.