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Biomedical subjects

Y Horio

Publications and source records attributed to Y Horio.

At least 127 records · Page 7Linked to original sources
PubMed1983

Precursor of mitochondrial glutamic oxaloacetic transaminase isozyme exists as a dimer.

Mitochondrial glutamic oxaloacetic transaminase is synthesized in the cytoplasm as a larger precursor and then imported into mitochondria in association with its processing to mature form. The precursor corresponded to about 0.05-0.1% of the total proteins synthesized on membrane-free polysomes. Gel permeation chromatography showed that the molecular weight of the precursor was about 100,000 daltons, which was slightly larger than that of mature enzyme (homodimer: 45,000 x 2). On the other hand, sodium dodecylsulfate treated precursor had the molecular size (about 50,000 daltons) slightly larger than that of the subunit of mature one by the gel permeation chromatography. These results suggest that the precursor of mitochondrial glutamic oxaloacetic transaminase exists as a dimer.

Animals↗
PubMed1982

Electrophysiological characteristics of ischemic cardiac cells in hypoxic and hyperkalemic conditions.

The difference in the electrophysiological properties between the subepicardial cells and the subendocardial cells (Purkinje fibers and ordinary myocardial cells) was examined in dogs using a microelectrode technique. The preparations were obtained one hour after coronary occlusion. Immediately after exposure to a hypoxic solution, spontaneous activities could be recorded in neither the subepicardial nor the subendocardial cells. The electrical activities induced by electrical stimulation disappeared 5-10 min after exposure to the hypoxic solution in the subepicardial cells, while they remained in the subendocardial cells. Vmax, action potential amplitude, action potential duration and resting membrane potential of the subendocardial cells were all reduced significantly in the hypoxic solution containing 7 mK K+ in contrast to those in the hypoxic solution containing 4 mM K+ (p less than 0.001). In the hypoxic solution containing 15 mM K+, all cardiac cells depolarized partially and became electrically quiescent in both normal and ischemic cardiac cells. These findings support the idea that during regional hypoxia and hyperkalemia resulting from acute coronary occlusion, heterogeneous changes in electrical activities occur between the subepicardium and the subendocardium in the ischemic regions.

Animals↗
PubMed1982

Effect of lidocaine on conduction within normal and acutely ischemic ventricular myocardium of dogs.

The effect of lidocaine on conduction within normal and acutely ischemic ventricular myocardium was studied in 45 dogs in vivo. By recording pairs of local electrograms from the endocardium and epicardium and by stimulating the ventricle close to one of a pair of electrodes, we measured conduction times in the subendocardial layer (Endo 1-2), in the subepicardial layer (Epi 1-2), and from the endocardium to the epicardium (Endo-Epi). We then estimated the effect of lidocaine on each of them. In normal myocardium, lidocaine in a therapeutic dose (serum level 2.5 +/- 0.4 micrograms/ml) did not affect any of the three conduction times, but in a larger dose (serum level 6.5 +/- 0.7 micrograms/ml) it prolonged Endo-Epi significantly (P less than 0.05) and Endo 1-2 and Epi 1-2 slightly. In acutely ischemic myocardium caused by single stage ligation of the left anterior descending coronary artery, lidocaine in a therapeutic dose prolonged Endo 1-2 and Endo-Epi significantly (P less than 0.001) in the early stage after administration but did not affect Epi 1-2 simultaneously. Lidocaine in a larger dose, however, prolonged all three conduction times (P less than 0.001). The data indicate that within normal ventricular myocardium, lidocaine does not influence conduction unless its dose is toxic, and that within acutely ischemic ventricular myocardium, at a therapeutic dose, lidocaine prolongs conduction rapidly, but this effect is produced heterogeneously in the ischemic myocardium and is poor in the subepicardial layer.

Animals↗
PubMed1979

Effects of 2-nicotinamidoethyl nitrate (SG-75) on dog coronary artery and cat papillary muscle.

Effects of 2-nicotinamidoethyl nitrate (SG-75) on isolated dog coronary artery and cat papillary muscle were investigated. SG-75 dose-dependently relaxed the isolated coronary arterial strips contracted with potassium. Large doses of SG-75 depressed contraction of papillary muscle driven with electrical stimulation and inhibited enhancement of contraction of papillary muscle induced by calcium and isoproterenol. From these results it is suggested that SG-75 may have a weak Ca++-antagonistic action.

Animals↗
PubMed1979

Inhibition of constrictor responses of dog coronary artery by atropine. A possible effectiveness of atropine on variant form of angina pectoris.

A possible effectiveness of atropine on variant form of angina pectoris was investigated using the left circumflex coronary arterial strips of dogs. Acetylcholine 10(-5)--10(-3) Gm/ml dose-dependently constricted the isolated arterial strips during potassium-contracture in 6 cases, and repetitive applications of acetylcholine could produce the similar contractions to the control. In 18 strips atropine 10(-6) Gm/ml significantly depressed the contractions of coronary arteries induced by acetylcholine 10(-5)--10(-3) Gm/ml. In 5 arterial strips atropine 10(-6) Gm/ml significantly inhibited norepinephrine-induced responses of these arteries, and by 10(-5) Gm/ml further suppression of the responses was obtained. The results suggest that atropine may suppress the contractile responses of the coronary artery induce by acetylcholine and nonrepinephrine through a muscarinic-receptor blocking action and simultaneously partly through an adrenergic alpha-receptor blocking action.

Acetylcholine↗