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Biomedical subjects

M Arita

Publications and source records attributed to M Arita.

At least 379 records · Page 21Linked to original sources
PubMed1977

Comparative studies of several vaccinia virus strains by intrathalamic inoculation into cynomolgus monkeys.

From the comparative studies of the virulence of several vaccinia virus strains by intrathalamic inoculation into cynomolgus monkeys, the following results were observed. The CV1 virus was most virulent, the New York City Board of Health, Ikeda, EM63, and Lister viruses were slightly less virulent, and DIs and LC16 viruses least virulent. The characteristic findings were widespread inflammatory lesions in the meninges and choroid plexus which were closely associated with the replication of vaccinia virus, and parenchymal lesions which might be referred to a encephalopathy in the deceased monkeys. Meningoencephalitis was, however, ofter recognized in the monkeys sacrificed at 14 days postinoculation and those dying late.

Animals↗
PubMed1977

Electrophysiologic effects of diltiazem, a new slow channel inhibitor, on canine cardiac fibers.

The effect of diltiazem hydrochloride (CRD-401), a coronary vasodilator, was investigated in isolated perfused canine ventricular muscles and Purkinje fibers using microelectrodes. The drug at a concentration of 1 microng/ml lowered the level of action potential plateau and shortened the duration in both ventricular and Purkinje fibers without change in maximum rate of rise (Vmax) or resting potential. Contractile tension of ventricular muscle was markedly decreased with shortening of plateau. With higher drug concentrations (5 microng/ml), Vmax in both ventricular muscle and Purkinje fiber decreased about 20% without change in resting potential, and the effect on repolarization became more marked. The drug blocked spontaneous firing which appeared in depolarized Purkinje fibers and abolished the automaticity elicited in electrically depolarized ventricular muscles. Input resistance of ventricular muscle, measured by small, hyperpolarizing short pulses, was not changed appreciably by the drug; suggesting no change in potassium conductance. These results suggest that the drug is a slow channel inhibitor, and its clinical implication is discussed in terms of antiarrhythmic activity.

Action Potentials↗
PubMed1977

Factors concerning the immunity to poxvirus infection.

Two kinds of early antigens were shown in vaccinia-infected cells, one heat (56 degrees, 30 min)-stable (ES antigen) and the other heat-labile (EL antigen). Both antigens do not induce circulating neutralizing antibody in rabbits, but resistance to intradermal inoculation of active virus was observed when animals were immunized with either antigen in combination with Freund's complete adjuvant. Vaccinia-specific haemagglutinin (VHA) associated with infected cell membrane was purified and its antigenicity was also studied. Rabbits showed a good antibody response to VHA and some animals also showed neutralizing antibody, though in a small amount, to either intracellular (ICV) or extracellular (EVC) virus. Rabbits immunized with membrane antigens obtained from either VHA-positive or negative virus in combination with Freund's adjuvant showed skin restance to challenge with active virus. It was suggested that antibody against ECV might be responsible for the resistance.

Animals↗
PubMed1976

Cytotoxic effect of the thermostable direct hemolysin produced by Vibrio parahaemolyticus on FL cells.

The thermostable direct hemolysin produced by Vibrio parahaemolyticus showed cytotoxic activity on FL cells derived from human amniotic membrane. Scanning electron micrographs of the whole cells showed that the microvilli on the cell surface decreased in number and changed in shape on treatment with the hemolysin. Most of the microvilli disappeared before death of the cells, as judged from the results of staining the cells with trypan blue and measuring release of alkaline phosphatase from the cells. Electron micrographs of thin sections ofthe cells showed that the cytoplasm of the cells was not significantly affected by treatment with sublethal amounts of hemolysin, even when the microvilli on the cell surface were significantly affected. Lethal amounts of hemolysin affected the cytoplasm and caused disarovilli on the cell surface are affected by treatment with the hemolysin before cytoxic effects develop.

Alkaline Phosphatase↗
PubMed1976

Automaticity and time-dependent conduction disturbance produced in canine ventricular myocardium. New aspects for initiation of ventricular arrhythmias.

1) In isolated canine ventricular myocardium, automaticity could be induced by a passage of small depolarizing DC-currents. The mechanism was attributed to inflowing Ca++ and Na+ currents and time-dependent deactivation of outward K+ current under a condition of high membrane resistance due to an anomalous rectification. Significance of the automaticity was discussed in relation to the ventricular arrhythmias encountered in very early stage of myocardial infarction. 2) In in situ canine hearts, chloropromazine induced time (preceding cycle length)-dependent decrease in conduction velocity within the ventricle. Thus QRS-duration of non-premature beats was lenghtened at rapid pacing rates while QRS-duration of atrial premature beats was lengthened also at short coupling intervals in the drug-treated dogs. These slow conductions were not due to reduced take-off potential of action potentials bue due to drug-induced slow recovery of rapid Na+ system. The phenomenon may be responsible for reported QRS-prolongation and fatal ventricular arrhythmias encountered in the patients receiving phenothiazines.

Action Potentials↗
PubMed1976

Spontaneous electrical activity induced by depolarizing currents in canine ventricular myocardium. A preliminary note.

Spontaneous action potential (AP) discharge could be induced by an application of long (5-10 sec) depolarizing currents in 68% of canine ventricular myocardium tested in the voltage range between about -65 and -10 mV. The constant currents of various intensities were applied across a sucrose gap, and intracellular potentials were recorded with a microelectrode. The firing rate of the AP's was voltage-dependent and ranged between 0.7 and 2.5 Hz. The AP was dependent on both [Ca++]0 and [Na+]0. Increase of [Na+]0. Increase of [Na+]0 from 37 to 149 mM increased the firing rate, maximum rate of rise, and overshoot of the AP's while increase of [Ca++]0 from 0.45 mM to 1.8 and 7.2 mM increased the firing rate and maximum rate of rise, but did not change the amplitude of overshoot. AP discharges were not blocked by tetrodotoxin (10(-5) Gm/ml), but were effectively blocked by verapamil (6 X 10(-6) Gm/ml). Adrenaline (5 X 10(-6) Gm/ml) initiated AP's in otherwise quiescent preparations. The results suggest that spontaneous AP's may be produced by inflowing of slow Na+ and Ca++ currents modified by underlying change of K+-permeability. Possible clinical significance of this phenomenon is discussed in relation to ventricular arrhythmia.

Action Potentials↗
PubMed1976

The prolongation of QRS-duration resulting from delayed recovery of ventricular excitability. A new mechanism for intraventricular conduction disturbance. A preliminary note.

Chlorpromazine (1, 5, and 20 mg/Kg) was injected intravenously to anesthetized and open-chest dogs under artificial respiration. Using right atrial pacing, the heart rate was increased stepwise from intrinsic sinus rate to higher rate where the A-V block first developed. ECG (II) was recorded simultaneously with arterial blood pressure, ventricular monophasic action potentials and left atrial electrogram. In the control, QRS-duration was constant (46.9 +/- 0.8 msec) irrespective of heart rate. After the drug injection, however, the duration increased significantly with increasing heart rate, the effect depending on the injected dosage (r==0.283, P less than 0.1 in 1 mg/Kg; r==0.406, P less than 0.01 in t mg/Kg; r==0.631, P less than 0.001 in 20 mg/Kg). During the drug action, QRS-duration of atrial premature beats was also longer than that of sinus beats, and the lengthening increased with shortening of preceding cycle length. The observed QRS-prolongations were due to neither incomplete ventricular repolarization nor bundle branch block. The mechanism of prolongation was attributed to delayed or time-dependent recovery of ventricular excitability, i.e., slowed removal of inactivation in rapid sodium system in the ventricular muscle fibers.

Animals↗