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Biomedical subjects

I Sato

Publications and source records attributed to I Sato.

At least 379 records · Page 21Linked to original sources

Effect of cianidanol (KB-53) on the activity of mouse cytotoxic-T-lymphocytes.

The effect of cianidanol (KB-53) on the mouse cytotoxic-T-lymphocyte (CTL) activity of the splenic cells was investigated. The CTL activity of the splenic cells prepared from C3H/He, DBA/2 and CBA strain mice which had been sensitized with EL-4 cells were recognized markedly 11 d after the sensitization. The CTL activity showed an antigen specificity. KB-53, in a dose range of 125-1000 mg/kg, augmented the mouse CTL activity in a dose-dependent manner by oral administration once daily for 5 d beginning immediately after the sensitization. This CTL activity disappeared with treatment of the splenic cell with anti-thy-l serum and normal guinea pig serum, therefore, it was confirmed that the cytotoxic activity of the splenic cells which were prepared from the mice sensitized with EL-4 cells depended on the T-cell activity.

Animals↗

Effect of cianidanol (KB-53) on the activity of mouse natural killer cells.

The effect of cianidanol (KB-53) on the mouse natural killer (NK) cell activity of the splenic cells was investigated using YAC-1 cells as target cells. The oral administration of KB-53 at a dose of 500 mg/kg augmented significantly the NK cell activity. The activity was observed maximally 3 d after the administration, and significant difference from the control was observed even at 7 d after the administration of KB-53. The oral administration of KB-53, at a dose range of 125-500 mg/kg, augmented the NK cell activity in a dose-dependent manner at 3 d after the administration.

Animals↗

Relation between the widening of the fragmented atrial activity zone and atrial fibrillation.

Fragmented electrical activity is often recorded by a local atrial electrogram in response to atrial extrastimuli. To assess the relation between fragmented activity and the spontaneous occurrence of atrial fibrillation or flutter (AFF), the fragmented activity zone was measured in 57 patients. The electrograms of the high right atrium, low right atrium and left atrium (through the coronary sinus) were recorded simultaneously during high right atrial stimulation. The fragmented activity zone was defined as the S1-S2 interval (S1 = stimulus of a basic beat, S2 = stimulus of a premature beat) during which a significant fragmented activity was recorded by a high right atrial electrogram after S2. Fifteen patients had neither sinoatrial disease nor atrial arrhythmias (Group I, controls), 16 had sick sinus syndrome (SSS) with a history of paroxysmal AFF (Group II), 14 had SSS without a history of paroxysmal AFF (Group III), and 12 had idiopathic paroxysmal AFF (Group IV). The fragmented activity zone was significantly wider in Group II (112 +/- 26 ms [mean +/- standard deviation], p less than 0.001), Group III (77 +/- 38 ms, p less than 0.001) and Group IV (86 +/- 19 ms, p less than 0.001) than in Group I (31 +/- 25 ms). Patients in Group II had a wider fragmented activity zone than those in Group III (p less than 0.01). Thus, the widening of the fragmented atrial activity zone is characteristic of AFF and may be a good index of a tendency to develop spontaneous AFF.

Adolescent↗

Limiting factor for the initiation of reentrant tachycardia in concealed Wolff-Parkinson-White syndrome.

We studied the limiting factor for the initiation of reentrant tachycardia in 14 patients with concealed Wolff-Parkinson-White syndrome by comparing atrial refractoriness and echo times. When relatively late atrial premature beats (A2) were not accompanied by an atrial echo (Ae), the echo times were estimated from the antegrade A2-V2 conduction time of A2, since the retrograde conduction time via the accessory pathway remained constant regardless of the degree of prematurity. Thus, A2-Ae curves including the minimal echo time and the longest A2-Ae without Ae could be drawn in all patients. Then the curve was compared with the atrial effective refractory periods and the functional refractory periods of A2 in each patient. Atrial refractoriness which might limit the occurrence of an Ae is not that of basic beats (A1) but that of premature beats (A2). In all patients the atrial effective refractory periods of A2 were much shorter than the minimal echo time and the longest A2-Ae without Ae, suggesting that the atrial effective refractory period is not responsible for limiting the initiation of an Ae. Also in 13 of 14 patients, the atrial functional refractory periods were shorter than the minimal echo time and the longest A2-Ae without Ae. In one patient, the atrial functional refractory period was sandwiched between the minimal echo time and the longest A2-Ae without Ae suggesting the atrial functional refractory period of Ae might be responsible for limiting the occurrence of an Ae in this patient.

Adult↗

The effect of pacing site on the echo zone in patients with concealed Wolff-Parkinson-White syndrome.

In 14 patients with the left-sided concealed Wolff-Parkinson-White syndrome, the effects of changing atrial pacing site on the echo zone were evaluated. In 12 patients, re-entrant tachycardia was induced by premature stimuli both in the coronary sinus (CS) and the high right atrium (HRA). In the remaining 2 patients, the tachycardia was induced by premature stimuli only in the CS. The lower limit of the echo zone was shifted to a longer coupling interval during CS pacing in 12 patients. The longer effective refractory period (ERP) of the CS was responsible for the shifting of the lower limit of the echo zone to a longer coupling interval. The upper limit of the echo zone was shifted to a longer coupling interval during CS pacing in 10 patients. The difference of atrial conduction times from the site of stimulation to the 2 conduction pathways (the normal conduction pathway and the accessory pathway) is thought to be responsible for the shifting of the upper limit of the echo zone.

Adult↗

Exercise-induced cyclic episodes of S-T segment elevation in a patient with variant angina.

A unique case of variant angina is described in which cyclic S-T segment elevation was reproducibly induced by exercise. The treadmill test revealed cyclic S-T segment elevation to occur from the first minute onward, recurring with a cycle length of 2 min throughout the exercise while the work load was being increased. Similar cyclic episodes were also induced by the cold pressor test, and the ambulatory electrocardiogram demonstrated spontaneous episodes of S-T segment elevation with a similar cycle length in early mornings. Coronary arteriography revealed a fixed lesion in the mid-portion of right coronary artery with a 90% narrowing associated with coronary spasm leading to subtotal occlusion. The cyclic episodes were abolished by the administration of the calcium antagonist diltiazem. The spontaneous phasic activity of coronary arterial muscle is discussed as a possible cause or mechanism.

Angina Pectoris, Variant↗

[Effects of cianidanol (KB-53) on experimental liver injury in mice--histopathological, histochemical and enzyme-histochemical studies].

Protective effects of KB-53 on acute liver injury induced by carbon tetrachloride (CCl4) and 1-naphtylisothiocyanate (ANIT) in mice was investigated by means of histopathological, histochemical and enzymehistochemical examinations. Diffuse centrilobular necrosis, ballooning degeneration of hepatocytes and hemorrhage were markedly observed in the livers of the mice one to three days after a subcutaneous injection of CCl4. On the other hand, in the livers of KB-53 pretreated mice, forcal necrosis was observed and inflammatory cells had already infiltrated one day after CCl4-intoxication. Three days later, remarkable development of absorbent granulation tissues with syncytium and hepatocytic mitosis was observed. Furthermore, a number of PAS positive materials such as mucopolysaccharides and mucoproteins were detected in the livers of KB-53 pretreated mice. KB-53 inhibited the disappearance of glucose-6-phosphatase (G-6-Pase) in the liver after CCl4-intoxication and the rise of alkaline phosphatase (Al-Pase) in the liver after ANIT-intoxication. In addition, KB-53 inhibited the rise of Al-Pase and total bilirubin in the serum of mice after CCl4 and ANIT-intoxication. All these findings suggest that KB-53 protects liver against the morphological and functional changes, and it potentiates the proliferative and regenerative activity of the liver impaired with CCl4 and ANIT.

1-Naphthylisothiocyanate↗