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T Kohya

Publications and source records attributed to T Kohya.

At least 37 records · Page 2Linked to original sources
PubMed1997

Metabolic abnormality of calf skeletal muscle is improved by localised muscle training without changes in blood flow in chronic heart failure.

OBJECTIVE: To investigate whether localised skeletal muscle training, which does not have a great influence on the heart, improves abnormalities of calf muscle metabolism in patients with chronic heart failure. METHODS: Seven cardiac patients in New York Heart Association class II and III undertook a random order crossover trial. Training consisted of unilateral calf plantar flexion exercise. Before and after training, the patients' metabolic responses were examined during the calf exercise test with phosphorus-31 nuclear magnetic resonance spectroscopy (31P-MRS) and calf blood flow with plethysmography. The new Borg scale was employed as a subjective fatigue scale. RESULTS: In a constant load exercise test (70% of maximum load achieved during the incremental exercise), standardised phosphocreatine and intracellular pH decreased less after training (p < 0.05, repeated measures analysis of variance). The new Borg scale improved significantly after training (p < 0.05). Blood flow did not change significantly in either test. CONCLUSIONS: In patients with chronic heart failure, localised calf skeletal muscle training improved oxidative capacity without changes in calf blood flow. This training also improved the subjective fatigue scale. This training method may therefore alleviate leg fatigue experienced in daily activities.

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PubMed1997

[Evaluation of myocardial perfusion by 99mTc-tetrofosmin SPECT before and after emergent percutaneous transluminal coronary angioplasty for acute myocardial infarction].

To assess clinical performance of coronary perfusion in patients with acute myocardial infarction following successful PTCA, various 99mTc-tetrofosmin (TF) SPECT were obtained. Twenty-eight patients with acute myocardial infarction underwent TF SPECT before emergent PTCA (acute phase), after 7 days (subacute phase) and 4 weeks (chronic phase) later. Twenty-eight patients divided into 2 groups. Early group; time lug from onset of AMI till PTCA is 6 hours or shorter (n = 17), delayed group; time lug is more than 6 hrs (n = 11). The defect scores were graded by 4 points grading system (0 as normal to 3 as defect) in 14 myocardial segments. In early group, the mean defect score was 13 +/- 7 at acute phase, 6 +/- 5 at subacute phase, and 3 +/- 4 at chronic phase. In delayed group, the mean value of defect score at each phases were 18 +/- 7, 14 +/- 7, and 13 +/- 7. The improvement of defect score of early group was significantly larger than that of delayed group (p < 0.005). These data indicate that PTCA therapy for acute MI patients is useful particularly in the early stage following acute MI.

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PubMed1996

Expression of vascular endothelial growth factor in human myocardial infarction.

To define mechanisms that may influence collateral circulation and angiogenesis, we investigated vascular endothelial growth factor (VEGF) mRNA expression in human hearts. In non-ischemic human hearts, VEGF mRNA was not detected in vessels, but was found in cardiomyocytes. In hearts with myocardial infarction, the intensity of the VEGF signal was much higher in smooth muscle cells of arterioles adjacent to necrosis and in infiltrating macrophages than in myocytes around the site of the necrosis. This study suggests that levels of VEGF expression are high in smooth muscle cells and macrophages around infarcted areas after myocardial infarction and that VEGF may play a role in promoting collateral circulation and angiogenesis in human ischemic hearts.

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PubMed1995

Abrupt augmentation of ST segment elevation associated with successful reperfusion: a sign of diminished myocardial salvage.

To investigate the significance of abrupt augmentation of ST segment elevation immediately after reperfusion, 36 patients with an initial acute anterior myocardial infarction successfully treated with thrombolysis were studied. Immediately after reperfusion was performed, 17 (47%) patients showed abrupt augmentation of ST segment elevation of anterior area (E group), and 19 (53%) patients did not (N group). The time to reperfusion was not significantly different between the two groups. In the E group the peak level of creatine kinase MB isozyme was higher (p < 0.05) than in the N group. The left ventricular ejection fraction (EF) did not increase in the E group from acute to chronic phase. However, in the N group EF increased significantly. The difference in EF in the chronic phase was significant between the two groups (p < 0.05). The infarcted regional wall motion (RWM) did not increase in the E group, whereas in the N group it increased markedly (p < 0.05). In addition, the infarcted RWM in the chronic phase was worse in the E group than in the N group (p < 0.05). Abrupt augmentation of ST segment elevation associated with successful reperfusion appears to reflect diminished myocardial salvage.

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PubMed1995

Regression of left ventricular hypertrophy prevents ischemia-induced lethal arrhythmias. Beneficial effect of angiotensin II blockade.

To evaluate the preventive effect of regression of left ventricular hypertrophy (LVH) on sudden cardiac death (SCD), the incidence of ventricular tachycardia or ventricular fibrillation (VT/Vf) after left coronary artery occlusion in Langendorff preparations was studied in the following five groups: (1) spontaneously hypertensive rats (SHR) without treatment (SHR-N), (2) SHR treated with captopril (SHR-C), (3) SHR treated with the angiotensin II receptor antagonist TCV-116 (SHR-A), (4) SHR treated with hydralazine (SHR-H), and (5) Wistar-Kyoto (WKY) rats. Although blood pressure was equally lowered in all treated groups, SHR-C and SHR-A but not SHR-H showed regression of LVH. The incidence of VT/Vf was 5% in WKY rats, 63% in SHR-N (P < .005 versus WKY rats), 0% in SHR-C, 10% in SHR-A, and 45% in SHR-H (P < .05 versus WKY rats). Further evaluation of the effect of TCV-116 revealed that SHR treated with a low dose of TCV-116 (1 mg/kg per day) showed a decrease in left ventricular mass with only a little decrease in blood pressure and that the incidence of VT/Vf was reduced in association with the degree of regression of LVH. Electrophysiological study using microelectrode techniques revealed that in the LVH groups (SHR-N and SHR-H), the action potential duration (APD) of the left ventricular papillary muscle was more prolonged than in WKY rats, whereas APD shortened to a greater extent during superfusion with a hypoxia/no-glucose solution. APD showed no difference in the regression groups (SHR-C and SHR-A) compared with the WKY group.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1994

Involvement of muscarinic M1 receptor in the central pathway of the serotonin-induced Bezold-Jarisch reflex in rats.

The involvement of central muscarinic receptors in mediating the Bezold-Jarisch reflex elicited by injection of 5-hydroxytryptamine (5-HT) was studied in urethane/chloralose-anesthetized rats. Intravenous bolus injection of 5-HT (3.1 to 50 micrograms/kg) evoked a short-lasting dose-related bradycardia and hypotension, the Bezold-Jarisch reflex, accompanied with bursts of the efferent cervical vagus nerve. Systemic administration of atropine (0.1 and 1 mg/kg) blocked not only the cardiac responses but also the efferent cervical vagus nerve activity changes. Although the afferent cervical vagus nerve was also activated by an intravenous bolus injection of 5-HT, these responses were not altered by the systemic administration of even a high dose of atropine (1 mg/kg). Intracerebroventricular (i.c.v.) administration of pirenzepine (1 and 10 micrograms/10 microliters), a selective M1 receptor antagonist, caused a rightward shift of the 5-HT dose-response curve for efferent vagus nerve activity. In contrast, i.c.v. administration of muscarinic type 2 receptor antagonist, gallamine, and type 3 receptor antagonist, p-fluorohexahydrosiladifenidol, failed to alter the response in nerve activity to 5-HT. These results suggest that the activation of central nervous muscarinic receptors might be involved in mediating the Bezold-Jarisch reflex and that the subtype might belong to type 1.

Animals↗
PubMed1989

Silent myocardial ischemia during Holter monitoring in ischemic heart disease.

The purpose of this study was to investigate the frequency and characteristics of silent myocardial ischemia in patients with proven ischemic heart disease using ambulatory ECG monitoring, and to clarify possible mechanisms for the absence of symptoms during these attacks. A total of 182 patients, including 78 patients with stable effort angina (EA), 12 with unstable angina (UA), and 92 with prior myocardial infarction (MI), were examined. During daily activities, 43% and 56% of all transient ST-segment depression observed was asymptomatic in patients with EA and MI, respectively. In addition, 74% of all ischemic episodes were asymptomatic in patients with UA. In patients with EA, 35% exhibited both symptomatic and asymptomatic attacks, and the duration and magnitude of ST-segment depression were greater for symptomatic attacks than for asymptomatic attacks. On the other hand, in patients with MI, 55% had only asymptomatic attacks. When asymptomatic episodes in patients who had only asymptomatic attacks were compared with symptomatic episodes in patients who had only symptomatic attacks, asymptomatic episodes tended to be associated with a greater magnitude of ST depression. They were also significantly longer in duration than the symptomatic episodes. All patients with UA had both symptomatic and asymptomatic episodes, and the magnitude and duration were significantly greater during the former. These results lead us to conclude that: (1) silent myocardial ischemia is observed frequently in patients with EA and MI during daily activities. In particular, patients with MI tend to have more severe silent ischemia. (2) In patients with EA and UA, the severity of ischemia is a fundamental factor in determining the presence or absence of pain during an ischemic attack.(ABSTRACT TRUNCATED AT 250 WORDS)

Activities of Daily Living↗
PubMed1988

Susceptibility of hypertrophied rat hearts to ventricular fibrillation during acute ischemia.

This study compared arrhythmias induced by acute ischemia in Langendorff preparations of normal and hypertrophied rat hearts. Left ventricular pressure overload was induced by partial ligation of the abdominal aorta 6 to 8 weeks prior to study. The ratio of left ventricular weight to body weight (LVW/BW) and systolic blood pressure (SBP) were significantly higher in two groups of rats with hypertrophied hearts (moderate hypertrophy: 2.68 +/- 0.06 mg/g, 182 +/- 3 mmHg; severe hypertrophy: 3.31 +/- 0.03 mg/g, 238 +/- 5 mmHg) than in normal hearts (2.18 +/- 0.03 mg/g, 125 +/- 3 mmHg), while there were no differences in body weights. During 30 min of ischemia produced by left coronary artery occlusion in the Langendorff preparations, ventricular fibrillation occurred in six of 20 (30%) normal, six of nine (67%) moderately hypertrophied, and 14 of 14 (100%) severely hypertrophied preparations (P less than 0.001 normal vs severely hypertrophied). Tachyarrhythmias occurred in 15 of 20 (75%) normal, eight of nine (89%) moderately hypertrophied, and 14 of 14 (100%) severely hypertrophied hearts. Heart rate and coronary efflux before and during the ischemic period did not differ between normal and hypertrophied hearts. The ratio of non-perfused to perfused areas of the left ventricle, measured by Evans blue dye staining and with computerized planimetry, also was not different for normal (57.6 +/- 2.3%) and hypertrophied hearts (moderate hypertrophy 62.5 +/- 3.3%, and severe hypertrophy 59.1 +/- 2.0%). Additional control studies using larger hearts from older rats also indicate that myocardial mass was not an important determinant of ischemic arrhythmias in hypertrophy. Prolongation of endocardial and epicardial conduction time during 30 min of ischemia was not different between normal and hypertrophied hearts. Action potential duration and refractory periods were significantly longer in ventricular cells of hypertrophied hearts than in normals, and superfusion with hypoxia/zero glucose solution shortened these parameters to a greater extent in hypertrophied cells. These results lead us to conclude that hypertrophied hearts have a greater susceptibility to ventricular fibrillation during acute ischemia, and that dispersion of refractoriness may play a role in this phenomenon.

Action Potentials↗
PubMed1987

Automaticity, triggered activity, and responses to adrenergic stimulation in cat subendocardial Purkinje fibers after healing of myocardial infarction.

We studied automaticity, triggered activity, and responses to alpha- and beta-adrenergic stimulation in subendocardial Purkinje fibers overlying healed infarct scars (infarct preparation) and from remote normal zones (noninfarct preparation) of cat left ventricles. The preparations were studied 2 to 4 months after ligation of multiple distal tributaries of the left anterior descending and circumflex arteries. Subendocardial Purkinje fibers from corresponding areas of normal hearts served as control samples (control preparation). Transmembrane action potential characteristics and rates of automaticity (spontaneous phase 4 depolarization) did not differ among control, noninfarct, and infarct preparations. However, overdrive at cycle lengths of less than 400 msec suppressed automaticity to a greater degree in Purkinje fibers of infarct preparations than those of control and noninfarct preparations. Changes in automatic rate during superfusion with isoproterenol (10(-10)M to 10(-6)M) were not different among the three groups of preparations, but exposure to phenylephrine (10(-9)M to 10(-5)M) in the presence of 5 X 10(-7)M propranolol reduced the automatic rate to a greater degree in Purkinje fibers of infarct preparations than those of control or noninfarct preparations. Triggered activity arising from delayed afterdepolarizations was recorded in 10 of 29 infarct preparations (34%), but not in 12 control and 10 noninfarct preparations. These afterpotentials were augmented by increasing extracellular Ca++ concentration, 10(-7)M isoproterenol, and 10(-5)M phenylephrine in the presence of 5 X 10(-7)M propranolol. We conclude that Purkinje fibers overlying healed infarct scars have altered physiology of spontaneous automaticity, enhanced responses to alpha-adrenergic interventions, and a tendency to triggered activity, and that both alpha- and beta-adrenergic effects may result in worsening of arrhythmias by augmentation of afterpotentials in healed myocardial infarction.

Action Potentials↗