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Biomedical subjects

T Kinugawa

Publications and source records attributed to T Kinugawa.

At least 73 records · Page 4Linked to original sources
PubMed1991

Response of sympathetic nervous system activity to exercise in patients with congestive heart failure.

To investigate the serial sympathetic nervous system response to exercise, plasma norepinephrine (NE) and epinephrine (E) concentrations were measured at rest, during each stage of treadmill exercise, and immediately and 5 minutes after exercise in 68 congestive heart failure (CHF) patients (NYHA functional class I 24, II 25, III 19) and 30 normal subjects. Circulatory responses of NYHA class II patients increased at early stages of exercise. Systolic blood pressure and double product at peak exercise were significantly lower in NYHA class III patients. Plasma NE response of NYHA class I patients was similar to that of normal subjects. However, plasma NE at rest, and during and after exercise were significantly higher in NYHA classes II and III patients than in normal subjects and NYHA class I patients (peak NE (pg ml-1); Normals: 547 +/- 37, I: 535 +/- 53, II: 867 +/- 87, III: 1033 +/- 157). There was no significant difference in plasma E levels among the four groups. NE response to exercise was augmented according to the severity of heart failure, which suggested compensatory activation of sympathetic nervous system activity. Circulatory responses were reduced in NYHA class III patients despite the exaggerated compensatory activation of the sympathetic nervous system. Blunted circulatory responses to increased NE concentration in NYHA class III patients might relate to a decreased cardiac responsiveness to sympathetic activity in severe CHF patients.

Adult↗
PubMed1990

Excess purine degradation caused by an imbalance in the supply of adenosine triphosphate in patients with congestive heart failure.

To evaluate purine degradation in patients with congestive heart failure concentrations of serum hypoxanthine, lactate, and noradrenaline were measured before and after submaximal treadmill exercise in 12 patients with chronic congestive heart failure and nine healthy volunteers. In four patients the concentration of hypoxanthine was significantly higher than in the controls or in the remaining eight patients with congestive heart failure. Venous lactate and noradrenaline in the four patients with high concentrations of hypoxanthine were also significantly higher than those in the eight patients with normal concentrations of hypoxanthine. Patients who responded normally were also more likely to have been treated with vasodilators and angiotensin converting enzyme inhibitors. Exercise induced arrhythmias were more common in the patients with high concentrations of hypoxanthine. These results suggest that the excess purine degradation in patients with congestive heart failure might be the result of a "relative" disturbance in the supply of adenosine triphosphate caused by the shift of cellular metabolism from aerobic glycolysis to anaerobic glycolysis during submaximal exercise and that hypoxanthine (a substrate for xanthine oxidase and a source of free radicals) was increased after submaximal exercise in some patients with congestive heart failure.

Adenosine Triphosphate↗
PubMed1990

Diagnostic value of R-wave amplitude increase during treadmill exercise testing for detecting coronary artery disease.

To evaluate the diagnostic value of an exercise-induced increase in R-wave amplitude (RWA) for detecting coronary artery disease (CAD), treadmill testing using the modified Bruce protocol was performed on a CASE II computerized system (Marquette) in 10 healthy young men, 35 patients (pts) with CAD, 22 subjects with normal coronary arteries, and 11 pts with aortic or mitral regurgitation. Based on the analysis of the patterns of serial changes in RWA in lead V5, we proposed new RWA criteria for detecting CAD. (1) During exercise, RWA increases in stage 1 and subsequently increases further or remains unchanged. (2) During exercise, RWA decreases in the early phase of exercise and subsequently increases. (3) In the recovery period, RWA shows a gradual and excessive increase. A combination of the above RWA criteria showed a sensitivity, specificity and accuracy of an equal value of 86%. We conclude that an exercise-induced RWA increase is a useful indicator for detecting CAD, especially when taking the patterns of serial changes into consideration, and that the abnormal RWA increase may be related to an increase in left ventricular (LV) end-diastolic volume due to exercise-induced LV dysfunction.

Adult↗
PubMed1989

Transient QRS axis shift to the right during right coronary artery and/or left circumflex artery spasms.

The QRS axis was measured in 24 patients during ergonovine malate provocation test (EM test). Of 12 patients with significant spasm of the right coronary artery (RCA) and/or left circumflex artery (LCX), the QRS axis shifted to the right in 7 patients after the EM test (mean 8.2 degrees), and the axis shifted back to the left in 9 patients after nitroglycerin administration (mean -9.1 degrees). The sensitivity of right axis shift for RCA and LCX spasm was 58% and the specificity was 80%. Thus, right axis shift seems to be associated with myocardial ischemia due to RCA and LCX spasm and to be useful for the detection of RCA and/or LCX spasms.

Coronary Vasospasm↗
PubMed1989

A case of paroxysmal ventricular tachycardia during pregnancy.

We report a case of a 37-year-old woman who had paroxysmal ventricular tachycardia (VT) during early pregnancy. She had severe hyperemesis, palpitation at 6 weeks of gestation and many episodes of paroxysmal VT, but no apparent organic heart disease. At that time she had a transient increase of thyroid hormone levels. With bed rest and without medication, her symptoms and episodes of VT disappeared in accordance with the improvement of hyperemesis and thyrotoxicosis. She demonstrated a rare course of arrhythmias in which the deterioration of VT was observed at transient thyrotoxicosis and hyperemesis.

Adult↗
PubMed1989

[Sympathetic nervous system response to exercise in patients with congestive heart failure].

The response of the sympathetic nervous system to exercise in patients with congestive heart failure was studied in 65 patients (NYHA functional class I 28, II 23, and III 14) and 22 normal subjects (N) by submaximal treadmill testing with the modified Bruce's or Sheffield's protocols. Plasma norepinephrine (NE) and epinephrine (E) levels were also measured at rest, at the end of each stage, and immediately after and 5 min after exercise. In accordance with the severity by NYHA functional class, the exercise duration became shorter and the discontinuation of exercise with symptoms occurred more frequently. Systolic blood pressure and double products (DP) at the peak exercise were significantly lower in patients with NYHA class III. NE and increments of NE increased during exercise [peak NE (pg/ml); N: 589, I: 646, II: 1253, and III: 997] and were higher at rest, during exercise and in recovery in patients with NYHA classes II and III than in the normal subjects and NYHA class I patients. E increased gradually during exercise [peak E (pg/ml); N: 60, I: 66, II: 63, and III: 66] and there were no significant differences among the four groups. A negative correlation (r = -0.53) between the peak NE and exercise duration was observed in normal subjects, while a positive correlation (r = 0.55) was observed in patients with NYHA class II. A positive correlation (r = 0.54) between DP at the peak exercise and the peak NE was observed in patients with NYHA class I, whereas a negative correlation (r = -0.46) was observed in patients with NYHA class III. The NE response in patients with NYHA classes II and III increased significantly, suggesting compensatory activation of the sympathetic nervous system for impaired cardiac function. In conclusion, the NE response to submaximal exercise testing differs in each NYHA functional class and it might be a useful indicator to evaluate cardiac function of patients with congestive heart failure.

Aged↗
PubMed1988

Electrophysiological studies on the effects of mianserin, a tetracyclic antidepressant agent, on isolated guinea-pig papillary muscle.

We studied the effects of mianserin on the action potentials of papillary muscle from the guinea-pig. Mianserin (above 10 microM) reduced the maximum rate of the rise (Vmax) of the action potential, and shifted the Vmax-Em relationship to more negative potentials. The compound also depressed the slow action potentials of K+-depolarized papillary muscles. It is concluded that relatively high concentrations of mianserin had an inhibitory action on the electrophysiological properties of both the fast- and slow-response fibers of the heart.

Action Potentials↗
PubMed1988

The usefulness of exercise-induced QRS axis shift as a predictor of coronary artery disease.

The QRS axis of 101 patients with coronary artery disease (CAD) and 57 normal subjects without CAD who underwent coronary arteriograms were measured before and after exercise testing. There was no improvement in the sensitivity of positive axis shifts (15 degrees or greater) for CAD (18%) when compared to the value of positive ST depression (61%). However, the specificity of positive axis shifts for CAD was significantly increased (98%) when compared to the value of positive ST depression (77%). In addition, 39% of those patients with CAD (39 of 101) showed false negative ST depression, but 18% of these patients (7 of 39) showed a positive axis shift. In normal subjects 21% (12 of 57) showed false positive ST depression, but all of the 21% (12 of 12) showed negative axis shift. There was no significant difference in the increments of heart rate between positive ST depression, positive axis shift, and negative ST depression, negative axis shift. No statistical differences in the sensitivity of ST depression and an axis shift for one-, two- and three-vessel diseases were noted. The specificity of left-axis shift for the left anterior descending artery lesion was 98% and the specificity of right-axis shift for the right coronary artery and/or left circumflex artery lesion was 91%. Therefore, the axis shift response is no more sensitive for the detection of CAD than ST depression. However, when a positive axis shift is observed, one can predict two things: the CAD and the localization of the coronary stenosis.

Arrhythmias, Cardiac↗
PubMed1988

Effects of pirmenol hydrochloride on the spontaneous action potentials and membrane current systems of rabbit sinoatrial node cells.

The electrophysiologic effects of pirmenol hydrochloride on rabbit sinoatrial node cells were examined and compared with those of several class I antiarrhythmic agents. At 1 microM, pirmenol decreased the heart rate and the rate of diastolic depolarization and increased the action potential duration at half-amplitude. Above 10 microM, the agent also decreased the maximum rate of rise (Vmax) and the action potential amplitude significantly. The order of the inhibitory potency on Vmax was apridine greater than 711389-S greater than pirmenol greater than mexiletine greater than tocainide. With respect to the current systems, pirmenol decreased the slow inward current (Isi) and the time-dependent potassium outward current (IK). The agent also prolonged the recovery time constant of Isi without any changes in the decay process of the tail current (IK). These findings suggest that pirmenol depresses the spontaneous discharge of the sinoatrial node through a decrease in Isi and Ik.

Action Potentials↗
PubMed1988

Effects of amoxapine on electrophysiological properties of rabbit sinoatrial node.

The effects of amoxapine on membrane potentials and membrane currents of rabbit sinoatrial node were studied using the double microelectrode voltage clamp method. Amoxapine (greater than 1 mumol.litre-1) decreased the heart rate and the maximum rate of rise and the rate of diastolic depolarisation in a dose dependent manner. Above 3 mumol.litre-1, amoxapine also decreased the action potential amplitude and prolonged the action potential duration at half amplitude. These electrophysiological changes induced by amoxapine were relatively reduced in a high calcium medium (extracellular calcium concentration 4.0 mmol.litre-1). In voltage clamp experiments amoxapine depressed the slow inward current, the time dependent potassium current, and the hyperpolarisation activated inward current. The major effect, however, was considered to be a reduction of the slow inward current. It is concluded that amoxapine produced an inhibitory action on the electrical activity of sinoatrial node, and this action is mainly explained by an inhibition of calcium influx through the cell membrane.

Action Potentials↗
PubMed1988

Inhibitory actions of amoxapine, a tricyclic antidepressant agent, on electrophysiological properties of mammalian isolated cardiac preparations.

1. The electrophysiological effects of amoxapine were examined in guinea-pig isolated papillary muscles and rabbit sinoatrial nodes using a conventional microelectrode technique. 2. In papillary muscles, amoxapine above 10 microM caused a dose-dependent decrease in the maximum upstroke velocity (Vmax) of the action potential and in the action potential amplitude (APA), whereas the action potential duration at 90% repolarization (APD90) was significantly prolonged. For a decrease in Vmax, amoxapine produced a negative shift of the curve relating Vmax to the resting potential (Em) along the voltage axis to more negative membrane potentials. 3. Amoxapine also decreased Vmax and the overshoot potential of K+-depolarized slow action potentials of papillary muscle preparations. 4. In spontaneously beating sinoatrial node preparations, amoxapine above 3 microM reduced the heart rate, Vmax, APA and the slope of phase 4 depolarization in a dose-dependent manner. 5. It was concluded that amoxapine exerts inhibitory actions on fast- and slow-response fibres of the heart and these actions can be mainly explained by inhibition of both fast Na+ and slow Ca2+ channels.

Action Potentials↗
PubMed1988

Actions of flunarizine dihydrochloride on the electrical activity of isolated guinea-pig papillary muscle and rabbit sino-atrial node.

Effects of flunarizine on electrophysiological properties of isolated guinea-pig papillary muscles and rabbit sino-atrial nodes were examined using conventional microelectrode and double-microelectrode voltage clamp methods. Although flunarizine did not affect the maximum rate of rise of the action potential (Vmax) in fast response fibers, the compound depressed the slow action potentials of K+-depolarized papillary muscle (at above 10 microM) and reduced the automaticity of sino-atrial node (at above 3 microM). In voltage clamp experiments, flunarizine selectively suppressed the slow inward current of sino-atrial node specimens. It is concluded that relatively high concentrations of flunarizine directly modify the electrical activity of isolated mammalian myocardium via a suppression of Ca2+ influx through the cell membrane.

Action Potentials↗
PubMed1987

Effect of trimebutine maleate on sinus node pacemaker activity of the rabbit.

The electrophysiological effects of trimebutine maleate were studied on rabbit sinus node cells with the two-microelectrode voltage clamp method. Trimebutine (above 10 microM) produced a negative chronotropic effect accompanied by decreases in the maximum upstroke velocity at phase 0, slope of phase 4 depolarization and action potential amplitude. The effects on the current systems were depression of the slow inward current and a decrease in the current oscillations induced by elevating [Ca]0. It is concluded that trimebutine exerts a Ca2+ channel blocking effect on the sinus node pacemaker cells.

Action Potentials↗
PubMed1987

Comparison of the chronotropic responses to tri- and tetracyclic antidepressants in isolated sinoatrial node preparations from the rabbit.

The effects of maprotiline and mianserin, tetracyclic antidepressant agents, on membrane potentials and currents of rabbit sinoatrial node cells were studied and compared to those of a tricyclic antidepressant compound, imipramine. Imipramine (10 microM), maprotiline (30 microM) and mianserin (100 microM) significantly decreased the spontaneous rate, the maximum rate of rise and the action potential amplitude. The slope of the diastolic depolarization was also decelerated by these drugs. On the current systems, imipramine (10 microM), maprotiline (10-30 microM) and mianserin (40-100 microM) decreased the slow inward current, the time-dependent potassium outward current and the hyperpolarization-activated inward current. Although all these antidepressant agents have qualitatively similar depressant effects, the inhibitory potency on the electrical activity of sinoatrial node was: imipramine greater than maprotiline greater than mianserin. These electrophysiological observations suggest that tetracyclic antidepressant agents might have less pronounced cardiotoxicity than did tricyclic antidepressants in slow response fibers.

Action Potentials↗
PubMedDate not supplied

Effects of enalapril on the exercise capacity and neurohumoral factors during exercise in patients with chronic heart failure.

The effects of enalapril on exercise capacity and neurohumoral factors during exercise were evaluated in 10 patients with heart failure. Echocardiograms and exercise testing with expired gas analysis were performed before and after enalapril. Blood samples were obtained before and after exercise. Both ejection fraction and percent fractional shortening increased with enalapril (p < 0.05). The anaerobic threshold and peak VO2 did not change with enalapril. Epinephrine and norepinephrine levels at peak exercise decreased with enalapril (p < 0.1). Plasma renin both at rest and at peak exercise increased with enalapril (p < 0.1). Angiotensin II was lower after enalapril both at rest and at peak exercise (p < 0.1 and p < 0.05, respectively). Aldosterone was lower after enalapril both at rest and at peak exercise (p < 0.05). Atrial natriuretic peptide (ANP) was lower after enalapril both at rest and at peak exercise. There was no significant correlations between peak VO2 and changes in neurohumoral factors before and after enalapril during exercise. In conclusion, neurohumoral changes with enalapril occurred during exercise even if exercise capacity did not improve. Moreover, the improvement of cardiac function at rest and neurohumoral factors with enalapril did not lead to a change of exercise capacity.

Aged↗
PubMedDate not supplied

Responses of plasma catecholamines, renin-angiotensin-aldosterone system, and atrial natriuretic peptide to exercise in patients with essential hypertension.

Neurohormonal responses to exercise have not been studied fully in patients with essential hypertension (HT). This study determined if neurohormonal responses to exercise are altered between three subgroups of HT categorized by basal plasma renin activity (PRA). Plasma norepinephrine, epinephrine, atrial natriuretic peptide (ANP), PRA, angiotensin II (AII), and aldosterone were measured at rest and after submaximal treadmill exercise in 39 patients with essential HT (WHO classes I-II) and 13 controls. Patients with HT were divided into three subgroups based on the PRA level [low-renin (< 0.5) HT (n = 14), normal-renin (0.5-2.0) HT (n = 13), and high-renin (> 2.0) HT (n = 12)]. Patients with HT had higher blood pressure during exercise compared to controls, but blood pressure responses were similar among low-, normal-, and high-renin HT. Neurohormonal factors were comparable between all hypertensives and controls, except for higher plasma AII at rest in patients with HT. When neurohormones were compared among three subgroups of HT, plasma norepinephrine and epinephrine responses were similar. Patients with high-renin HT had higher PRA and AII, and lower ANP levels at rest and after exercise. In all hypertensives, negative correlations were observed between resting PRA and resting ANP (r = -0.41, p < 0.01), as well as peak PRA and peak ANP (r = -0.33, p < 0.05). Thus, neurohormonal responses to exercise varied with similar cardiac responses among subgroups of essential HT stratified according to renin levels. Patients with high-renin HT had augmented renin-angiotensin system activity with a decrease in ANP levels both at rest and after exercise. A reciprocal relationship between renin-angiotensin system activity and ANP was observed both at rest and after exercise in HT.

Adult↗