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Biomedical subjects

T Kinugawa

Publications and source records attributed to T Kinugawa.

At least 55 records · Page 3Linked to original sources
PubMed1995

Nicorandil suppressed myocardial purine metabolism during exercise in patients with angina pectoris.

To elucidate the effect of Nicorandil on myocardial energy metabolism and myocardial sympathetic activity, we administered Nicorandil orally to eight patients with angina pectoris prior to exercise testing. Arterial and coronary sinus levels of lactate, ammonia, hypoxanthine (HX), adrenaline and noradrenaline were measured during exercise in order to determine the irrespective myocardial extraction ratios (MER). Compared to placebo, Nicorandil increased the time to development of significant ST depression (322 vs 390 s) while decreasing the maximum amplitude of ST depression (0.244 vs 0.216 mV). Heart rate, systolic blood pressure, and the rate pressure product during exercise were not significantly affected. The MER of lactate, measured during exercise, was significantly higher after Nicorandil than placebo (13.6 vs 27.9). Similarly, the MERs of ammonia and HX were significantly higher after Nicorandil (-46.0 vs 7.4% and -47.0 vs 9.9% respectively). Nicorandil, had no apparent effect on myocardial sympathetic activity as the MERs of adrenaline and noradrenaline were essentially unaffected. We conclude that Nicorandil decreased myocardial ischaemia and suppressed myocardial accelerated purine metabolism (a marker of cellular energy metabolism) during exercise in patients with angina pectoris. This effect appears not to be related to myocardial sympathetic activity.

Administration, Oral↗
PubMed1995

Treatment with enalapril fails to prevent impaired cardiopulmonary baroreflex control in dogs with left ventricular dysfunction.

That the cardiopulmonary baroreflex control of sympathetic nerve activity is impaired in dogs with left ventricular (LV) dysfunction has been shown previously. This study tested the hypothesis that treatment with the angiotensin-converting enzyme inhibitor enalapril prevents or delays the development of abnormalities of cardiopulmonary baroreflexes in dogs with LV dysfunction. Serial changes in LV volumes and neurohumoral profiles (plasma norepinephrine and renin activity) were assessed in conscious dogs with progressive LV dysfunction due to rapid ventricular pacing. Enalapril 5 mg orally twice daily was administered from days 4 to 12 of pacing. Cardiopulmonary baroreflexes were assessed in enalapril-treated paced dogs (n = 8) and untreated paced dogs (n = 8) by recording changes in renal nerve activity and pulmonary capillary wedge pressure during volume infusion in anesthetized sinoaortic denervated dogs on day 12 of rapid pacing. There was no difference in LV volume in the two groups. Neurohumoral factors were similar in both groups except for the expected high plasma renin activity in enalapril-treated dogs. Hemodynamic parameters also were comparable in the two groups. Cardiopulmonary baroreflex sensitivity for enalapril-treated dogs was not different from that of untreated paced dogs, and baroreflex gain in both groups was significantly lower than for the nonpaced control dogs (P < .05). Despite adequate converting enzyme blockade, treatment with enalapril failed to prevent the development of attenuated cardiopulmonary baroreflex control of sympathetic nerve activity in dogs with developing LV dysfunction.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Altered vagal and sympathetic control of heart rate in left ventricular dysfunction and heart failure.

We investigated alterations in autonomic control of heart rate in conscious dogs with left ventricular (LV) dysfunction in the presence and absence of heart failure (HF) due to rapid pacing. In dogs with LV dysfunction but no HF, indexes of parasympathetic control decreased significantly after only 4 days of pacing. In dogs with fully developed HF, both vagal and sympathetic contributions were small. Vagomimetic doses of atropine increased both R-R interval (419 +/- 25 to 466 +/- 34 ms, P < 0.05) and standard deviation (SD) of the R-R interval (13 +/- 2 to 34 +/- 9 ms, P < 0.05). The digitalis glycoside deslanoside (Cedilanid-D) alone prolonged R-R interval (420 +/- 33 to 492 +/- 44 ms, P < 0.01) and tended to increase SD (14 +/- 4 to 28 +/- 8 ms, P = 0.08). After Cedilanid-D, low-dose atropine resulted in no significant further change in R-R interval or SD. These data indicate that changes in vagal control of heart rate become apparent at a very early developmental stage of LV dysfunction, and we speculate that this may provide important prognostic information in patients who are at risk for developing progressive myocardial dysfunction and HF.

Animals↗
PubMed1995

Exercise-induced ST-segment elevation--role of left ventricular wall motion abnormalities and coronary artery narrowing.

We studied the causes of exercise-induced ST-segment elevation. Group I consisted of 15 patients with anterior myocardial infarction in the absence of a coronary artery luminal narrowing of 75% or more. Group II consisted of 36 patients with predominantly exertional angina and a luminal narrowing of 90% or more in the left anterior descending coronary artery in the absence of previous myocardial infarction. In group I, exercise-induced ST-segment elevation occurred frequently during treadmill exercise (15/15, 100%). None of the patients showed 201Tl redistribution. The standard deviation of the phase in radionuclide ventriculography increased during bicycle exercise. Of group II patients, only those with 99% narrowing and poor collaterals showed exercise-induced ST-segment elevation (13/14, 93%), whereas none of those with complete occlusion or 99% narrowing and good collaterals, or 90% narrowing showed ST-segment elevation. In group II, patients with exercise-induced ST-segment elevation showed lower 201Tl uptake during exercise and washout in the territory of the diseased vessel than those without exercise-induced ST-segment elevation. In conclusion, wall motion abnormalities may cause exercise-induced ST-segment elevation independently of myocardial ischemia. In patients with predominantly exertional angina, exercise-induced ST-segment elevation may be a marker for 99% narrowing with poor collaterals and severe myocardial ischemia.

Adult↗
PubMed1993

Acute hemodynamic effects of bunazosin in congestive heart failure--differing responses according to degree of cardiac dysfunction.

1. Hemodynamic responses to Bunazosin (BZN) in congestive heart failure (CHF) were evaluated for 6 hours (hr) in 30 patients (A, normal cardiac function; B, mild cardiac dysfunction; C, severe cardiac dysfunction). 2. For 6 hr after BZN, the increments of cardiac index (delta CI) and stroke volume index (delta SVI) with BZN were higher in groups A and B than in group C. 3. A significant positive correlation was observed between ejection fraction and maximum delta CI and SVI, and between % fractional shortening and maximum delta CI and SVI. 4. These data showed that BZN improved the hemodynamics of CHF patients and that patients in groups A and B responded well to this vasodilator, however, patients in group C did not.

Adrenergic alpha-Antagonists↗
PubMed1993

Abnormalities of baroreflex control in heart failure.

This brief review summarizes abnormalities of arterial and cardiopulmonary baroreflex control of heart rate and sympathetic nerve activity. The potential role of these abnormalities in the development of the neurohumoral excitatory state associated with heart failure is discussed. Major emphasis is placed on the identification of important issues still to be investigated in this area. The potential importance of altered cardiovascular reflexes in the context of the interaction of the patient with heart failure and environmental stresses is discussed. The use of the canine rapid ventricular pacing model of biventricular failure in the investigation of abnormalities of baroreflexes in heart failure is emphasized. Insights obtained from this model should be extended to human investigations.

Animals↗
PubMed1993

Case report: a case of multiple coronary artery to left ventricular communications.

A 39-year-old man with anginal pain had multiple coronary artery to left ventricular communications. His electrocardiogram showed evidence of left ventricular hypertrophy, and an echocardiogram revealed a dilated left ventricle. A coronary angiogram revealed multiple coronary artery to left ventricular fistulae involving three major coronary arteries with no evidence of atherosclerotic lesions. Only 17 cases of such fistulous communications involving three major coronary arteries have been reported in the literature. It is suggested that the fistulous communications to the left ventricle was a cause of his angina pectoris, probably because of the coronary steal phenomenon.

Adult↗
PubMed1993

Activation of cardiac sympathetic afferents: effects of exogenous adenosine and adenosine analogues.

Adenosine is released during myocardial ischemia and can cause angina-like chest pain when given by intracoronary administration. We tested the hypothesis that intracoronary adenosine activates cardiac sympathetic afferent fibers and results in reflex sympathoexcitation. In dogs with sinoaortic denervation and vagotomy, we administered 2 mg of adenosine into the left anterior descending artery over 2 min. Before dipyridamole infusion, intracoronary adenosine resulted in no change in blood pressure or renal sympathetic nerve activity. After dipyridamole infusion, which blocks adenosine uptake, intracoronary adenosine resulted in a peak increase in sympathetic activity of 34 +/- 7%. We also investigated the adenosine-receptor subtype responsible for this sympathoexcitatory response. We found that the adenosine1 agonist N6-cyclopentyladenosine elicited a dose-dependent sympathoexcitatory response similar to adenosine but that the adenosine2 agonist 5'-(N-cyclopropyl)carboxamidoadenosine failed to elicit a sympathoexcitatory response. We conclude that adenosine activates cardiac sympathetic afferent fibers and leads to a sympathoexcitatory response due to activation of adenosine1 receptors.

Adenosine↗
PubMed1993

Reflex sympathoexcitation by cardiac sympathetic afferents during myocardial ischemia. Role of adenosine.

BACKGROUND: Stimulation of cardiac sympathetic afferents during myocardial ischemia has been attributed to bradykinin released from the ischemic myocardium. Recent data from human studies suggest that adenosine may serve as this mediator. Our experiments were done to determine whether reflex sympathoexcitatory responses to activation of cardiac sympathetic afferents during myocardial ischemia could be inhibited by blockade of adenosine receptors and augmented by increasing the local concentrations of adenosine in the ischemic myocardium. METHODS AND RESULTS: Experiments were done in 29 anesthetized dogs with bilateral vagotomy and carotid sinus denervation. Activation of cardiac sympathetic afferent fibers was induced by occlusion of the left anterior descending coronary artery (LAD) combined with rapid atrial pacing (pacing rate, 200 beats per minute). LAD occlusion plus rapid atrial pacing increased renal sympathetic nerve activity by 20 +/- 4% before but by only 7 +/- 1% after administration of aminophylline (100 mg i.v.), an adenosine receptor antagonist. In contrast, LAD occlusion during rapid atrial pacing increased renal sympathetic nerve activity by 18 +/- 8% before and 61 +/- 15% after treatment with dipyridamole (0.57 mg/kg i.v.), an inhibitor of adenosine reuptake. In a separate group of dogs, LAD occlusion during rapid atrial pacing increased renal sympathetic nerve activity similarly before and after sham treatment. CONCLUSIONS: These data suggest that adenosine released during myocardial ischemia activates cardiac sympathetic afferents to cause reflex sympathoexcitation. These findings are consistent with observations made in humans that suggest that adenosine is the mediator of the sensation of angina pectoris, which also results from stimulation of cardiac sympathetic afferents.

Adenosine↗
PubMed1993

Effects of volume and pressure overloads and myocardial hypertrophy on exercise-induced changes in electrocardiographic QRS amplitude.

To investigate the effects of volume and pressure overloads and myocardial hypertrophy on exercise-induced changes in QRS amplitude, we reviewed treadmill exercise electrocardiograms. In 10 normal young men, Rv5 amplitude decreased and Sv1 amplitude increased at peak exercise, and returned to the resting value in the recovery period. In 10 patients with aortic regurgitation, Rv5 and Sv1 amplitudes increased after 5 min of recovery. In 12 patients with essential hypertension and 10 with idiopathic hypertrophic non-obstructive cardiomyopathy, Rv5 amplitude remained unchanged or higher at peak exercise compared with the resting value, but patterns of serial changes were similar to that of normal subjects. In 9 patients with atrial septal defect, R'v1 amplitude increased with exercise, whereas it remained unchanged in 12 with isolated complete right bundle branch block. In 5 patients with mitral stenosis, Sv1 amplitude decreased at peak exercise. In conclusion, changes in QRS amplitude with exercise are influenced by hemodynamic abnormality and myocardial hypertrophy, and a major determinant of these serial changes seems to be the change in ventricular volume.

Adult↗
PubMed1993

Effects of an angiotensin-converting enzyme inhibitor, alacepril, on cardiovascular and sympathetic nervous responses to mental stress in patients with essential hypertension.

The effects of an angiotensin-converting enzyme inhibitor, alacepril, on cardiovascular and plasma catecholamine responses to mental stress were studied. A mental arithmetic test (MAT) was carried out in 9 patients with essential hypertension before and after treatment with alacepril, 25 mg once daily for 2 weeks, and in 9 age- and sex-matched normal subjects. Systolic blood pressure at rest and during MAT and the change in plasma norepinephrine concentrations during MAT were significantly greater in the hypertensive subjects than in the normal subjects. Alacepril significantly reduced systolic blood pressure, both at rest and during MAT, as compared to before treatment in the hypertensive subjects. Furthermore, alacepril significantly attenuated the change in plasma norepinephrine concentrations during MAT (from 127 +/- 76 pg/ml to 66 +/- 42 pg/ml, p < 0.05). These results suggest that alacepril significantly suppresses the augmented cardiovascular and sympathetic nervous responses to mental stress in patients with essential hypertension.

Adult↗
PubMed1992

Suppression of sympathetic nervous system activity by nicorandil during exercise.

1. Treadmill testing was done and plasma epinephrine and norepinephrine were measured during exercise and recovery in 21 patients with coronary artery disease given nicorandil. 2. Epinephrine levels during exercise did not change significantly with nicorandil, but the percent change in epinephrine with nicorandil tended to be lower during exercise. 3. Norepinephrine levels after exercise were suppressed with nicorandil (with, 424 +/- 15 pg/ml; without, 760 +/- 16, P less than 0.05). 4. Also, the percent change in norepinephrine with nicorandil was significantly decreased during exercise and recovery (with, 259 +/- 11%; without, 555 +/- 19, P less than 0.01). 5. Therefore, nicorandil suppressed the sympathetic nervous system hyper-response to exercise.

Adult↗
PubMed1992

Effect of alacepril on blood pressure and neurohumoral factors at rest and during dynamic exercise in patients with essential hypertension.

We assessed blood pressure and neurohumoral factors at rest and during exercise in 10 patients with essential hypertension before and after treatment with the new angiotensin converting enzyme inhibitor, alacepril (25-50 mg day-1). Alacepril significantly lowered mean blood pressure at rest and at the same exercise load as before treatment without affecting heart rate response. The response of plasma renin activity, plasma aldosterone, and plasma adrenaline were not changed by alacepril, but increase of plasma angiotensin II and plasma noradrenaline during exercise were significantly attenuated after alacepril treatment (ANOVA, P = 0.04, both). The change in mean blood pressure during exercise was positively correlated with the decrease in plasma angiotensin II (r = 0.65, P < 0.05). These results demonstrated that alacepril was effective in essential hypertension both at rest and during exercise, suggesting that the antihypertensive effect during exercise might be related to the decrease in pressor hormones, especially in plasma angiotensin II.

Adult↗
PubMed1992

Plasma catecholamine responses to dynamic exercise in patients with coronary artery disease--the relationship between sympathetic activity and systolic blood pressure and exercise-induced ventricular arrhythmias.

In order to investigate the relationship between sympathetic activity and postexercise systolic blood pressure (SBP) and exercise-induced ventricular arrhythmias in patients with coronary artery disease (CAD), we studied 38 patients and 9 normal subjects who underwent treadmill testing. Peak pressure-rate product was similar in the 2 groups. The plasma concentrations of norepinephrine and epinephrine at rest and immediately after exercise were significantly higher in patients with CAD compared with normal subjects (norepinephrine at rest, p < 0.01; norepinephrine immediately after exercise, p < 0.05; epinephrine at rest, p < 0.05; epinephrine immediately after exercise, p < 0.05). The level of norepinephrine immediately after exercise was significantly higher in 15 patients with a postexercise SBP increase than in 23 patients without that SBP change (p < 0.05), whereas the level of epinephrine was similar in the 2 groups. The level of epinephrine immediately after exercise was significantly higher in 10 patients with exercise-induced premature ventricular contractions than in 28 patients without those arrhythmias (p < 0.05), whereas the level of norepinephrine was similar in the 2 groups. We conclude that a postexercise SBP increase is related to the augmentation of sympathoneural activity and that exercise-induced ventricular arrhythmias are related to the augmentation of sympathoadrenal activity.

Arrhythmias, Cardiac↗
PubMed1992

Determinants of subsequent late postoperative left ventricular function and reversal of ventricular dilatation after mitral valve replacement for chronic mitral regurgitation.

We studied 16 patients with chronic mitral regurgitation by echocardiography before, and at 3 weeks, at 6-8 months and at 1-9 years after mitral valve replacement (MVR) to investigate serial changes in left ventricular (LV) function and reversal of ventricular dilatation. All patients at an average of 2.6 years after, and 8 patients before MVR were also studied by echocardiography and, except for 3 patients by measuring plasma catecholamines from the right atrium during bicycle exercise. Before operation, all patients were divided into group A (n = 12) with end-systolic dimension (ESD) < 4 cm and systolic blood pressure (SBP)/ESD > 3, and group B (n = 4) with ESD > 4 cm and SBP/ESD < 3. Maximum reduction in end-diastolic dimension (EDD) occurred at 3 weeks in all patients after MVR (from 60.5 +/- 3.7 to 49.0 +/- 4.5 mm, p < 0.05). ESD was reduced significantly (p < 0.5) only in group A. LV function was normal in group A, but it was depressed in group B at early and late periods after MVR. The slopes of the relationship between the mean velocity of circumferential fiber shortening (Vcf) and plasma norepinephrine (NE) during exercise in all patients in group B decreased along with the depression in LV function. After operation, all patients in group A reached New York Heart Association (NYHA) functional class I, while patients in group B were in NYHA class II. It is concluded that the surgical outcome after MVR for chronic MR will be better if preoperative ESD < 4 cm and SBP/ESD > 3. The relationship between mean Vcf and plasma NE during exercise seemed to be a useful index to evaluate the inotropic reserve of the LV.

Echocardiography↗
PubMed1992

Cardiovascular and sympathetic nervous response to dynamic exercise in patients with essential hypertension.

To investigate the relationship among systolic blood pressure (SBP) during exercise (EX), left ventricular hypertrophy (LVH) and plasma norepinephrine concentration (NE) in patients with essential hypertension (HT), 20 patients with HT and 20 age- and sex-matched normal subjects were studied using treadmill testing. According to the change in SBP from rest to EX (delta SBP), patients with HT were classified into two groups (group I, n = 12, delta SBP less than 72 mmHg: group II, n = 8, delta SBP greater than or equal to 72 mmHg). There were no significant differences between the two groups with regard to SBP at rest, NE at rest and NE on EX. However, SBP at peak EX, delta SBP and the incidence of LVH were greater in group II than in group I. We conclude that exaggerated SBP response to EX in patients with HT is related to LVH.

Adult↗
PubMed1992

[Cardiac and plasma catecholamine response to dynamic exercise in hyperthyroidism].

To investigate cardiac and sympathoadrenal responses to dynamic exercise, heart rate, systolic blood pressure, serial plasma norepinephrine (NE) and epinephrine (E) concentrations during multistage treadmill exercise were measured in 24 hyperthyroid patients (mean age; 42 +/- 16) and 24 age-sex matched control subjects. Eleven patients were re-examined in the euthyroid state after antithyroid therapy. Exercise duration was shorter in patient with hyperthyroidism. Also, the heart rates and systolic blood pressures at rest and in the early stage of exercise were significantly higher in hyperthyroidism. NE at rest (normal vs hyperthyroid: 124 +/- 10 vs 80 +/- 7 pg/ml, p < 0.01) and NE at peak exercise (475 +/- 38 vs 310 +/- 38 pg/ml, p < 0.01) were lower in hyperthyroidism. E at rest (22 +/- 2 vs 29 +/- 4 pg/ml, n.s.) did not differ, however, E during the first stage of exercise (30 +/- 3 vs 69 +/- 12 pg/ml, p < 0.01) was higher in hyperthyroidism. Re-examination for the euthyroid state revealed the decreases in the heart rates and systolic blood pressures at rest and in the early stage of exercise, and the normalization of the NE and E response. Thus, patients with hyperthyroidism was in the hyperdynamic cardiac state at rest and during dynamic exercise, which was accounted for by decreased sympathetic nervous activity and increased adrenomedullary responses. These modifications of sympathoadrenal response seemed reversible when patients were controlled by antithyroid therapy.

Adolescent↗