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Biomedical subjects

H Fukuzaki

Publications and source records attributed to H Fukuzaki.

At least 181 records · Page 10Linked to original sources
PubMed1987

[Cardiac function and prognosis in hypertrophic cardiomyopathy].

To assess pathophysiological changes and prognoses in hypertrophic cardiomyopathy (HCM), the clinical courses of 190 patients with HCM between 1968 and 1985 were reviewed and analyzed. Their average follow-up period was 4.0 years. During the course of follow-up, 24 patients died of heart disease at annual mortality of 3.3%; 22 sudden death, and two congestive heart failure. Among the 190 cases, 70 were studied by echocardiography with an average follow-up period of 4.4 years. The subjects were categorized in three groups: 10 who died suddenly (SD group), 16 with ventricular tachycardia (VT group) and the remaining 44 without ventricular tachycardia (non-VT group). Initially, the VT group had significantly greater left ventricular end-diastolic dimension (LVDd), smaller % fractional shortening (FS), and normalized rapid felling rate (RFR) compared with the other two groups. However, there were no significant differences in the echocardiographic parameters between the SD and non-VT groups. During the follow-up period, no changes in echocardiographic parameters were observed in the non-VT group. However, LVDd was increased in both the SD and VT groups, and normalized RFR and atrial filling rate (AFR) were decreased in the SD group. These results suggested that close observations using echocardiography are useful for evaluating the natural history and prognoses of HCM.

Adolescent↗
PubMed1987

Nifedipine suppressed atherosclerosis in cholesterol-fed rabbits but not in Watanabe heritable hyperlipidemic rabbits.

We studied the effects of nifedipine, a calcium antagonist, on atherosclerosis in cholesterol-fed rabbits and Watanabe heritable hyperlipidemic rabbits (WHHL rabbits). Japanese White rabbits were fed 120g of 2% cholesterol rabbit chow daily, and WHHL rabbits were fed standard rabbit chow. In each experiment, the rabbits were divided into two groups. Twenty milligrams of nifedipine was given orally twice a day to the nifedipine group, and the control group was given a placebo in the same way. The rabbits were sacrificed at the end of the 12th week in the case of cholesterol-fed rabbits, and the 20th week in the case of WHHL rabbits. Among the cholesterol-fed rabbits, the percentage of aortic intimal surface area covered by atherosclerotic lesions (AS%) was 25.9 +/- 7.6% (mean +/- S.D.) in the nifedipine group (n = 7), and 55.6 +/- 22.8% in the placebo group (n = 8) (p less than 0.01). The cholesterol content of thoracic and abdominal aorta in the nifedipine group was lower than those in the placebo group (p less than 0.05). Among the WHHL rabbits, the AS% was 33.4 +/- 14.1% in the nifedipine group (n = 5), and 27.0 +/- 11.7% in the placebo group (n =6) (n.s.). The aortic cholesterol and calcium contents also showed no significant differences between the two groups. We concluded that nifedipine suppressed atherosclerosis in cholesterol-fed rabbits but not in WHHL rabbits. The different responses suggest that the effect of nifedipine could be mediated by low density lipoprotein receptors or that the early exposure to hyperlipidemic serum from birth might affect cell functions of WHHL rabbits.

Administration, Oral↗
PubMed1986

Activation of protein kinase C by the action of 9,11-epithio-11,12-methano-thromboxane A2 (STA2), a stable analogue of thromboxane A2, in human platelets.

Incubation of human washed platelets with 9,11-epithio-11, 12-methano-thromboxane A2 (STA2), a stable analogue of thromboxane A2, caused the activation of protein kinase C and myosin light chain (MLC) kinase to the same extents as those induced by thrombin as judged by measuring the phosphorylation of a 40-kilodalton protein and MLC, respectively. However, STA2 stimulated much less phosphoinositide turnover than thrombin. Furthermore, the doses of STA2 necessary for protein kinase C activation and phosphoinositide turnover were higher than those necessary for MLC kinase activation, although the doses of thrombin necessary for these three reactions were nearly the same. These results suggest that protein kinase C may be activated at the Ca2+ concentrations higher than those required for MLC kinase activation by the action of STA2, presumably due to the inability of this agonist to produce diacylglycerol in an amount enough to increase the affinity of the enzyme for Ca2+.

Blood Platelets↗
PubMed1986

Twenty-four hour ambulatory ECG monitoring of junior high school students in Miki City.

To evaluate incidence of serious arrhythmias among school age youths, 24-hour ambulatory ECG monitoring was performed in 100 junior high school students, including 60 subjects with some ECG abnormalities and 40 without. With this monitoring 2 cases with multifocal VPCs and 2 cases with paired VPCs or nonsustained ventricular tachycardia were found; the case with VT died suddenly after having been lost during careful follow up. It is emphasized from these results that ambulatory ECG monitoring is quite useful in selected cases in this age group and careful follow up of students with advanced grade VPCs is very important.

Adolescent↗
PubMed1986

Regulation of coronary blood flow by counteraction of coronary vascular alpha and beta adrenergic activation during experimental pliable coronary stenosis.

In order to evaluate the role of adrenergic receptor-mediated vasomotions of large epicardial coronary arteries in changing coronary blood flow (CBF), the effects of intracoronary norepinephrine (NE), 1.0 microgram/min, were examined in dogs with coronary stenosis which preserved stenosis vasomobility. In untreated dogs, NE caused no significant changes in CBF and stenosis resistance (SR). In dogs treated with propranolol, NE decreased CBF by 65 +/- 7.0% (mean +/- SE) and produced 12-fold intensification of SR followed by LV dP/dt reduction. Similar detrimental responses to NE were observed in dogs treated with atenolol. In dogs treated with phentolamine, NE increased CBF by 33 +/- 5.6% and decreased SR by 65 +/- 7.1%. When NE was administrated directly distal to the stenosis to exclude responses of the stenosed coronary segment, NE failed to affect CBF and SR. These results indicated that alpha receptor stimulation intensified stenosis severity, profoundly decreased CBF and evoked myocardial ischemia, whereas beta stimulation dilated coronary stenosis and increased CBF. The net effects of NE were due to balanced alpha and beta stimulation. Thus, disproportionate activation of alpha and beta (probably beta 1) adrenergic receptors in large coronary arteries with pliable stenosis could modulate their tone and plays an important role in the regulation of CBF.

Adrenergic alpha-Antagonists↗
PubMed1986

Time lag between pulmonary congestion and pulmonary edema in dogs.

The time course of pulmonary congestion and pulmonary edema was examined using a gravimetric method in 19 open-chest anesthetized dogs. Balloon catheters in the left atrium (LA) were inflated to elevate LA pressure more than 25 mmHg. The dogs were divided into 4 groups (G) according to the duration of the elevated LA pressure: G.1 (n = 6) as control; G.2 (n = 4) for 15 minutes; G.3 (n = 4) for 30 minutes; and G.4 (n = 5) for 60 minutes. Although no significant increase of extravascular lung water content (an indicator of pulmonary edema) was observed in G.2 (4.97 +/- 0.85 g/kg) and G.3 (4.46 +/- 0.96) compared with G.1 (4.02 +/- 0.88), a significant increase was observed in G.4 (6.81 +/- 1.21, p less than 0.05). Residual pulmonary blood content (an indicator of pulmonary congestion) was significantly increased in G.2, 3 and 4 compared with G.1. By light and electron microscopes, pulmonary congestion was revealed in G.2, whereas interstitial pulmonary edema was demonstrated only in G.4. Thus, it was concluded that pulmonary congestion occurred within 15 minutes, but pulmonary edema occurred 30 to 60 minutes after left atrial pressure was elevated more than 25 mmHg. This time lag may be an important factor in explaining the discrepancy between the elevated left atrial pressure and the clinical manifestation of pulmonary edema.

Animals↗
PubMed1986

Hemodynamic effects of digoxin on congestive heart failure.

To assess the hemodynamic effects of digoxin (0.01 mg/kg) on congestive heart failure, we evaluated 19 patients with decreased contraction force of left ventricle (old myocardial infarction n = 9, and dilated cardiomyopathy n = 10, group 1) and 8 patients with mechanical impaired left ventricular filing (mitral stenosis n = 8, group 2). In groups 1 and 2, heart rate and pulmonary capillary pressure significantly decreased (p less than 0.05). In group 1, stroke volume increased, but not significantly. In group 2, stroke volume increased significantly (p less than 0.05). There were no significant changes in blood pressure and systemic vascular resistance in either group. We divided group 1 into two groups (group 1A: cardiac index increased more than 15%, group 1B: cardiac index increased less than 15%). In group 1A, cardiac index and % fractional shortening before digoxin administration were lower than in group 1B (1.97 + 0.27 vs 2.80 + 0.481/min/m2, p less than 0.001, and 10.9 + 8.0 vs. 19.5 +11.9%, p less than 0.05, respectively). These data suggested that digoxin exerted a positive inotropic effect with decreased pulmonary capillary pressure but cardiac index did not always increase in congestive heart failure.

Digoxin↗
PubMed1986

Usefulness of intravenous dipyridamole combined with pacing stress for detection of myocardial ischemia in coronary artery disease.

In order to establish a more clinically useful diagnostic method to detect myocardial ischemia, a stress test of 0.56 mg/kg of intravenous dipyridamole (D), an atrial pacing (P) and the combination of both (D + P) were administered to 14 patients with significant coronary stenosis and 8 patients with normal coronary arteriogram. The effects on regional coronary hemodynamics and myocardial metabolism were subsequently studied. Treadmill exercise tests in 15 patients and thallium-201 exercise myocardial scintigraphy in 14 patients were also performed at another time. When the uptake ratio of myocardial lactate less than 0% was used as an indicator of myocardial ischemia, 100% (12/12) of sensitivity and 100% (6/6) of specificity were obtained with (D + P)-test in diagnosis of significant coronary stenosis and its sensitivity was significantly higher than that with P-test (43%) or with D-test (31%). Even though sensitivity and specificity of exercise electrocardiogram (70% and 50%) or thallium-201 exercise myocardial scintigram (88% and 80%) in diagnosis of coronary stenosis were not significantly lower than those of (D + P)-test respectively, myocardial ischemia could also be detected with (D + P)-test in two patients at the region perfused by the infarct-related artery, which had not been detected by thallium-201 exercise myocardial imaging. We conclude, (D + P)-test combined with investigation of myocardial lactate metabolism is quite useful to detect myocardial ischemia.

Aged↗
PubMed1986

Enhanced red cell sodium permeability in patients with borderline hypertension.

Red cell membrane sodium permeability was studied in 41 untreated patients with essential hypertension (20 borderline hypertensives and 21 established hypertensives) and 21 age matched normotensive subjects by means of the measurement of unidirectional passive influx of 22Na+ into ouabain-treated erythrocytes. The mean value (+/- SD) of 22Na+ influx was greater in the hypertensives than in the normotensives (0.183 +/- 0.047 vs 0.152 +/- 0.047 mmol/l . cells/hr, respectively, p less than 0.02). Among the patients with essential hypertension, the borderline hypertensives demonstrated a higher 22Na+ influx than the established hypertensives (0.207 +/- 0.043 vs 0.160 +/- 0.038 mmol/l . cells/hr, respectively, p less than 0.001), and 22Na+ influx positively correlated with plasma renin activity (r = 0.44, p less than 0.005). In 16 of 20 borderline hypertensives, 5 year blood pressure changes were examined retrospectively, and a positive correlation was observed between mean blood pressure increase and 22Na+ influx value in these subjects (r = 0.64, p less than 0.01). These results suggest that passive sodium influx may be altered in the course of the development of hypertension in relation to the changes in blood pressure level and that enhanced sodium permeability may be a characteristic of the early stage of essential hypertension.

Adult↗
PubMed1986

A circulating Na+-K+ATPase inhibitor, erythrocyte sodium transport and hypertension in patients with chronic renal failure.

The level of circulating Na+-K+ATPase inhibitor (% inhibition), erythrocyte ouabain-sensitive 22Na+ efflux rate constant (Kos) and erythrocyte sodium content (RBC Na) were measured in 11 undialysed patients with chronic renal failure, 16 patients on chronic hemodialysis and 16 age-matched normotensive healthy controls. In uremics, % inhibition was significantly higher than that in the controls (p less than 0.001). There were significant correlations between % inhibition and both mean blood pressure (r = 0.74, p less than 0.001) and Kos (r = -0.47, p less than 0.005) for all the groups combined. Hypertensive uremics showed significantly higher % inhibition, lower Kos and higher RBC Na compared with normotensive ones. These data suggest that the elevated level of circulating Na+-K+ ATPase inhibitor may, at least in part, account for the pathogenesis of hypertension in patients with chronic renal failure.

Adult↗
PubMed1986

[Mitral valve prolapse with myocardial disarrangement and familial hypertrophic cardiomyopathy: a case report].

This is a report of a patient with mitral valve prolapse (MVP) and myocardial abnormalities on endomyocardial biopsy in whose relatives hypertrophic cardiomyopathy (HCM) was identified. A 19-year-old woman was admitted to our hospital for evaluation of a heart murmur. A systolic ejection murmur was audible in the third intercostal space at the left sternal border, and a standard 12-lead electrocardiogram showed ST-T wave changes in leads II, III and aVF. Echocardiography revealed prolapse of the anterior leaflet of the mitral valve, but no left ventricular hypertrophy. Endomyocardial biopsy disclosed mild hypertrophy and disarrangement of the myocardium. The family study revealed asymmetrical septal hypertrophy in her mother, who had no history of hypertension. Her younger sister had mild hypertrophy of the interventricular septum on echocardiography, and her histopathological findings suggested a diagnosis of HCM. This case was clinically regarded as MVP, but development of left ventricular hypertrophy as noted in her mother may occur in the future.

Adolescent↗
PubMed1986

[Severity and non-uniformity of regional wall motion in dilated cardiomyopathy evaluated by two-dimensional echocardiography].

A two and a half year follow-up study of segmental left ventricular wall motion was performed by two-dimensional echocardiography for 26 patients with dilated cardiomyopathy (DCM). Segmental analysis of left ventricular wall motion abnormalities (WMA) was performed using 11 segments obtained by short- and long-axis views of the left ventricle. Wall motion in each segment was classified and assigned a numerical score as normal (0), hypokinetic (1), severely hypokinetic (2), and akinetic or dyskinetic (3). Based on this categorization, a wall motion abnormality index (WMAI) was derived as an overall assessment of left ventricular asynergy. The intersegmental standard deviation of the wall motion abnormality score was used as an index of left ventricular asynergy (non-uniformity index: NUI). During the follow-up period, the wall motion abnormality index increased in all of the 26 patients (from 1.23 to 1.82, p less than 0.001), but the non-uniformity index did not change (from 0.72 to 0.73). When comparing the non-uniformity index among three groups classified according to the grade of wall motion abnormality, both at the initial and during follow-up studies, the moderate wall motion abnormality group (1.0 less than or equal to WMAI less than 2.0) had larger non-uniformity indexes (0.83, 0.84) than the other groups, and the severe non-uniformity index (greater than or equal to 0.9) was observed solely in the moderate group. In the follow-up study, these 26 patients were categorized in two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

[Malignant familial cardiomyopathy with sudden death, typical asymmetric septal hypertrophy and dilated cardiomyopathy-like features].

Twenty-one members of a family were traced for three generations including the propositus, who had typical dilated cardiomyopathy (DCM)-like features. Clinical, radiological, electrocardiographic and echocardiographic examinations were performed for 13 of 16 still living. Five of 21 members died including three of sudden death. Among living 16 members, five had congestive heart failure, greater than grade III of the NYHA, and cardiomegaly on chest radiography in five. Left ventricular hypertrophy, abnormal Q waves, and ST-T changes were observed on electrocardiography in two, five and eight members, respectively. Echocardiography revealed asymmetric septal hypertrophy (ASH) in four, two of whom had systolic anterior motion (SAM) of the mitral valve. Two had features simulating DCM, and five had mitral valve prolapse. Among six patients with ASH or features simulating DCM, four had cardiac catheterization, coronary angiography and endomyocardial biopsy. None had significant coronary stenosis, but all had high left ventricular end-diastolic pressure (LVEDP) (23 +/- 7 mmHg). Endomyocardial biopsy showed moderate myocardial cellular hypertrophy, interstitial myocardial fibrosis, nuclear changes and myocardial disarrangement, with features characteristic of HCM. In this family with malignant HCM, patients had various clinical features including typical HCM, simulated DCM, DCM coexisted with mitral valve prolapse, and sudden death occurred frequently.

Adolescent↗
PubMed1985

Comparison of the modes of action of Ca2+ ionophore A23187 and thrombin in protein kinase C activation in human platelets.

In human platelets, the Ca2+ ionophore A23187 stimulated the phosphorylation of a 40 kDa protein and myosin light chain (MLC) to the same extents as those induced by thrombin, but the doses of A23187 for 40 kDa protein phosphorylation were higher than those for MLC phosphorylation, although the doses of thrombin for both reactions were nearly the same. Moreover, A23187 produced much less diacylglycerol than thrombin. However, the sites of the 40 kDa protein phosphorylated by the action of A23187 and thrombin were identical, and the 40 kDa protein phosphorylation induced by A23187 and thrombin was inhibited by tetracaine, an inhibitor for protein kinase C. Neither A23187 nor thrombin induced the production of a catalytic fragment of protein kinase C which might be generated by limited proteolysis with Ca2+-dependent protease. These results indicate that A23187 induces protein kinase C activation which phosphorylates the 40 kDa protein, but higher doses of A23187 are required for the activation of this enzyme than for the activation of MLC kinase.

Blood Platelets↗