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Biomedical subjects

H Fukuzaki

Publications and source records attributed to H Fukuzaki.

At least 199 records · Page 11Linked to original sources
PubMed1985

Induction of protein kinase C activation and Ca2+ mobilization by fibroblast growth factor in Swiss 3T3 cells.

Addition of fibroblast growth factor (FGF) to quiescent cultures of Swiss 3T3 cells rapidly induced diacylglycerol formation, protein kinase C activation and Ca2+ mobilization. Protein kinase C-activating agents such as 12-O-tetradecanoylphorbol-13-acetate (TPA) and 1-oleoyl-2-acetylglycerol (OAG) mimicked the action of FGF and stimulated DNA synthesis in the presence of insulin. Prolonged treatment of the cells with phorbol-12,13-dibutyrate (PDBu) led to the down-regulation and complete disappearance of protein kinase C. In these cells, TPA and OAG did not induce DNA synthesis any more. FGF still elicited Ca2+ mobilization and DNA synthesis, but the magnitude of DNA synthesis was reduced to almost half as compared with that in the control cells. These results clearly indicate that both diacylglycerol and Ca2+ may serve as second messengers for FGF and suggest that these messengers may be involved in the mitogenic action of this growth factor.

Animals↗
PubMed1985

Plasma concentrations of platelet-specific proteins in different stages of essential hypertension: interactions between platelet aggregation, blood lipids and age.

Plasma beta-thromboglobulin (beta TG) and platelet factor 4 (PF4) were significantly higher in a group of 116 hypertensive men than in a normotensive group of 142 men. They increased with the stage of hypertension but the level did not correlate with the age of the subjects. Platelet aggregation was similar in the two groups and positively correlated with the age of the subjects in the normotensive group but not in the hypertensive group. A strong positive correlation was observed between the levels of plasma beta TG and PF4 and between platelet aggregation to ADP and that to epinephrine in both the hypertensive and normotensive groups. However, there was no correlation between the level of plasma beta TG or PF4 and platelet aggregation. Plasma antithrombin III was lower in the hypertensive group than in the normotensive group. These studies suggest that plasma levels of beta TG and PF4 are closely related to the stage of hypertension and are better indicators than aggregation of in vivo platelet activation in hypertensive subjects. Enhanced platelet activation may be involved in the acceleration of hypertensive arteriovascular damage and atherosclerosis.

Adenosine Diphosphate↗
PubMed1985

The relation between left ventricular asynchrony, relaxation, outward wall motion and filling characteristics during control period and pacing-induced myocardial ischaemia in coronary artery disease.

To assess the relation between left ventricular asynchrony, relaxation, outward wall motion and filling in patients with coronary artery disease and normal systolic function, pressure measurements and left ventricular angiography were performed at rest and after pacing. Asynchrony and outward wall motion were quantified by segmental area-time curves. At rest, there were no differences in asynchrony and time constant between 10 patients with coronary artery disease and 10 normal subjects, while the early-filling rate was less in patients with coronary artery disease than in normal subjects. Six coronary artery disease patients with isolated left anterior descending disease displayed anterior outward wall motion which was less than that of normal subjects. In 10 coronary artery disease patients with pacing-induced angina, asynchrony increased, time constant prolonged and the early-filling rate decreased. In 6 coronary artery disease patients with isolated left anterior descending disease, anterior outward wall motion decreased after pacing. Thus, impaired early diastolic filling at rest in patients with coronary artery disease and normal systolic function may result not from asynchrony nor impaired relaxation, but from reduced regional outward wall motion of the affected area supplied by diseased coronary artery during early diastole. However, during ischaemia temporal asynchrony and impaired relaxation possibly add to left ventricular filling impairment in patients with coronary artery disease.

Adult↗
PubMed1985

Effects of left ventricular asynchrony on time constant and extrapolated pressure of left ventricular pressure decay in coronary artery disease.

To elucidate the effects of ventricular asynchrony with or without myocardial ischemia on the time constant of left ventricular pressure decay and asymptote, that is, the level to which pressure would decrease if isovolumic pressure decrease continued infinitely, left ventriculography and pressure measurements were investigated in 14 normal subjects and 25 patients with coronary artery disease. Ventricular asynchrony was quantitated by the segmental area-time curve. This study consisted of two parts. 1) After a right atrial pacing stress test, the time constant and asymptote remained unchanged in eight normal subjects. In 18 patients with coronary artery disease and pacing-induced angina, asynchrony increased, the time constant was prolonged (64 +/- 13 to 94 +/- 17 ms, p less than 0.01) and the asymptote decreased (-22 +/- 10 to -46 +/- 20 mm Hg, p less than 0.01) after the pacing. 2) During right ventricular pacing at 80, 100 and 120 beats/min in the patients, asynchrony increased and the time constant was prolonged (55 +/- 7 versus 70 +/- 10, 47 +/- 11 versus 66 +/- 19, 36 +/- 7 versus 53 +/- 13 ms, respectively, p less than 0.01 versus right atrial pacing), whereas the asymptote was unchanged in six normal subjects compared with the value during right atrial pacing at each pacing rate. In seven patients with coronary artery disease, right ventricular pacing at 80, 100 and 120 beats/min also produced an increase in the time constant, while the asymptote was unchanged. Thus, prolongation of the time constant of left ventricular pressure decay may result from ventricular asynchrony even in the absence of myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Catheterization↗
PubMed1985

Myocardial ischaemia produced by ergonovine-induced vasoconstriction during preexisting coronary stenosis: experimental conditions for the geometric theory.

Experiments were designed to determine the contribution of active vasomotor tone of a large coronary artery during a preexisting coronary stenosis to the production of myocardial ischaemia. The quantitative relations between ergonovine dose and systemic and coronary haemodynamic and electrocardiographic responses during various degrees of coronary stenosis were evaluated in 55 anaesthetised open-chest dogs. In the absence of coronary stenosis, intracoronary infusion of ergonovine (0.04 to 4 micrograms X min-1) had no systemic or coronary haemodynamic effects. In dogs with coronary stenosis created with intraluminal microballoon occluder, ergonovine produced marked decreases in coronary blood flow and distal coronary pressure followed by a decline in left ventricular dP/dt and ST-elevation in epicardial electrogram in the presence of moderate (28 +/- 1.1 mmHg in pressure gradient) and severe (41 +/- 1.4 mmHg), but not mild (15 +/- 0.9 mmHg) stenosis. These detrimental effects of ergonovine were dependent on its dose as well as the severity of preexisting coronary stenosis. Interventions such as aspirin pretreatment or endothelial denudation did not attenuate the coronary vasomotor response or ergonovine, but pretreatment with nifedipine (3 micrograms X kg-1 iv) prevented this response. Intravenous injection of ergonovine (4 to 15 micrograms X kg-1) in doses relevant to clinical usage during intraluminal obstruction resulted in similar changes in coronary haemodynamics as those of intracoronary ergonovine. In contrast, in dogs with various degrees of coronary stenosis produced with an externally applied constrictor device, ergonovine did not affect systemic and coronary haemodynamics. These experiments demonstrate that normal vasomotion superimposed on moderate and severe pliable coronary stenosis can cause transient myocardial ischaemia, which helps to clarify the conditions to produce myocardial ischaemia according to geometric theory.

Animals↗
PubMed1985

A comparison of two exponential models of the time constant during left ventricular isovolumic pressure decay in coronary artery disease.

To make a comparison of two exponential models of the time constant (Tw: Weiss's method, Tc: exponential analysis with a variable asymptote) during left ventricular (LV) isovolumic relaxation, we assessed LV pressure decay in 104 patients with coronary artery disease (CADpts) and 21 normal subjects at rest and after pacing, and investigated the hemodynamic determinants of these two models using forward-backward stepwise multiple regression analysis. At rest, Tw was prolonged as the left ventricular minimal pressure (LVPmin), the left ventricular end-diastolic pressure (LVEDP) and the end-systolic volume (ESV) increased (multiple regression coefficient: R = 0.87), whereas Tc was prolonged as ESV and regional wall motion abnormality (RWMA) increased (R = 0.72). Pacing-induced changes in Tw were augmented as LVPmin and RWMA increased (R = 0.75), whereas changes in Tc were augmented as RWMA increased (R = 0.63). Thus, the changes in Tw may be due to an increase in LVPmin rather than to any direct effect of ischemia on the relaxation rate. The relaxation rate can be evaluated more reliably by Tc than by Tw, irrespective of associated pressure changes during ischemia in CADpts.

Adult↗
PubMed1985

Exercise capacity correlating to exercise hemodynamics in coronary artery disease.

Forty-seven patients with coronary artery disease characterized by angina pectoris and/or old myocardial infarction underwent two maximal exercise tests, the supine ergometer test and the upright treadmill test, to study the relationship between exercise capacity and exercise hemodynamics. Subjects were divided into 3 groups: Group I (n = 19) achieved 25 or 50 watts, Group II (n = 15) achieved 75 watts and Group III (n = 13) achieved 100 or 125 watts. During ergometer exercise, the mean pulmonary capillary pressure elevated by 25.3 +/- 8.3 mmHg in Group I, 20.8 +/- 8.8 mmHg in Group II and 12.0 +/- 8.4 mmHg in Group III; the Group III value was significantly smaller than the other groups. The stroke volume index decreased by 3.6 +/- 8.8 ml/m2 in Group I, and increased by 10.9 +/- 8.7 ml/m2 in Group II and 10.7 +/- 14.7 ml/m2 in Group III. Thus, the impaired exercise capacity correlated with the abnormal exercise hemodynamics and its severity. In addition, the exercise capacity in the treadmill test was comparable to that in the ergometer test. It was concluded that the impaired exercise capacity in the both supine and upright exercise tests was well related to the development of abnormal exercise hemodynamics in patients with coronary artery disease.

Adult↗
PubMed1985

Hemodynamic effects of digoxin on congestive heart failure in old myocardial infarction, dilated cardiomyopathy, acute myocardial infarction and mitral stenosis.

The hemodynamic effects of digoxin (0.01 mg/Kg) on congestive heart failure were compared in 32 patients with old myocardial infarction (OMI) (n = 9), dilated cardiomyopathy (DCM) (n = 10), acute myocardial infarction (AMI) (n = 5) and mitral stenosis (MS) (n = 8). The responses of heart rate (HR) and pulmonary capillary pressure (PCP) to digoxin in OMI, DCM and MS were marked but different in each of these groups and no significant changes were found in patients with AMI. The responses of cardiac index (CI) to digoxin in patients with OMI and DCM in whom left ventricular myocardial contractile force was impaired were divided into 2 groups (Group 1: CI increased more than 15% and Group 2: less than 15%). In Group 1, both CI and percent fractional shortening (%FS) before digoxin administration were lower than in Group 2, i.e., 1.97 +/- 0.27 vs 2.80 +/- 0.48 L/min/m2 (p less than 0.001) and 10.9 +/- 8.0 vs 19.5 +/- 11.9% (p less than 0.05), respectively. In MS, CI increased after digoxin administration only in the 2 patients with low CI and rapid HR in the control state. These results indicate that the mode of hemodynamic response to digoxin is considerably different in various diseases. They further suggest that digoxin should not be used in the early phase of AMI, although digoxin was of great clinical benefit in patients with OMI and DCM through such mechanisms as its positive inotropic and negative chronotropic effects and lowering of PCP.

Adult↗
PubMed1985

Effects of diltiazem and nitroglycerin on left ventricular diastolic properties in patients with coronary artery disease.

To determine the effects of diltiazem (DTZ) and nitroglycerin (NTG) on left ventricular (LV) diastolic relaxation and filling in patients with cornary artery disease (CADpts), LV graphy and time constant (Tc) of LV isovolumic pressure decay were studied before and 5 min after intravenous DTZ (10 mg) in 16 CADpts and sublingual NTG (0.3 mg) in 11 CADpts. Diastolic regional ventricular filling dynamics were quantitated by segmental area-time curves during early-, mid- and late-filling periods. After NTG, LV systolic pressure (LVSP), end-diastolic pressure (EDP) and end-diastolic volume (EDV) decreased. Early-filling rate (EFR) decreased (165 +/- 82 to 122 +/- 61 ml/sec/m2) due to a decrease in the regional early-filling rate in the normokinetic area and late-filling rate (LFR) increased (95 +/- 38 to 145 +/- 45 ml/sec/m2), while LV peak positive dp/dt, peak LVSP/end-systolic volume (ESV) ratio, Tc and mid-filling rate (MFR) were unchanged. After DTZ, LVSP decreased and EDV increased. EFR increased. EFR increased (127 +/- 54 to 166 +/- 60 ml/sec/m2) due to an enhanced regional early-filling rate in the mildly hypokinetic area, while EDP, LV peak positive dp/dt, peak LVSP/ESV ratio, Tc, MFR and LFR were unchanged. From these results, it was postulated that NTG caused a decrease in LV early filling and an increase in LV late filling, probably due to LV preload reduction. In contrast, DTZ caused significant improvement of LV early filling particularly in the mild hypokinetic area. Thus, DTZ but not NTG was able to relieve local myocardial dysfunction secondary to a stenosed coronary artery during the filling period, resulting in clinical improvement in CADpts.

Benzazepines↗
PubMed1985

Ventriculo-atrial conduction in patients with normal and impaired atrio-ventricular conduction.

Ventriculo-atrial (VA) conduction was studied in 133 patients with various kinds of arrhythmias using intracardiac electrograms and programmed stimulation. One-to-one VA conduction was observed during RV pacing at the rate just above the sinus rate in 6 of 31 patients (19.4%) with advanced AV block, in 7 of 26 patients (26.9%) with impaired AV nodal conduction, in 25 of 71 patients (35.2%) with normal AV nodal conduction and 3 of 5 patients (60%) with enhanced AV nodal conduction. However, the differences between these groups were not significant. There was no significant difference in either the AH block rate during RA pacing or the antegrade functional refractory period (FRP) of the AV node in patients with or without VA conduction, and the VA block rate during RV pacing was not significantly correlated with the AH block rate or the FRP of the AV node. VA conduction time (S-HRA) also showed no significant differences between these groups. The mean VA conduction time during RV pacing at rates of 60 to 80 bpm was 208 +/- 87 msec, ranging from 100 to 395 msec. In conclusion, AV conduction disturbances may influence VA conduction, but VA conduction cannot be predicted from antegrade conductivity.

Arrhythmias, Cardiac↗
PubMed1985

Autonomic hyperactivity in patients with vasospastic angina.

To evaluate the role of the autonomic nervous system in vasospastic angina, plasma catecholamine and cyclic nucleotide levels were measured and the pilocarpine test was performed in 19 patients with vasospastic angina, 14 patients with nonvasospastic angina and 7 control subjects who were hospitalized patients without heart disease. Diurnal and nocturnal levels of plasma catecholamines were significantly higher in patients with angina pectoris, especially in patients with vasospastic angina, as compared with those of controls. In addition, an increase in plasma catecholamines preceded the onset of spontaneous and pilocarpine induced anginal attacks associated with significant increases in plasma catecholamines in patients with vasospastic angina. On the other hand, while nifedipine significantly suppressed both spontaneous and pilocarpine induced anginal attacks, the increase in plasma catecholamines remained. These results indicate that increased activity and responsiveness of the sympathetic nervous system may possibly contribute to the development of vasospastic angina on the basis of parasympathetic hyperactivity.

Angina Pectoris↗
PubMed1985

Relationships between red cell cation contents and blood pressure level.

Red cell sodium (R-Na), potassium (R-K) and sodium to potassium ratio (R-Na/K) were studied in 2,542 adults participating in periodic medical examinations. The mean values of R-Na and R-Na/K in untreated borderline (n = 406) and definite hypertensives (n = 485) were higher than those in normotensives (n = 1,651), but that of R-K was not different among the groups. The increased R-Na and R-Na/K in the hypertensives were observed only in those under 50 years, but not in those 50 years and over. In the normotensive subjects, age and sex affected the intraerythrocyte cation contents, but a positive family history of hypertension did not. Although a few characteristics correlated with both R-Na and mean blood pressure, and with both R-Na/K and mean blood pressure, multiple regression analyses revealed that R-Na and R-Na/K independently and significantly contributed to the variation in mean blood pressure. It was also indicated that these relations of R-Na and R-Na/K to mean blood pressure were significant in those under 50 years, but not in those 50 years and over. While several characteristics confound the relationships between red cell cation contents and blood pressure, these results suggest that the contributions of R-Na and R-Na/K to the mechanisms of human hypertension still persist in young to middle-aged people.

Adult↗
PubMed1985

Abnormal relationship between dietary sodium intake and red cell sodium transport in salt-sensitive patients with essential hypertension.

The effects of high sodium intake on erythrocyte 22Na efflux rate constants were studied in 25 patients with essential hypertension and 9 normal subjects. With changes in sodium intake from 100 mEq to 300 mEq/day, both total and ouabain sensitive 22Na efflux rate constants decreased significantly (p less than 0.001) in "salt-sensitive" patients (-0.031 +/- 0.005 and -0.035 +/- 0.006 /hr, respectively), but these responses were variable in "nonsalt-sensitive" patients and in normal subjects. The "salt-sensitive" patients showed a significant increase in their body weight, while intraerythrocyte sodium contents remained unchanged in the both groups. These results suggest that the abnormal change in membrane Na-K-ATPase activity may, at least in part, be involved in the mechanism of sodium susceptibility in patients with essential hypertension.

Adult↗
PubMed1985

[Hypertensive heart disease simulating dilated cardiomyopathy].

Echocardiography was performed for 246 patients with hypertension. Among the 246 patients, echocardiographic features simulating dilated cardiomyopathy (DCM) were observed in 12. These patients had past history of hypertension and prominent left ventricular dilatation with reduced left ventricular contractility, but no left ventricular wall thickening. To elucidate the mechanism producing DCM-like features in patients with hypertension, the clinical and echocardiographic findings of the 12 hypertensive patients (HT-DCM) were compared with those of 50 hypertensive patients without dilated left ventricles and of 31 patients with DCM. On admission, all patients with HT-DCM had congestive heart failure (CHF) without high blood pressure and their echocardiograms revealed the abnormal findings described above. There were no differences of the clinical and echocardiographic findings on admission between HT-DCM and DCM. Following medical treatment, relatively early improvement of CHF was noted in all patients with HT-DCM; the LV dimension decreased and diffuse wall motion abnormality improved steadily with gradual elevation of blood pressure during the follow-up periods. The LV function of most patients with HT-DCM improved markedly but never reached normal levels. There were no significant differences the right ventricular endomyocardial biopsy findings of between DCM and HT-DCM. It was suggested the DCM-like features in these cases are caused, not only by hypertension, but by other factors, as well.

Adult↗
PubMed1985

[Right ventricular dysplasia: clinical characteristics of five patients].

The purpose of this study was to elucidate the clinical features of right ventricular (RV) dysplasia, a recently described clinical entity characterized by RV myopathic changes and ventricular tachycardia of left bundle branch block morphology. Five cases were reported, in which the diagnosis was established according to the criteria of Marcus. Case 1, a 33-year-old man, was referred to us for evaluation of his paroxysmal ventricular tachycardia of five years duration. Case 2, a 38-year-old man, was admitted because of shock caused by ventricular tachycardia. In both cases, the QRS configurations during ventricular tachycardia were those of the left bundle branch block pattern, and electrocardiograms during sinus rhythm showed T wave inversions in the right precordial leads and late ventricular potentials. Two-dimensional echocardiography, radionuclide angiography and contrast angiography disclosed RV dilatation and dysfunction with normal left ventricular (LV) function. The biopsied myocardium from the right and left ventricles in Case 2 revealed myocytolysis, a paucity of myofibrils and proliferation of collagen fibers. Case 3, a 73-year-old woman began to experience exertional dyspnea since 16 years of age. Her treatment consisted of bed rest, diuretics and digitalis. In December 1983, her New York Heart Association functional class was III, and physical examinations disclosed a Levine III/VI systolic murmur suggestive of tricuspid regurgitation, jugular vein dilatation, hepatomegaly, and pretibial edema. Electrocardiogram showed atrial fibrillation, incomplete right bundle branch block and T wave inversions in the precordial leads. Chest radiograph revealed marked cardiomegaly (cardiothoracic ratio of 92%). Echocardiography, radionuclide angiography and contrast angiography revealed marked RV dilatation, depressed ejection fraction (RV end-diastolic volume index of 342 ml/m2, and RV ejection fraction of 28%). Case 4, a 20-year-old man, was admitted with a chief complaint of palpitation. Case 5, a 19-year-old man, was referred to us for the evaluation of asymptomatic cardiomegaly, and his cardiothoracic ratio was 54%. A 12-lead electrocardiogram showed right bundle branch block and T wave inversions in the right precordial leads. Ambulatory electrocardiography revealed frequent premature ventricular complexes of the left bundle branch block pattern. Echocardiography, radionuclide angiography, and contrast angiography disclosed RV dilatation and dysfunction in both cases, and mild LV dilatation and dysfunction (LV end-diastolic volume index of 149 ml/m2, LV ejection fraction of 48%) in Case 4.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗