Biomedical subjects

H Fukuzaki

Publications and source records attributed to H Fukuzaki.

At least 127 records · Page 7Linked to original sources

PubMed1988

Dynamic behaviour of coronary stenosis in response to increasing heart rate in the dog.

In order to assess the responses of coronary stenosis to an elevation of myocardial metabolic demand, the effects of pacing induced tachycardia on systemic and coronary haemodynamics were examined during four grades of compliant coronary stenosis which preserved stenosis vasomotility in eight open chest dogs. Grades of the coronary stenosis were defined as trifling, mild, moderate, and severe by pressure gradients of 12(0.5), 19(1.0), 28(1.4) and 37(1.6) mm Hg (mean [SEM]), respectively. Stepwise increases in heart rate (+30, +60 and +90 beats.min-1) decreased the resistance caused by trifling and mild coronary stenosis by 47(11.9) and 26(8.8)%, respectively, with an increase in coronary blood flow and a decrease in pressure gradient across the stenosis. By contrast, the resistance caused by moderate and severe stenosis increased by 96(24.2) and 148(63.2)%, respectively, with a decrease in coronary blood flow and an increase in pressure gradient. During lower grades of coronary stenosis, flow-dependent dilatation of large epicardial coronary arteries reduced the stenosis severity, whereas during higher grades of stenosis, passive narrowing of the stenosed arterial segment due to arteriolar vasodilatation outstripped the flow-dependent stenosis dilator effects and resulted in an intensification of the stenosis.

Animals↗

PubMed1988

Left ventricular filling characteristics in sodium-depleted and sodium-loaded patients with mild essential hypertension.

To determine left ventricular early diastolic function and transmitral blood-flow characteristics during periods of sodium depletion (50 mmol/day) and sodium loading (300 mmol/day), Doppler and standard echocardiography were performed in 13 patients with untreated mild hypertension. A high sodium intake for 7 days significantly increased (P less than 0.05) the ratio of Doppler atrial contraction phase peak velocity A to rapid filling phase peak velocity R. The isovolumic relaxation time was prolonged (P less than 0.001) and the left atrial emptying index was reduced (P less than 0.05). During sodium loading the changes in isovolumic relaxation time and the atrial emptying index were correlated with the increase in mean wall stress (r = 0.600, P less than 0.05 and r = -0.695, P less than 0.01, respectively), but not with the increase in end-diastolic volume. These results suggest that during excess salt intake, left ventricular relaxation and filling may be impaired due to a salt-induced increase in afterload in patients with mild hypertension.

Echocardiography, Doppler↗

PubMed1988

Inhibition by cyclic AMP of phorbol ester-potentiated norepinephrine release from guinea pig brain cortical synaptosomes.

The involvement of Ca2+/phospholipid-dependent protein kinase (protein kinase C, PKC) and cyclic AMP-dependent protein kinase in the K+-evoked release of norepinephrine (NE) was studied using guinea pig brain cortical synaptosomes preloaded with [3H]NE. 12-O-Tetradecanoylphorbol-13-acetate (TPA), a potent activator of PKC, enhanced the K+-evoked release of [3H]NE, in a concentration-dependent manner, but with no effect on the spontaneous outflow and uptake of [3H]NE in the synaptosomes. The apparent affinity of the evoked release for added calcium but not the maximally evoked release was increased by TPA (10(-7) M). Inhibitors of PKC, polymyxin B, and a more potent inhibitor, staurosporine, counteracted the TPA-induced potentiation of the evoked release. Both forskolin and dibutyryl cyclic AMP (DBcAMP) enhanced the evoked release, but reduced the TPA-potentiated NE release. A novel inhibitor of cyclic AMP-dependent protein kinase, KT5720, blocked both the forskolin-induced increase in the evoked release and its inhibition of TPA-induced potentiation in the evoked release, thereby suggesting that forskolin or DBcAMP counteracts the Ca2+-dependent release of NE by activating cyclic AMP-dependent protein kinase. These results suggest that the activation of PKC potentiates the evoked release of NE and that the activation of cyclic AMP-dependent protein kinase acts negatively on the PKC-activated exocytotic neurotransmitter release process in brain synaptosomes of the guinea pig.

Alkaloids↗

PubMed1988

Clinical significance of dipyridamole Tl-201 emission computed tomography perfusion abnormality for evaluating pathophysiological and pathological aspects in hypertrophic cardiomyopathy.

A dipyridamole-induced Tl-201 perfusion abnormality was evaluated from its clinical features, echocardiography and myocardial histopathology in 39 patients with hypertrophic cardiomyopathy (HCM). From the findings of Tl-201 emission computed tomography (ECT), subjects were divided into three groups: group 1 (n = 16) which did not show a perfusion abnormality in the hypertrophic region; group 2 (n = 12) which showed a perfusion defect on the initial image with complete redistribution on the delayed image; and group 3 (n = 11) which showed a persistent perfusion defect--this group included most patients who revealed partial and/or incomplete redistribution. Echocardiography revealed that group 2 showed a marked asymmetrical septal hypertrophy and an incidental obstructive pattern, and that group 3 had a significantly dilated left ventricular diastolic dimension and a decreased percentage of fractional shortening. Group 3 also showed frequent ventricular tachycardia and a familial history of cardiomyopathy. As for the myocardial biopsy findings, group 3 had significantly advanced myocardial fibrosis, the percentage being 6.0 +/- 3.1% in group 1; 5.5 +/- 2.5% in group 2; and 11.9 +/- 3.4% in group 3. Thus, it was concluded that the persistent perfusion defect on dipyridamole stress Tl-201 ECT testing is an important finding corresponding to the advanced clinical and pathological aspects of HCM.

Adult↗

PubMed1988

Pulsed Doppler echocardiographic assessment of transmitral flow in pacing-induced angina pectoris.

We analyzed transmitral flow using pulsed Doppler echocardiography during anginal attack provoked by atrial pacing in 11 patients with coronary artery disease (CAD). Left ventricular (LV) filling period was divided into 4 time intervals (Tr1: the time interval to peak velocity of rapid filling (peak R), Tr2: the time interval from peak R to the end of rapid filling, Ts: the time interval of slow filling, Ta: the time interval of atrial contraction). The velocity in each interval was integrated by planimeter as IR1, IR2, IS or IA which indicates relative filling volume in each interval. During angina, IR1 was unchanged due to prolongation of Tr1 (82 +/- 21 to 102 +/- 23 msec, p less than 0.02), despite a decrease in peak R (54 +/- 11 to 43 +/- 11 cm/sec, p less than 0.005), while IR2 decreased (5.8 +/- 1.9 to 4.3 +/- 1.4 cm, p less than 0.005) and IA increased (6.7 +/- 1.4 to 7.3 +/- 1.3 cm, p less than 0.005). In conclusion, these results suggested that in acute myocardial ischemia in CAD a decrease in transmitral flow from the time of peak R to the end of rapid filling (IR2) reflected the impairment of the LV rapid filling, which was incompletely compensated by an increase in atrial contraction.

Adult↗

PubMed1988

Effects of left ventricular dysfunction on left atrial performance in previous myocardial infarction and during pacing-induced myocardial ischemia in angina pectoris.

This study aimed to evaluate acute and chronic response of left atrial function to left ventricular dysfunction in patients with coronary artery disease. We studied simultaneous measurements of left atrial volume by biplane cineangiography and left ventricular pressure at rest and after pacing in 59 patients with coronary artery disease and 11 normal subjects. At rest, 35 patients with previous myocardial infarction (MI group) had low left ventricular filling rate of the first third in diastolic time, large left atrial volume before contraction (LA pre-ACV) and large left atrial ejection volume (LAEV), compared with control group. Left atrial ejection fraction (LAEF), the ratio of LAEV to LA pre-ACV, was similar between both groups. LAEF was maintained within a wide range of values in accordance with left ventricular peak A pressure, except for 3 patients who had high values of left ventricular peak A pressure and low values of LAEF. After a right atrial pacing stress test, time constant was prolonged and mean emptying rate of left atrial volume during early diastole decreased in 11 patients with angina pectoris who had an increase greater than 5 mmHg in left ventricular end-diastolic pressure after pacing. In these group, LA pre-ACV increased, LAEF decreased and LAEV was unchanged. These results suggest that left atrial performance responds differently to acute and chronic left ventricular dysfunction in patients with coronary artery disease.

Angina Pectoris↗

PubMed1988

Intracellular magnesium deficiency and effect of oral magnesium on blood pressure and red cell sodium transport in diuretic-treated hypertensive patients.

The effects of magnesium supplementation were tested in 20 patients with essential hypertension receiving long-term thiazide diuretic treatment (Th group) and 21 age-matched untreated patients (EHT group). Intra-erythrocyte cations, water content and the ouabain-sensitive sodium efflux rate constant were measured. The Th group received magnesium supplementations as MgO (600 mg Mg/day) for 4 weeks. In the Th group intra-erythrocyte magnesium and the sodium efflux rate constant were lower and red cell sodium was higher than in the EHT group. During magnesium supplementation, there were significant decreases (p less than 0.01) in intra-erythrocyte sodium content and mean blood pressure, and increases (p less than 0.005) in red cell magnesium content and the sodium efflux rate constant. These effects of magnesium were more evident in 9 patients who were unresponsive to diuretic therapy, a definite reduction in mean blood pressure, from 104.8 +/- 2.7 mmHg to 94.4 +/- 2.2 mmHg (p less than 0.001), being observed. In the remaining 11 patients, however, blood pressure remained unchanged. The sodium efflux rate constant was positively correlated with red cell magnesium content and negatively correlated with sodium content (r = 0.61, p less than 0.005 and r = -0.57, p less than 0.01, respectively). These results indicate that long-term diuretic treatment may give rise to intracellular magnesium deficiency and a suppression of cell membrane active sodium transport. The results also suggest that oral magnesium may decrease intracellular sodium, possibly through the activation of Na-K-ATPase, which in turn may contribute to the reduction in blood pressure. Therefore, magnesium supplementation may be a worthwhile additional therapy for diuretics.

Administration, Oral↗

PubMed1988

Clinical study of late potentials--comparison of late potentials in myocardial infarction, cardiomyopathy and idiopathic ventricular tachycardia.

Late potentials (LPs) were studied using the signal averaging technique in 80 patients with myocardial infarction (MI), idiopathic cardiomyopathy (CM) and idiopathic ventricular tachycardia (IVT). In MI, LP duration was 28.4 +/- 12.6 ms in the sustained VT group (I; 8 cases); 18.6 +/- 9.0 ms in the non-sustained VT group (II; 11 cases); and 14.4 +/- 8.6 ms in the non-VT group (III; 21 cases); (p less than 0.05 in I vs II, p less than 0.01 in I vs III and not significant in II vs III). In CM, it was 33.7 +/- 13.0 ms in group I (6 cases); 20.1 +/- 5.9 ms in group II (12 cases); and 7.1 +/- 9.2 ms in group III (14 cases); (p less than 0.01 in I vs II, I vs III and II vs III). The LP duration in IVT (8 cases) was 15.6 +/- 10.4 ms, which was significantly shorter than that of group I in MI and CM (p less than 0.05 vs MI and p less than 0.01 vs CM). Late potential duration was also compared between a pacing-inducible VT group and a non-inducible VT group. The mean value of LP duration in the inducible VT group of MI was significantly longer than that in the non-inducible group (27.8 +/- 3.9 ms in 4 cases vs 17.3 +/- 2.5 ms in 4 cases, p less than 0.05). However, there was no significant difference in LP duration between the inducible and non-inducible groups of CM (22.0 +/- 11.0 ms in 5 cases vs 22.2 +/- 13.6 ms in 5 cases).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1988

The diagnostic value and clinical significance of light exercise 201T1 ECT in coronary artery disease.

To examine the clinical significance of scintigraphic transient perfusion defects preceding the occurrence of anginal pain and ischemic ST depression, we performed both maximal and light exercise thallium-201 emission computed tomography in 13 patients with effort angina pectoris. The target heart rate in the light test was set at 80% of the peak heart rate in the maximal test. The scintigraphic transient perfusion defect was observed in all cases in both tests, while the incidence of anginal pain and/or ischemic ST depression was lower in the light test (5/13 cases) comparing to the maximal test (13/13 cases). However, the number of defect segments in the light test was smaller than that in the maximal test (13 vs 19 segments). In the former 13 segments, the initial relative activity in the maximal test was not significantly different from that in the light test (69.4 +/- 9.3 vs 70.1 +/- 10.0%). These results suggest that the light test can precipitate a transient perfusion defect preceding anginal pain and/or ischemic ST depression, therefore the light test is useful to detect coronary artery disease in patients who cannot perform the maximal test.

Aged↗

PubMed1988

The hemodynamic and metabolic basis for decreased aerobic capacity in the supine exercise compared with the upright exercise in coronary artery disease.

To elucidate the mechanism of reduced exercise tolerance in the supine position, 14 patients with coronary artery disease were studied by both supine ergometer exercise and upright treadmill exercise. Maximal oxygen consumption in the supine position amounted to 80% of that in the upright position (1110 +/- 453 vs 1387 +/- 470 ml/min; p less than 0.001). Maximal cardiac output was identical in both positions (12.07 +/- 4.44 vs 12.55 +/- 4.49 l/min; ns). Maximal arteriovenous oxygen difference in the supine position amounted to 83% of that in the upright position (9.22 +/- 1.92 vs 11.14 +/- 1.88 vol%; p less than 0.01). Thus, the lower maximal oxygen consumption in the supine position was not caused by the decreased cardiac output but by the impaired augmentation of arteriovenous oxygen difference. Lactate concentration at the same oxygen consumption was higher in the supine position, which means early augmentation of anaerobic metabolism. We concluded that the aerobic capacity in the supine position was significantly lower than that in the upright position in patients with coronary artery disease, and the impaired utilization of transported oxygen was considered to be one of the mechanisms of the decreased aerobic capacity in the supine position.

Adult↗

PubMed1988

Cardiovascular effects of dibutyryl cyclic AMP in patients with congestive heart failure--comparison with dobutamine and captopril.

To assess the effect of dibutylyl cyclic AMP (DBcAMP) on patients with congestive heart failure (CHF) in comparison with dobutamine and captopril, these three agents were administered to 9 patients with CHF. DBcAMP was infused at a rate of 0.2 mg/kg.min for 30 min, dobutamine was infused at a rate of 8 micrograms/kg.min and captopril 25 mg was administered orally. Hemodynamic and echocardiographic studies were performed before and after administration of each agent. Systolic arterial pressure (SAP) fell with DBcAMP and captopril but rose with dobutamine. Cardiac output (CO) rose and systemic vascular resistance (SVR) fell with each agent but the magnitude of the change was greater with DBcAMP than with the other two agents. Left ventricular end-systolic dimension decreased and percent fractional shortening increased with all these drugs. Comparing DBcAMP and captopril, although the degree of change in CO was closely correlated with that in SVR by captopril, the degree of increase in CO by DBcAMP was more than that expected from the degree of the decrease of SVR. Comparing DBcAMP and dobutamine, SAP and pressure rate product increased with dobutamine, but the former fell and the latter was not changed by DBcAMP. Arrhythmia was not increased by DBcAMP, though it was markedly increased by dobutamine. In conclusion, the magnitude of positive inotropic and vasodilator effect of DBcAMP was equal to or greater than that of dobutamine or captopril. So DBcAMP is thought to be useful for the treatment of CHF.

Aged↗

PubMed1988

Stimulation of phospholipase C-mediated hydrolysis of phosphoinositides by adenosine 5'-triphosphate via P2-purinoceptors in cultured rat aortic vascular smooth muscle cells.

Incubation of [3H] inositol-labeled cultured rat aortic vascular smooth muscle cells with angiotensin II caused the dose- and time-dependent formation of inositol mono-, bis- and trisphosphates. Under these conditions, adenosine triphosphate (ATP) stimulated the formation of these inositol phosphates. The maximal reaction velocities obtained by ATP and angiotensin II were roughly the same. The doses of ATP giving half maximal and maximal reaction velocities were about 100 microM and 1 mM, respectively. This action of ATP was mimicked by other nucleotides such as adenosine diphosphate (ADP) and guanosine triphosphate (GTP), but these nucleotides were far less effective than ATP. Adenosine monophosphate (AMP), adenosine, guanosine diphosphate (GDP), guanosine monophosphate (GMP), deoxythymidine trisphosphate (dTTP), and cytosine triphosphate (CTP) were almost ineffective. The formation of inositol phosphates induced by ATP was inhibited partially by pretreatment of the cells with pertussis toxin. This toxin ADP-ribosylated a protein with a molecular mass of about 40,000. These results indicate that ATP induced the phospholipase C-mediated hydrolysis of phosphoinositides probably via P2-purinoceptors in rat aortic vascular smooth muscle cells, and suggest that a pertussis toxin-sensitive GTP-binding protein is involved at least partially in the coupling of this receptor to the phospholipase C in this cell type.

Adenosine Triphosphate↗

PubMed1988