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E Nozaki

Publications and source records attributed to E Nozaki.

6 recordsLinked to original sources
PubMed1996

Coronary angioplasty ameliorates hypoperfusion-induced endothelial dysfunction in patients with stable angina pectoris.

OBJECTIVES: This study sought to investigate the effect of coronary angioplasty on chronic hypoperfusion-induced endothelial dysfunction in patients with coronary heart disease. BACKGROUND: The endothelium is an important component for organ flow regulation. Ischemia with or without reperfusion is known to cause endothelial dysfunction. We tested the hypothesis that chronic hypoperfusion impairs endothelial function in the angiographically normal coronary artery segment distal to stenosis and that the impairment by chronic hypoperfusion is reduced by coronary angioplasty. METHODS: In 13 patients with stable angina pectoris, substance P (10, 30 and 100 pmol) and nitroglycerin (200 micrograms) were sequentially infused into the coronary artery in a cumulative manner on the day after coronary angioplasty. In 10 of these patients, vascular responses to these agents were again investigated 3 months after angioplasty. Changes in vascular diameter were evaluated in vessels located proximal and distal to the target lesion, both of which were angiographically normal, by performing computer-assisted quantitative coronary angiography. In five patients, the transstenotic pressure gradient was also measured with a pressure sensor-mounted guide wire before angioplasty. RESULTS: On the day after angioplasty, the magnitude of dilation by substance P in distal segments was significantly less than that in proximal segments and inversely correlated with the transstenotic pressure gradient (p < 0.05) and lesion stenosis (p < 0.05). There was no difference in nitroglycerin-induced vasodilation between the two vessel segment groups. Three months later, the impaired response to substance P in the distal segment was restored to normal. CONCLUSIONS: We conclude that chronic hypoperfusion impairs endothelium-dependent dilation of coronary artery distal to critical stenosis in patients with ischemic heart disease and that coronary angioplasty ameliorates the endothelial dysfunction within 3 months.

Aged↗
PubMed1993

Effects of arterial distensibility on left ventricular ejection in the depressed contractile state.

OBJECTIVE: The aim was to evaluate the effects of arterial distensibility on ventricular ejection in various ventricular contractile states: (1) control; (2) a regionally depressed contractile state due to left circumflex coronary artery occlusion (ligation); (3) a globally depressed contractile state induced by lignocaine (lignocaine); and (4) a globally augmented contractile state due to dobutamine infusion (dobutamine). METHODS: Arterial compliance was decreased from 2.3 x 10(-4) dyne-1.cm5 (C2.3) to 0.4 x 10(-4) dyne-1.cm5 (C0.4), maintaining other afterload components and left ventricular end diastolic pressure constant. Nine excised perfused and paced canine hearts, supported from donor dogs, were used. RESULTS: In control, ligation, lignocaine, and dobutamine groups, the difference in cardiac output between the compliance values of C0.4 and C2.3 was 124(SEM 32), 204(36), 163(33), and 130(24) ml, respectively. Thus cardiac output at C0.4, as a percentage of that at C2.3, was 88(2.8)% (control), 75(2.9)% (ligation), 82(2.9)% (lignocaine), and 88(2.4)% (dobutamine), respectively: control v ligation, and lignocaine v ligation, p < 0.001; control v lignocaine, and dobutamine v ligation, p < 0.01. Stroke work at C0.4 decreased in the ligation group (63%, p < 0.001) and in the lignocaine group (70%, p < 0.001). CONCLUSIONS: When cardiac dysfunction is already present, decreased arterial distensibility has a further deleterious effect on cardiac output. This may be due to the fact that the pressure at the end of ejection is higher and as a result the change in dimension during ejection is considerably reduced, especially in cases with depressed cardiac function caused by afterload dependency.

Animals↗
PubMed1989

Left ventricular pump function in right ventricular overload.

To clarify how left ventricular pumping action is altered in cor pulmonale, an experimental study was performed using canine heart preparations in which the effects on left ventricular performance of right ventricular overload, with and without depressed systolic function, were investigated. For this purpose, two methods using excised perfused hearts (n = 16) and in vivo hearts (n = 6) were employed, and in the latter condition, pulmonary artery constriction (n = 7), femoral arterial-venous (A-V) shunt (n = 3) and right coronary artery occlusion (n = 6) were induced. Left ventricular systolic function was assessed by the relationship between left ventricular isovolumic developed pressure and left ventricular volume in excised heart, and by ejection fraction with 2 dimensional echocardiogram in the vivo condition, taking into account preload and afterload changes. From the excised heart preparation, it was shown that left ventricular developed pressure significantly decreases when right and left ventricular diastolic pressure increases greatly. On the other hand, in vivo right ventricular overload due to pulmonary constriction and A-V shunt, the left ventricular ejection fraction increased following afterload reduction. When we compare the left ventricular ejection fraction in pulmonary constriction with that in right coronary occlusion, in which reduction of left ventricular diastolic area from the control was similar, the latter was significantly decreased despite afterload reduction. These results suggest that right ventricular overload does not necessarily induce left ventricular systolic dysfunction unless left ventricular end-diastolic pressure, as well as that of the right ventricle, increases definitely and simultaneously.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Myocardial imaging using 11C-CoQ10 with positron emission tomography.

The potential of 11C-labeled coenzyme Q10(CoQ10) as a myocardial imaging tracer was explored with positron emission tomography (PET). Serial myocardial imaging studies were performed using 11C-CoQ10, 45Ti-diethylenetriaminepentaacetic acid (45Ti-DTPA), and 2-deoxy-2-[18F]fluoro-D-mannose (18FDM) in the same dog. Cross sectional images of the heart with 11C-CoQ10 showed relatively high radioactivity in the blood pool, when compared with images taken with 18FDM. However, when the blood spillover of radioactivity is adequately corrected with 45Ti-DTPA data, it was found that 11C-CoQ10 accumulated in the myocardium with time.

Animals↗
PubMedDate not supplied

Different responses of left ventricular systolic function to changes in right ventricular volume and shortening--comparison between aorto-femoral vein and aorto-left atrium shunts in dog hearts.

It has been reported that left ventricular end-systolic volume decreases during arteriovenous shunt and increases during subclavian artery-left atrium shunt at a constant end-systolic pressure. The mechanism of the opposing changes in end-systolic volume during the two types of shunt is not clear. One possible cause is that left ventricular pump function with enhanced right ventricular ejection differs from that without enhancement. To investigate this hypothesis, we studied the two types of shunt (Aorto-femoral vein shunt, AoFV; aorto-left atrium shunt, AoLA) with matched reduction of systemic vascular resistance in open-chest dogs with beta-blockade. Both right and left ventricular volumes and shortenings were assessed from short-axis views by two-dimensional (2D)-echocardiogram. Left ventricular end-systolic short-axis area decreased from 76 +/- 3 to 62 +/- 3% in AoFV shunt (p less than 0.05), but tended to increase in AoLA shunt (76 +/- 4 in control state vs 81 +/- 5% in AoLA, NS) in spite of a similar reduction in left ventricular end-systolic pressure. There was no difference in left ventricular shortening, but significant differences were observed in right ventricular shortening (50 +/- 8 in AoFV vs 24 +/- 7% in AoLA, p less than 0.05) and right ventricular short-axis area at end-diastole (142 +/- 6 in AoFV vs 96 +/- 3% in AoLA, p less than 0.01), and at end-systole (92 +/- 8 in AoFV vs 73 +/- 7% in AoLA, p less than 0.05) between the two types of shunt. We conclude that the different changes in left ventricular end-systolic short-axis area found in the two shunts are not caused by the different left ventricular shortenings, but by the different right ventricular mechanical actions. These findings suggest that left ventricular pumping action in the high output state changes, depending on whether it is accompanied by augmented ejection of the right ventricle or not.

Animals↗