Search PubMed⌕ Search

Biomedical subjects

K Mizushige

Publications and source records attributed to K Mizushige.

108 records · Page 6Linked to original sources

[Noninvasive estimation of max (dP/dt) of the left ventricle based on maximum aortic flow acceleration as measured by pulsed Doppler echocardiography].

To obtain an index of left ventricular contractility, cardiac catheterization is necessary. In the present study, we ascertained whether max(dP/dt) could be obtained noninvasively in vivo based on the theoretical equation, max(dP/dt) not equal to rho cmax(du/dt), where rho is the density of blood, c is the pulse wave velocity of the aorta and max(du/dt) is the maximum acceleration of the aortic blood flow. This equation is based on the theory of pulse wave propagation, and was established in animal experiments. We further attempted to clarify the clinical usefulness of rho cmax(du/dt) by examining the effects of afterload and preload on rho cmax(du/dt). Twenty-seven patients without stenosis of their aortic valves and left ventricular outflow tracts were observed. During cardiac catheterization, we measured max(dP/dt) using a catheter-tip micromanometer, max (du/dt) using pulsed Doppler echocardiography and pulse wave velocity by simultaneously recording the femoral pulse wave and the carotid pulse wave. The measurements were performed at rest, before and after an increase in contractility with dobutamine administration, an increase in afterload with methoxamine administration and an increase in preload by leg elevation. There was good linear correlation (Y = 0.95X + 7.51, r = 0.84, p less than 0.0005) between max(dP/dt)[X] and rho cmax(du/dt)[Y] at rest. When the contractility was changed, rho cmax(du/dt) reflected changing of max(dP/dt). Moreover, when the afterload and preload were increased, the changing pattern of rho cmax(du/dt) was similar to that of max(dP/dt). Max(du/dt), index of cardiac performance previously proposed, showed a different changing pattern than max(dP/dt), indicating that max(du/dt) was influenced substantially by loading conditions. These results indicated that we can obtain max(dP/dt) noninvasively and reliably by measuring rho cmax(du/dt).

Aged↗

Influence of right ventricular pressure overload on left and right ventricular filling in cor pulmonale assessed with Doppler echocardiography.

We evaluated the influence of right ventricular (RV) pressure overload on RV and left ventricular (LV) filling using Doppler echocardiography in cor pulmonale. The LV and RV inflow signals were recorded by Doppler flowmetry. The end-diastolic (ED) and end-systolic (ES) LV short axis images were detected by 2-dimensional echocardiography in 20 healthy subjects and in 36 cases of chronic pulmonary disease (CPD) with pulmonary hypertension. We measured (1) the ratio of the peak velocity of inflow due to atrial contraction to the peak velocity of rapid inflow (A/R), (2) the deceleration half-time of rapid inflow (delta TD), (3) the corrected radius of curvature (cRC) of the interventricular septum (IVS) at ES and ED, and (4) the percent change of length of 16 radial grids (%CL) using the fixed method on the ED and ES short axis images. In 17 of 36 patients with CPD, we measured the systolic pulmonary artery pressure (sPAP), the cardiac index (CI), the mean pulmonary capillary wedge pressure (mPCWP), the end-diastolic right ventricular pressure and the partial oxygen pressure of arterial blood (PaO2). The results were as follows: in CPD, (1) both the RV and the LV diastolic behavior were impaired as shown by increased A/R (1.04 +/- 0.20, 0.98 +/- 0.17, respectively) and prolonged delta TD (115 +/- 20, 100 +/- 17 msec, respectively), (2) the IVS was flattened at ED (cRC of IVS = 0.67 +/- 0.12), (3) the IVS wall motion was impaired (%CL of IVS = 133 +/- 13), (4) the sPAP had an adequate correlation with RV A/R (r = 0.80, p less than 0.01), RV delta TD (r = 0.59, p less than 0.05), LV A/R (r = 0.82, p less than 0.01), LV delta TD (r = 0.61, p less than 0.05), cRC of IVS (r = 0.67, p less than 0.01), %CL of IVS (r = -0.59, p less than 0.05). There was no significant correlation between the LV diastolic behavior and the CI, the mPCWP, the PaO2. It is concluded that the impairment of RV diastolic behavior was caused by the decreased RV compliance due to RV free wall hypertrophy. Moreover, the RV pressure overload interfered with the IVS motion during diastole, this regional impairment of diastolic behavior of the IVS subsequently causing impairment of LV diastolic filling.

Adolescent↗

[The influence of the right or left ventricular pressure overload on right and left ventricular diastolic behaviors as examined by pulsed Doppler echocardiography].

The influence of morphological and dynamic changes in the interventricular septum (IVS) on right ventricular (RV) and left ventricular (LV) fillings in cases of LV or RV pressure overload was evaluated. Using pulsed Doppler echocardiography, LV and RV inflow signals were recorded in 20 healthy subjects, in 36 cases of chronic pulmonary disease (CPD) with pulmonary hypertension, and in 46 cases of essential hypertension (HT). Two-dimensional short-axis echocardiograms were recorded at end-diastole (ED) and end-systole (ES) in the healthy subjects and in the cases with CPD. M-mode echocardiograms of the LV were recorded in the healthy subjects and in the cases with HT. We measured (1) the ratio of the peak velocity of inflow due to atrial contraction to that of rapid inflow (A/R), (2) the deceleration half-time of rapid inflow (delta TD), (3) the corrected radius of curvature of the IVS at ED and ES, (4) the % change of lengthening (CL) of 16 radial grids using a fixed method on the ED and ES short-axis images, and (5) the IVS end-diastolic thickness (IVSEDTh). The results were as follows: 1. In the patients with CPD, (1) the diastolic behavior was impaired not only in the RV, but in the LV as well, as shown by the increased A/R and prolonged delta TD in both ventricles, (2) the IVS was flattened at ED, as shown by the decreased corrected radius of the curvature, (3) the regional wall motion of the IVS was impaired, as shown by the decreased CL of the IVS. 2. In the patients with HT, (4) the RV diastolic filling was not impaired, (5) the LV A/R correlated with IVSEDTh, but the RV A/R did not correlate with IVSEDTh. We concluded that RV pressure overload interferes with IVS motion during diastole, and that the regional impairment of diastolic behavior of the IVS causes impairment of LV diastolic filling. Furthermore, the increased IVS wall thickness due to LV pressure overload has a little or no influence on the RV inflow pattern because the RV free wall was so distensible as to overcome the effect of increased IVS stiffness.

Aged↗

[Effect of calcium antagonist (diltiazem) on left ventricular diastolic properties in essential hypertension: a pulsed Doppler echocardiographic study].

To evaluate the acute effect of diltiazem on left ventricular diastolic properties, we measured transmitral flow in 15 patients with essential hypertension using pulsed Doppler techniques. Before administering diltiazem, the peak velocity (R) and the deceleration rate of rapid inflow decreased significantly as compared with healthy subjects, but the peak velocity during atrial contraction (A) and the A/R increased significantly. Immediately after the intravenous administration of 10 mg diltiazem, blood pressure decreased from 157 +/- 22/96 +/- 12 mmHg to 135 +/- 19/82 +/- 11 mmHg (p less than 0.001) and the heart rate increased from 69 +/- 10/min to 74 +/- 10/min (p less than 0.05). However, 30 minutes after the injection, these returned to control values. The peak velocity and deceleration rate of rapid inflow were 52 +/- 9 cm/sec and 227 +/- 65 cm/sec2, respectively, before administering diltiazem, and five minutes after injection, these parameters increased to 63 +/- 13 cm/sec (p less than 0.001) and 292 +/- 82 cm/sec2 (p less than 0.001), respectively. Thirty minutes later, these values leveled off at 58 +/- 12 cm/sec (p less than 0.01) and 257 +/- 76 cm/sec2 (p less than 0.05), respectively. The peak velocity during atrial contraction was 67 +/- 12 cm/sec before administration, and this did not change significantly after injecting diltiazem. Significant increases in peak velocity and deceleration rate of rapid inflow and decreases in the A/R continued after the blood pressure and heart rate returned to control values. It was therefore concluded that diltiazem improves impaired early diastolic left ventricular filling in essential hypertension.

Adult↗

[Pre-ejection flow in the left ventricular outflow tract elucidated by pulsed Doppler technique].

Pulsed Doppler technique has elucidated the blood flow towards the cardiac base in the left ventricular (LV) outflow tract prior to onset of ejection flow. This pre-ejection flow (PE flow) is observed immediately after the beginning of atrial contraction and it lasts until immediately after completion of mitral closure. This study was designed to clarify the mechanism and physiological significance of PE flow by investigating the temporal relationship between PE flow and cardiac dynamics and by examining its velocity distribution in the LV outflow tract. Observations were made for 21 healthy subjects (H), 12 patients with atrial fibrillation (Af), three with first degree AV block and two with second degree AV block of the Wenckebach type. A Doppler-Echocardiograph (Hitachi Medico EUB-10B) was used, and PE flow was detected in all subjects. The Doppler frequency, which corresponded to blood flow velocity, increased when the sampling site was near the tip of the anterior mitral valve leaflet as opposed to the upper portion of the LV outflow tract. Results of the temporal analysis of PE flow were as follows: The PE flow pattern was monophasic both in H and patients with Af. Its peak appeared 0.18 +/- 0.05 (mean +/- SD) sec after the beginning of the P wave and 0.02 +/- 0.02 sec after the Q wave in H, but 0.06 +/- 0.01 sec after the Q wave in Af. In first degree AV block, the PE flow consisted of two peaks. The interval between the first PE flow peak and the beginning of the P wave was constant and nearly 0.2 sec apart. It was nearly the same as in H. The second peak occurred 0.05 sec after the Q wave as in Af. In second degree AV block of the Wenckebach type, the first peak occurred at constant interval following the P wave, while the second peak related to left ventricular contraction and disappeared when an atrial contraction failed to initiate a ventricular response. These findings indicate that PE flow consists of two components with different mechanisms. 1) The first component is caused by the atrial blood inflow turning up from the apex towards the cardiac base. This flow component may participate in closure of the anterior mitral leaflet. 2) The second component consists of a rise in LV pressure due to LV contraction, and achieves complete closure of the mitral leaflets. We conclude that PE flow with its atrial and ventricular components contributes to closure of the mitral leaflets.

Aged↗

Sodium sensitivity and sympathetic nervous system in hypertension induced by long-term nitric oxide blockade in rats.

1. Pharmacological inhibition of nitric oxide (NO) synthesis is known to produce acute and chronic hypertension in many animal species, but the underlying mechanisms mediating the hypertension are not completely understood. In particular, the pathogenetic roles of sodium sensitivity and the sympathetic nervous system in this model of hypertension are controversial. The present study was designed to test the hypothesis that long-term administration of the NO synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME) to male Sprague-Dawley rats would produce a sodium-sensitive hypertension and that the enhanced activity of the sympathetic nervous system in this type of hypertension contributes to the sodium sensitivity. 2. NG-Nitro-L-arginine methyl ester was added to drinking fluid for 8 weeks at a concentration of 16 mg/dL. Rats received tap water for the first 4 weeks of the study and were then divided into two groups and placed on either a normal or high sodium intake (ingestion of either tap water or 0.9% NaCl, respectively). Awake systolic blood pressure was measured by the tail-cuff method every week. Urinary excretion rates of the stable NO metabolites and catecholamines during NO synthesis inhibition were examined. 3. Long-term administration of L-NAME produced a marked and sustained elevation in arterial pressure without altering urine flow, or sodium excretion rate. NG-Nitro-L-arginine methyl ester-induced hypertension was accompanied by a decreased urinary excretion of the stable NO metabolites NO2- and NO3- and was aggravated when rats drank 0.9% NaCl in place of tap water. Urinary excretion of adrenaline and noradrenaline, but not dopamine, in L-NAME-treated rats increased significantly within the first week of the study compared with control rats. L-Arginine (2 g/dL in drinking fluid) completely reversed the elevation of arterial pressure as well as the decrease in urinary NO2- and NO3- excretion and the increased urinary excretion of catecholamines associated with L-NAME treatment by 3 weeks of concomitant administration. 4. These results suggest that long-term inhibition of NO synthesis produces a sodium-sensitive hypertension and that changes in sympathetic nerve activity may, at least in part, contribute to the sodium sensitivity in this type of hypertension.

Animals↗

Inhibition by eicosapentaenoic acid of oxidized-LDL- and lysophosphatidylcholine-induced human coronary artery smooth muscle cell production of endothelin.

The objectives of the present study were (1) to determine whether oxidized low-density lipoprotein (LDL) and lysophosphatidylcholine (lyso-PC), a major phospholipid component of oxidized LDL, stimulate the production of endothelin-1 (ET)-1 in cultured human coronary artery smooth muscle cells (SMCs), and (2) to examine the possible effect of an antiatherogenic agent, eicosapentaenoic acid (EPA), on oxidized-LDL- and lyso-PC-stimulated ET-1 production in these cells. Oxidized LDL (10-50 microg/ml) and lyso-PC (10(-7) to 10(-5) mol/l) stimulated ET-1 production in a concentration-dependent manner. By contrast, the effects of native LDL and phosphatidylcholine were modest or absent. Lyso-PC (10(-7) to 10(-5) mol/l) and oxidized LDL (10-50 microg/ml) significantly induced particulate protein kinase C (PKC) activation. Lyso-PC- and oxidized-LDL-stimulated ET-1 production was significantly inhibited by PKC inhibitor, PKC (19-36). EPA (80-160 micromol/l) clearly suppressed ET-1 production stimulated by oxidized LDL and lyso-PC in a concentration-dependent manner. Furthermore, EPA (160 micromol/l) significantly inhibited lyso-PC (10(-5) mol/l)- and oxidized LDL (50 microg/ml)-induced particulate PKC activation. Results suggest that oxidized LDL and lyso-PC stimulate ET-1 production by a mechanism involving activation of PKC, and that EPA suppresses ET-1 production stimulated by lyso-PC as well as oxidized LDL probably through the modulation of PKC in human coronary artery SMCs. EPA may exert an antiatherosclerotic effect, in part, through these mechanisms.

Angiotensin II↗

Antioxidant effect of a new calcium antagonist, azelnidipine, in cultured human arterial endothelial cells.

Azelnidipine is a novel dihydropyridine-type calcium antagonist with long-acting anti-hypertensive action and a low reported incidence of tachycardia. We aimed to evaluate its antioxidant activity in cultured human arterial endothelial cells under oxidative stress. Endothelial cells were exposed to 1 mM H2O2 and treated with 100 microM alpha-tocopherol, 1 nM, 10 nM or 100 nM azelnidipine, 100 nM nifedipine or 100 nM amlodipine. After 3 h, the cell number and level of lipid peroxidation were evaluated by measuring the total protein and 8-iso-PGF2 alpha concentrations, respectively. The total protein concentration was similar with each treatment. Inhibition of 8-iso-PGF2 alpha was greatest with 10 nM azelnidipine (compared with the other drugs); the difference between 10 nM and 100 nM azelnidipine was not significant. We conclude that azelnidipine has a potent antioxidative effect that could be of significant clinical benefit when combined with its long-lasting anti-hypertensive action and low incidence of tachycardia.

Antioxidants↗

[Left ventricular diastolic behavior in patients with syndrome X during isometric exercise assessed by Doppler flowmeter].

Left ventricular (LV) diastolic filling during isometric exercise was evaluated in patients with syndrome X using pulsed Doppler echocardiography. The handgrip exercise was performed by 12 normal subjects (group N), 14 patients with syndrome X (group X), and 20 patients with effort angina, who were divided into 13 patients with single vessel disease (group SVD) and seven patients with multiple vessel disease (group MVD). The transmitral inflow patterns before and at the end of exercise were recorded using Doppler flowmetry, to measure the peak velocity of early diastolic flow (E) and the peak velocity of atrial contraction flow (A). The A/E ratio and the % change in A/E (% A/E) at the end of exercise compared with those before were calculated. 1. Group N: E, A, and A/E did not change significantly. 2. Group X: E decreased, A increased, and A/E increased. 3. Group SVD: E did not change significantly. A increased, and A/E increased. 4. Group MVD: E decreased, A increased, and A/E increased. 5. % A/E in group X and group MVD were larger than in group SVD. 6. Systolic blood pressure (SBP) and heart rate (HR) increased during exercise to the same extent in each group. The impairment of LV diastolic filling in group X was more severe than in group SVD, possibly due to more extensive ischemic areas in group X than in group SVD. The extension of ischemic areas in syndrome X may be similar to that in group MVD.

Adult↗