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Biomedical subjects

N Fukuda

Publications and source records attributed to N Fukuda.

At least 145 records · Page 8Linked to original sources

Cross sectional echocardiographic demonstration of the mechanisms of abnormal interventricular septal motion in congenital total absence of the left pericardium.

OBJECTIVE: To investigate the influence of the absence of the pericardium on the left ventricular wall, particularly on interventricular septal motion, using M mode and cross sectional short axis echocardiography in patients with congenital total absence of the left pericardium. METHODS: 21 patients with, congenital total absence of the left pericardium were divided into three groups according to the interventricular septal motion; systolic type (n = 6) with paradoxical motion during systole, diastolic type (n = 11) with abnormal posterior motion during mid to late diastole, and mixed type (n = 4) with paradoxical motion during systole and abnormal posterior motion during diastole. RESULTS: On cross sectional short axis echocardiograms of the left ventricle, in the diastolic type the degree of angular displacement of the papillary muscles during end diastole to end systole showed excessive anticlockwise rotation about the long axis of the left ventricle without marked anteroposterior displacement. In the systolic type, there was shift of the left ventricle towards the anteromedial portion in systole and towards the posterolateral portion in diastole without significant rotation. There was a significantly positive correlation between the degree of angular displacement and the amplitude of diastolic interventricular septal motion during mid to late diastole in all patients. CONCLUSIONS: There was abnormal interventricular septal motion during systole and diastole in patients with total absence of the left pericardium. Abnormal systolic motion was induced by anteroposterior displacement of the left ventricle, and abnormal diastolic motion by left ventricular rotation about the long axis of the heart during the cardiac cycle. Analysis using cross sectional echocardiography was useful for elucidating the mechanisms of abnormal interventricular septal motion.

Adult↗

Unusual left ventricular wall motion and a loud added sound during the isovolumic relaxation period in a patient with hypertensive heart disease.

A 69 year old woman with hypertensive heart disease had a loud added sound which coincided with a sudden interruption of the early diastolic motion of the left ventricular posterior wall, as visualised by M mode echocardiography, and came just before early diastolic transmitral flow, as measured by a pulsed Doppler echocardiogram. Early diastolic motion velocity from the base to the middle of the posterior wall, assessed by pulsed Doppler tissue imaging, was markedly high and sharp, and its peak coincided with the sound. A notch, similar to that in the posterior wall motion, occurred in the left ventricular pressure curve during early diastole. No intraventricular flow signal was detected during the isovolumic relaxation period, as measured by pulsed and colour Doppler imaging. The added sound was probably produced by impact between the dilated heart, with a relaxation abnormality, and the extracardiac structures during the isovolumic relaxation period.

Aged↗

In vitro antibacterial activity of vanadate and vanadyl compounds against Streptococcus pneumoniae.

All of the vanadate and vanadyl compounds tested in this study showed potent antibacterial activity against Streptococcus pneumoniae: the MIC (minimum inhibitory concentration) values of the vanadium compounds were 4-32 micrograms/ml, while the MIC values of tungstates and molybdates were 128-->8000 micrograms/ml. Scanning electron microscopy showed the elongation of S. pneumoniae strains under low concentrations (< MIC) of vanadium compounds such as (tert-BuNH3)4[V4O12] (1), (tert-BuNH3)6[V10O28] (2), Na3VO4 (7) and VOSO4 (8). The vanadium compounds non-selectively inhibited the incorporation of thymidine, uridine, leucine and glucose into the cells of S. pneumoniae and led to an efflux of potassium ions from the cells. It implies that the vanadium compounds interfere in or on the cell membrane with the transport of substrates and ions through the cell membrane, resulting in antibacterial activity against S. pneumoniae cells.

Cell Membrane↗

Concealed left ventricular hypertrophy and diastolic dysfunction in hypertrophic cardiomyopathy in the presence of acute left ventricular volume overload. A case report.

We report a patient in whom hypertrophic cardiomyopathy, with both left ventricular hypertrophy and diastolic dysfunction, was masked by acute severe aortic regurgitation and marked left ventricular dilation. Upon admission, 1) two-dimensional echocardiogram of the left ventricle revealed a dynamic and flail vegetation on the aortic right coronary cusp and marked left ventricular dilation, 2) a massive aortic regurgitant signal was recorded by color Doppler flow imaging, and 3) transmitral flow velocity by pulsed Doppler echocardiogram revealed a pseudonormalization. However, symmetric hypertrophy of the left ventricular wall, a decrease in early diastolic wave and a compensatory increase in atrial systolic wave of the transmitral flow velocity appeared after successful aortic valve replacement.

Aortic Valve↗

Transesophageal echocardiographic prediction of initially successful electrical cardioversion of isolated atrial fibrillation. Effects of left atrial appendage function.

Left atrial appendage (LAA) flow velocities prior to electrical cardioversion were recorded using transesophageal pulsed Doppler echocardiography to predict initially successful cardioversion of isolated atrial fibrillation (AF). Patients with AF were placed into either a success group (19 patients) in which sinus rhythm was maintained for at least 2 days or a failure group (12 patients). The duration of AF was shorter in the success group. The maximum left atrial diameter was the same for the two groups. The maximum LAA area was smaller in the success group. The maximum forward and backward LAA velocities were greater in the success group, as were the mean forward and backward LAA velocities. In the patients with mean LAA flow velocities greater than 19 cm/sec, the success of cardioversion could be predicted with high sensitivity (80%) and specificity (88%). We conclude that the duration of AF, the maximum LAA area, and LAA flow velocities prior to cardioversion predict the initial recovery of sinus rhythm for isolated AF.

Adult↗

Molecular mechanisms of the exaggerated growth of vascular smooth muscle cells in hypertension.

The molecular mechanisms of the exaggerated growth of vascular smooth muscle cells (VSMC) in hypertension are reviewed based on our previous experimental data. Spontaneously hypertensive rats (SHR)-derived VSMC increasingly express angiotensinogen, cathepsin D and angiotensin-converting enzyme (ACE) mRNAs, compared to cells from normotensive Wistar-Kyoto (WKY) rats, indicating the presence of an Ang II generating system in a homogeneous culture of VSMC from SHR. The produced Ang II then induces TGF-beta. SHR-derived VSMC show the distinct expression and abnormal regulation by Ang II of TGF-beta receptors when compared with cells from WKY rats, which express TGF-beta type II receptor predominantly to induce PDGF A-chain stimulation of VSMC growth. These findings imply that the increased growth of VSMC in hypertension is a primary event independent of high blood pressure, and is associated with endogenous Ang II-related growth factors.

Animals↗

Tricuspid inflow and regurgitant flow dynamics after mitral valve replacement: differences relating to surgical repair of the tricuspid valve.

BACKGROUND AND AIMS OF THE STUDY: Changes in tricuspid inflow and regurgitant flow dynamics were evaluated in patients with functional tricuspid regurgitation (TR) who underwent mitral valve replacement (MVR) with and without tricuspid annuloplasty (TAP). METHODS: In a group of 30 patients, all with atrial fibrillation, 15 underwent TAP performed according to the modified De Vega technique; the remaining 15 did not undergo TAP. Patients were studied before and serially after surgery, using pulsed and color Doppler echocardiography. The mean follow up was 4.7 years in the TAP group and 5.1 years in the non-TAP group. RESULTS: In the TAP group, immediately after surgery, the area of the TR jet decreased markedly, and the deceleration time of the tricuspid inflow velocity wave was significantly prolonged compared with that before surgery. By contrast, in the non-TAP group, both the area of the TR jet and deceleration time of tricuspid inflow velocity were virtually unchanged. The area of the TR jet remained small for a long period in the TAP group, but in non-TAP patients was increased in four cases over seven years, with two patients developing right-sided heart failure. Recent data showed the area of the TR jet to be significantly smaller, with maximum tricuspid inflow velocity significantly increased, and deceleration time of the tricuspid inflow velocity wave significantly prolonged in the TAP group compared with the non-TAP group. CONCLUSIONS: In patients with functional tricuspid regurgitation undergoing MVR, concomitant TAP may cause mild tricuspid stenosis, but produces sustained preventive effects against TR. Careful follow up is needed in patients who have not undergone TAP, as TR is not markedly decreased and may even be exacerbated. Aggressive TAP is recommended in patients showing dilatation of the tricuspid annulus, even if TR is mild.

Adult↗

The 'sail sound' and tricuspid regurgitation in Ebstein's anomaly: the value of echocardiography in evaluating their mechanisms.

We describe a patient with Ebstein's anomaly in whom Doppler echocardiography was used to clarify the mechanism responsible for 'sail sound' and tricuspid regurgitation associated with this condition. Phonocardiography revealed an additional early systolic heart sound, consisting of a first low-amplitude component (T1) and a second high-amplitude component (T2, 'sail sound'). In simultaneous recordings of the tricuspid valve motion using M mode echocardiography and phonocardiography, the closing of the tricuspid valve occurred with T1 which originated at the tip of the tricuspid leaflets, while T2 originated from the body of the tricuspid leaflets. Using color Doppler imaging, the tricuspid regurgitant signal was detected during pansystole, indicating a blue signal during the phase corresponding to T1 and a mosaic signal during the phase corresponding to T2 at end-systole. Thus, 'sail sound' in patients with Ebstein's anomaly is not simply a closing sound of the tricuspid valve, but a complex closing sound which includes a sudden stopping sound after the anterior and/or other tricuspid leaflets balloon out at systole.

Diagnosis, Differential↗

[Modification of the surgical strategy based on intraoperative echographic findings of atherosclerotic ascending aorta].

To prevent the atheroembolic complications such as brain infarction due to the manipulation of atherosclerotic ascending aorta during cardiac surgery, the ascending aorta of 55 patients including 6 emergencies (mean age: 67.7 +/- 6.9 years, valvular disease: n = 12, ischemic heart disease only or combined with valvular disease: n = 43) were evaluated with intraoperative echography as a routine, to enable a proper placement of the cannulae, clamp etc. Irregular elevated lesions into the aortic lumen from the intima were identified in 7 patients (13%, mean age: 71.0 +/- 6.9 years) of ischemic heart disease, which included 2 emergent cases. Arch cannulation was employed in 3 patients with wide-spread lesions on the posterior wall and femoral cannulation was done in 1 patient with wide-spread lesions on the anterior wall. Two of these patients received CABG with in situ arterial conduits under ventricular fibrillation, and the other 2 patients received CABG with aortic cross clamping at the lesion-free site during proximal anastomosis of vein grafts (single clamp technique). Two patients with localized lesion were done CABG with partial aortic clamping and one of them had cerebral infarction during the operation. We recognized that manipulation of the ascending aorta has to be done with a meticulous care and well away from the diseased site. In another patient with localized lesion, the arch cannulation and the single clamp technique were used 2 cm away from that lesion. The brain infarcted patient completely recovered without any sequelae and the others also had no atheroembolic complications. Although calcified lesions on CT were correlated with atheromatous lesions on echogram (p = 0.004), these atheromatous plaques were not detected by enhanced CT, except in only one patient. For screening of the atherosclerosis of ascending aorta, the CT examination was not so effective and the intraoperative echography was the most sensitive and could be easily accomplished. In conclusion, in order to prevent the atheroembolism that might occur due to the improper manipulation of the diseased ascending aorta during usual procedures, surgical strategies have to be modified according to the position, extent and quality of the atherosclerotic lesions, diagnosed by intraoperative echoscanning of the aorta.

Aged↗

Vitamin B12 enhances the phase-response of circadian melatonin rhythm to a single bright light exposure in humans.

Eight young males were subjected to a single blind cross-over test to see the effects of vitamin B12 (methylcobalamin; VB12) on the phase-response of the circadian melatonin rhythm to a single bright light exposure. VB12 (0.5 mg/day) or vehicle was injected intravenously at 1230 h for 11 days, which was followed by oral administration (2 mg x 3/day) for 7 days. A serial blood sampling was performed under dim light condition (less than 200 lx) and plasma melatonin rhythm was determined before and after a single bright light exposure (2500 lx for 3 h) at 0700 h. The melatonin rhythm before the light exposure showed a smaller amplitude in the VB12 trial than in the placebo. The light exposure phase-advanced the melatonin rhythm significantly in the VB12 trail, but not in the placebo. These findings indicate that VB12 enhances the light-induced phase-shift in the human circadian rhythm.

Adult↗

Changes in left ventricular inflow and pulmonary venous flow velocities during preload alteration in dilated heart.

The aim of the present study was to assess the changes of left ventricular inflow (LVIF) and pulmonary venous flow (PVF) velocities during preload alteration in 30 patients with dilated heart (LV end-diastolic dimension > or = 6.0 cm) and impaired LV systolic function (% fractional shortening of the LV < or = 25%). We performed transesophageal pulsed Doppler echocardiography during lower body negative (LBNP, -40 mmHg) and positive pressure (LBPP, +40 mmHg) in 10 patients with dilated cardiomyopathy, in 20 with old myocardial infarction, and in 22 healthy controls. Eight of the patients showed a pseudonormalization (compliance failure) pattern, and 22 showed a decreased early diastolic wave and compensatorily increased atrial systolic wave (relaxation failure) pattern of LVIF in the control state. Mean pulmonary capillary wedge pressure (PCWP) was greater in the compliance failure group than in the relaxation failure group in the control state. LVIF in 6 of the 22 patients with the relaxation failure pattern changed to the compliance failure pattern during LBPP, and that in 3 of 8 patients in the compliance failure group changed to the relaxation failure pattern during LBNP. The 6 patients with a change from the relaxation failure to the compliance failure pattern showed significantly higher peak diastolic and atrial systolic PVFs during LBPP than in the control state, and significantly higher PCWPs in the control state than the 16 patients with no change in LVIF. These findings suggest that the compliance failure and relaxation failure patterns of LVIF are readily interchangeable in various hemodynamic conditions, and that pattern analysis of LVIF and PVF during preload alteration is useful for understanding the hemodynamic severity and for evaluating preload reduction therapy in the dilated heart.

Blood Flow Velocity↗

Clinical significance of the apical late systolic ejection murmur: a new phonocardiographic sign indicating dynamic mid-left ventricular obstruction.

Systolic ejection murmurs of the left heart usually have their peak during early to mid-systole. Few reports have addressed ejection murmurs with their peak at late systole. We evaluated the clinical significance of an apical systolic ejection murmur with a peak intensity during late systole using Doppler and two-dimensional (2-D) echocardiography and phonocardiography. The apical late systolic ejection murmur was observed in 9 of 13 consecutive patients with mid-left ventricular obstruction. We investigated the ejection flow velocity and the timing of maximum velocity at the three different sites of the left ventricle, the left ventricular cavity shape, and the timing of the peak murmur intensity in these nine patients (late-murmur group). The same parameters were also examined in 8 consecutive patients with mid-systolic ejection murmurs (mid-murmur group), 10 with early systolic ejection murmurs (early-murmur group), and 7 controls without murmurs. Patients with aortic stenosis were excluded. The mid-ventricular ejection flow velocity was significantly higher in the late-murmur group than in the other three groups; that of the outflow tract was markedly higher in the mid-murmur group. The ejection flow velocity at the aortic orifice of patients in the early-murmur group was significantly high compared with that of the controls. The timing of the peak murmur intensity in each group correlated with that of the peak flow signal at the corresponding site with maximum velocity. In all patients in the late-murmur group, 2-D echocardiography revealed a systolic narrowing of the cavity at the mid-ventricle. Amyl nitrite inhalation induced a marked increase in the intensity of the murmur without evidence of appearing or increasing mitral regurgitation. It was concluded that the apical ejection murmur with a late systolic peak intensity is a new phonocardiographic sign indicative of dynamic, mid-left ventricular obstruction. This murmur should be differentiated from the mitral regurgitant murmur.

Adult↗

Possible mechanisms of mitral regurgitation in dilated hearts: a study using transesophageal echocardiography.

HYPOTHESIS: This study was undertaken to clarify the mechanisms of mitral regurgitation (MR) in dilated hearts. METHODS: In all, 68 patients with dilated heart and MR, including 26 patients with dilated cardiomyopathy (DCM), 24 with prior anterior myocardial infarction (A-MI), and 18 with prior posteroinferior myocardial infarction (I-MI), as well as 25 normal subjects were examined by transesophageal two-dimensional and color Doppler echocardiography. RESULTS: The maximum area of the MR signal in the DCM group correlated positively with the anteroposterior diameter of the mitral annulus at late systole. Although the coaptation edge length of the anterior and posterior mitral leaflets appeared shorter in dilated hearts than in the hearts of controls, a significant difference did not exist. The length of the coaptation edge correlated negatively with the maximum area of the MR signal in all dilated hearts, and characteristic systolic displacement of the coaptation point of both mitral leaflets occurred. The MI groups demonstrated anterior and posterior displacement in the direction of the short axis of the left ventricle in the A-MI and I-MI groups, respectively. However, the DCM group demonstrated inferior displacement toward the long axis of the left ventricle; its magnitude correlated positively with the maximum area of the MR signal. CONCLUSION: A major cause of MR in dilated hearts is mitral malcoaptation due to displacement of the coaptation point of the mitral leaflets along the long or short axis of the left ventricle. This is caused by left ventricular enlargement and/or asynergy of the left ventricular wall, rather than by a decrease in mitral coaptation edge length due to mitral annular dilation.

Adult↗

Altered hepatic metabolism of fatty acids in rats fed a hypolipidaemic drug, fenofibrate.

The aim of this study was to examine the effects of dietary fenofibrate (0.05% in the diet) on ketone body production and lipid secretion in isolated perfused rat liver. Feeding with fenofibrate for 7-9 days caused an increased liver weight. Ketone body production was significantly greater in the livers perfused with oleic acid than in those perfused without fatty acid, with the elevation of the ratio of beta-hydroxybutyrate:acetoacetate indicating an increased redox potential in mitochondrial compartments by exogenous fatty acid. On the other hand, fenofibrate feeding caused a further stimulation of ketone body production from both endogenous and exogenous fatty acid substrates, respectively, with a decreased ratio of beta-hydroxybutyrate:acetoacetate as compared to respective control livers, indicating a decreased redox potential. Hepatic secretion of triglyceride, but not of cholesterol, was decreased markedly in the fenofibrate-fed rats, especially when oleate was provided, suggesting an inverse relationship between rates of ketogenesis and triglyceride secretion. These results suggest that the altered hepatic metabolism of long-chain fatty acids between oxidation and esterification caused by fenofibrate may thus be a factor responsible for the decreased secretion of triglyceride, hence leading to hypotriglyceridaemia in vivo.

Acetoacetates↗

Changes in transmitral and pulmonary venous flow velocity patterns after cardioversion of atrial fibrillation.

To examine the recovery time of left atrial mechanical function after electrical cardioversion of atrial fibrillation, we recorded transmitral flow, pulmonary venous flow velocities, and interatrial septal motion during atrial systole within 24 hours (16 +/- 5 hours) and 10 days after cardioversion in 25 patients with atrial fibrillation, including 6 patients with hypertension, 4 with ischemic heart disease, 2 with alcoholic heart disease, 5 with dilated cardiomyopathy, and 8 with no evidence of underlying heart disease. With the exception of the five patients with dilated cardiomyopathy, the peak atrial systolic transmitral and pulmonary venous flow velocities, peak first systolic velocity of pulmonary venous flow, duration of both atrial systolic waves, and amplitude of the interatrial septal motion during atrial systole decreased markedly within 24 hours after cardioversion and increased 10 days after cardioversion. These results suggest that active atrial systolic and relaxant variables obtained from transmitral and pulmonary venous flow velocities may reflect left atrial mechanical function after cardioversion of atrial fibrillation.

Atrial Fibrillation↗

Inhibitory effect of an angiotensin II type 1 receptor antagonist on growth of vascular smooth muscle cells from spontaneously hypertensive rats.

To investigate the role of endogenous angiotensin II (Ang II) in the growth of vascular smooth muscle cells (VSMC), we examined the effect of the novel nonpeptide Ang II type 1 (AT1) receptor antagonist CV-11974 on basal and stimulated-growth of VSMC from normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). CV-11974 inhibited basal DNA synthesis by VSMC from SHR, but not from WKY, in the absence of serum. In the presence of 10% calf serum, DNA synthesis was significantly higher in VSMC from SHR than in cells from WKY, and the inhibitory effect of CV-11974 was attenuated. Ang II dose-dependently stimulated DNA synthesis by VSMC from both rat strains, and this effect was abolished by CV-11974. CV-11974 slightly but significantly suppressed proliferation of VSMC from both rat strains. CV-11974 competitively inhibited the specific binding of 125I-labeled Ang II to VSMC from both rat strains. The angiotensin-converting enzyme inhibitor (ACEI) delapril also reduced basal DNA synthesis by VSMC from SHR, but did not affect proliferation of VSMC from either rat strain. These findings suggest that VSMC from SHR may synthesize Ang II which promotes their basal growth in an autocrine/paracrine manner through the AT1 receptor, and that this system may be associated with the exaggerated growth of VSMC from SHR.

Angiotensin II↗

Increased secretion of triglyceride and cholesterol following inhibition of long-chain fatty acid oxidation in rat liver.

The effects of emeriamine, a fungal metabolite and a potent inhibitor of mitochondrial fatty acid oxidation, on ketogenesis and lipid secretion were examined in isolated perfused livers from 2-day-fasted rats. Liver perfusion with increasing concentrations of emeriamine up to 3 mumol caused a dose-dependent inhibition of ketone body production. The hepatic uptake of exogenous oleic acid substrate was comparable in the control and emeriamine-treated livers. The addition of 2 mumol emeriamine to the perfusion medium at either the beginning of perfusion or 2 h later caused immediate and almost complete cessation of ketone body production, which was accompanied by a concomitant decrease in the beta-hydroxybutyrate: acetoacetate ratio, suggesting a decreased production of NADH via mitochondrial beta-oxidation. Conversely, both triglyceride and cholesterol secretions were elevated, indicating a reciprocal response in ketogenesis and lipid secretion by the livers. The proportion of oleate in the perfusate triglyceride obtained from emeriamine-treated livers was significantly higher than that from control livers. In the post-perfused liver triglyceride, oleate was progressively increased in the livers treated with the inhibitor 2 h after perfusion and at the beginning of perfusion, respectively. These results indicate that direct inhibition of fatty acid oxidation diverts the exogenous fatty acids to the esterification pathway, and subsequently stimulate the synthesis and secretion of triglyceride and cholesterol. The fatty acid oxidation rate in the liver is, therefore, a critical determinant for the synthesis and secretion of these lipid components.

3-Hydroxybutyric Acid↗