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Biomedical subjects

H Matsuo

Publications and source records attributed to H Matsuo.

At least 181 records · Page 10Linked to original sources
PubMed1999

Ventricular adrenomedullin levels correlate with the extent of cardiac hypertrophy in rats.

We investigated the pathophysiological significance of adrenomedullin (AM) in the development of left ventricular hypertrophy (LVH). LVH was produced by aortic banding (AB) in rats. The left ventricular weight/body weight (LV/BW) ratio, ventricular AM peptide and mRNA levels, and hemodynamics were measured at 1, 3, 7, and 21 days after the operation. Both LV/BW ratio and ventricular AM levels showed a significant increase from 1 day after the operation in the AB rats versus the sham-operated rats. Both increased in a time-dependent manner. The ventricular AM levels correlated with the LV/BW ratio (r=0.76, P<0.01). The AM mRNA levels were highly expressed at 1 day after the operation in the AB rats but showed no difference from 3 to 21 days after the operation between the AB and sham groups. The plasma AM levels showed a peak at 1 day after the operation in both groups. Then, we treated AB rats with an angiotensin-converting enzyme inhibitor (quinapril) in 2 doses (1 and 10 mg. kg-1. d-1) for 21 days. The quinapril treatment attenuated similarly both the LV/BW ratio and the ventricular AM levels. We also assessed the effects of AM and hydralazine administration for 7 days on the LV/BW ratio and hemodynamics of AB rats. Both AM and hydralazine administration reduced the blood pressure by approximately 10% compared with the nontreated AB rats, but a reduction of the LV/BW ratio was observed only in the AM-treated group (P<0.05). These results suggest that ventricular AM levels are elevated by chronic pressure overload in a time-dependent manner concomitant with the extent of LVH and that AM may play a pathophysiological role in the development of LVH in chronic pressure overload.

Adrenomedullin↗
PubMed1999

Increased plasma levels of adrenomedullin in patients with systemic inflammatory response syndrome.

We measured the plasma levels of adrenomedullin (AM), a novel vasodilating peptide, in 89 patients with various forms of systemic inflammatory response syndrome (SIRS) and 13 healthy volunteers serving as controls. Plasma levels of AM in SIRS (burns: 20.5 +/- 3. 2 fmol/ml [mean +/- SEM]; pancreatitis: 13.8 +/- 3.8 fmol/ml; trauma: 14.9 +/- 2.5 fmol/ml; traumatic shock: 41.1 +/- 7.8 fmol/ml; severe sepsis: 59.9 +/- 11.2 fmol/ml; septic shock: 193.5 +/- 30.1 fmol/ml) were significantly increased over those of controls (5.1 +/- 0.2 fmol/ml). The patients with traumatic shock or septic shock especially had higher levels of plasma AM than those with trauma or severe sepsis, respectively. These data showed that in patients with SIRS, plasma AM levels increased in proportion to the severity of illness. Subsequently, we measured the plasma levels of mediators such as tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-8, plasminogen activator inhibitor (PAI)-1, and thrombomodulin (TM) in patients with traumatic shock and septic shock. A significant correlation was observed between plasma AM and TNF-alpha levels in patients with septic shock, suggesting an important role for AM as well as of TNF-alpha in the pathophysiology of inflammation. Plasma AM and IL-8 levels correlated positively with Acute Physiology and Chronic Health Evaluation (APACHE) II score, peak multiple organ failure (MOF) score during the first month and prognosis in patients with septic shock, as did plasma IL-6 levels in patients with traumatic shock. The plasma AM level might serve as a useful marker for evaluating the severity of disease and as an early predictor of subsequent organ failure and outcome in septic shock.

APACHE↗
PubMed1999

Prolongation of left atrial augmentation after handgrip stress in coronary artery disease: observation using pulsed Doppler flowmetry.

Although alterations in left ventricular diastolic filling dynamics have been observed during myocardial ischemia, few data exist regarding temporal changes in left ventricular filling during recovery. Therefore, the authors evaluated transmitral inflow pattern during and after handgrip exertion in coronary artery disease (CAD) by using Doppler echocardiography. The study population consisted of 18 normal (N) subjects and 47 patients with CAD. Of the CAD patients, 17 had coronary lesions associated with a limited area of underperfused myocardium (seven with good collateral circulation and 10 with distal lesions) (MILD), 15 patients exhibited a proximal lesion in a single vessel (SVD), and 15 patients had significant multivessel disease (MVD). Transmitral inflow velocities were continuously recorded at baseline, during handgrip exercise (50% of maximal for 1 minute), and for 5 minutes of recovery. Mean blood pressure, heart rate, early diastolic (E) and late atrial (A) inflow velocities, A/E ratio, and percent changes in E, A, and A/E from baseline were measured. In N and MILD, respectively, left ventricular inflow pattern returned to baseline at 3 minutes after handgrip (%E: 0.7 +/- 7.6%, 6.4 +/- 13.7%; %A: -0.2 +/- 7.9%, 3.1 +/- 6.5%; %A/E: -0.1 +/- 9.7%, -1.7 +/- 12.9%). In SVD and MVD, respectively, change in left ventricular inflow pattern was continued at 3 minutes after handgrip (%E: 7.2 +/- 9.4%, -4.3 +/- 17.2%, %A: 15.4 +/- 11.7%, 20.4 +/- 14.6%, %A/E: 7.9 +/- 10.0%, 29.2 +/- 25.6%). Increases in A and A/E in SVD and MVD were significantly higher than in N and MILD. Impaired left ventricular inflow pattern was observed at 3 minutes after handgrip in CAD, which may be reflected from prolonged impairment of diastolic function produced by ischemia. Therefore, temporal observation of left ventricular inflow pattern using the handgrip stress Doppler method may be useful for detection or follow-up of CAD.

Aged↗
PubMed1999

Effect of disopyramide on left ventricular pressure gradient in hypertrophic obstructive cardiomyopathy in comparison with propranolol--a case report.

The effect of intravenous administration of disopyramide (total dose 100 mg, bolus 20 mg every 5 minutes) was compared with that of propranolol (total dose 10 mg, bolus 2 mg every 5 minutes) in a patient with hypertrophic obstructive cardiomyopathy. Left ventricular pressure gradient (LVPG) was assessed by continuous wave Doppler flowmetry. LVPG markedly decreased (97 to 16 mmHg), and preejection period (PEP) increased with an increase in heart rate (HR) during disopyramide injection. No changes were observed in LVPG and PEP, and a decrease occurred in HR during propranolol administration. These results indicate that disopyramide produced greater effects on the reduction of LVPG than propranolol, a negative inotropic agent, did.

Aged↗
PubMed1999

Evaluation of left atrial wall elasticity using acoustic microscopy.

Left atrial wall elasticity is one of the important factors regulating left atrial stiffness and functions. The authors evaluated left atrial wall elasticity by measuring the sound speed through the left atrial wall, based on the hypothesis that high elasticity tissues will yield larger sound speed values through the tissue, and examined age-associated changes in left atrial wall elasticity. Left atrium specimens were obtained from 30 normal subjects (age, 15-95 years) at autopsy. An acoustic microscope, operating at 450 MHz, was used to measure the sound speed in the endocardium and the myocardium of the left atrium. The sound speeds in endocardium and myocardium demonstrated significant correlation with age (r = 0.74, p<0.0001 and r = 0.47, p<0.01, respectively). These findings indicate that left atrial wall elasticity increased with advancing age. These changes may lead to deterioration of left atrial compliance and eventual left atrial failure in older subjects.

Adolescent↗
PubMed1999

Cyclic variation of thickness in an age-related thick mitral valve observed by transthoracic echocardiography.

The cyclic variation of thickness during the cardiac cycle in age-related degenerative mitral valve (MV) has not been reported. Transthoracic echocardiography was used to evaluate the cyclic alteration in MV thickness in 40 patients with age-related MV thickening (diastolic MV thickness > or = 4 mm, age 70 +/- 14 years), 10 with mitral valve prolapse (MVP, age 49 +/- 11 years), 10 with rheumatic mitral stenosis (MS, age 66 +/- 9 years), and 31 control subjects (diastolic MV thickness < or = 3.6 mm, 53 +/- 17 years). After determination of the site of maximal thickness during diastole, the maximal and minimal thickness during systole of the anterior MV were measured. The percent change in MV thickness from diastole to systole (%deltaT) was calculated. The mitral regurgitation (MR) area was measured on color Doppler echocardiogram. The %deltaT (mean +/- sd) in age-related thickened MV and MVP groups were similar and significantly greater than that in control (60 +/- 8%, 61 +/- 6% vs 32 +/- 9%, p < 0.001). MR area was significantly greater in the age-related thickened MV group than that in controls (160 +/- 205 mm2 vs 14 +/- 40 mm2, p < 0.05). The %deltaT in MS (10 +/- 6%) was smallest (p < 0.001). A large cyclic alteration in valvular thickness was observed in the age-related degeneration of the MV and may be the cause of large MR despite no leaflet prolapse. The echocardiographic assessment of cyclic variation of MV thickness is feasible for estimating the histologic damage in thick MV.

Adolescent↗
PubMed1999

Incidence and clinical significance of interatrial shunting in patients with atrial septal aneurysm detected by contrast transesophageal echocardiography.

The prevalence of atrial septal aneurysm (ASA) in a general referral population of patients was investigated by use of transthoracic (TTE) and transesophageal echocardiographies (TEE). Contrast TEE was performed to detect interatrial shunting in patients with ASA. In this population, the prevalence of ASA as determined by TTE was 0.47% (24/5,079), and 0.78% (40/5,079) by TEE. Of these 40 patients 16 (40%) were judged to be normal by TTE. Of the forty patients who were positive for ASA, 50% demonstrated interatrial shunting (atrial septal defects, 10; patent foramen ovale, 10). The authors concluded that TEE is of significant value in detecting the presence of ASA and associated cardiac abnormalities. Contrast TEE further enhances the detection of interatrial shunting in patients with ASA.

Adolescent↗
PubMed1999

Tissue characterization of myocardial cells by use of high-frequency acoustic microscopy: differential myocyte sound speed and its transmural variation in normal, pressure-overload hypertrophic, and amyloid myocardium.

The purpose of the present study was to evaluate the acoustic properties of myocytes in normal, pressure-overload hypertrophic, and amyloid myocardium. Myocardial tissue specimens at autopsy were obtained from 10 subjects without cardiovascular disease, six patients with left ventricular (LV) hypertrophy, and six patients with cardiac amyloidosis. Sound speed of myocytes was measured at subendocardial and subepicardial regions in myocardium by use of a high-frequency (450 MHz) acoustic microscope. In normal myocardium, the sound speed of myocytes was significantly higher in subendocardial region (1,728+/-19 m/sec) than in subepicardial region (1,645+/-22 m/sec) (p<0.0001). A significantly higher sound speed of myocytes was observed in the subendocardial region in LV hypertrophic myocardium (1,779+/-19 m/sec) than that in normal myocardium (p<0.001). In amyloid myocardium, a significantly lower sound speed of myocytes was observed in subendocardial (1,560+/-8 m/sec) and subepicardial (1,594+/-48 m/sec) regions than that in respective regions of the normal myocardium (p<0.0001 and p<0.05, respectively). Transmural variation in sound speed of myocytes measured by high-frequency acoustic microscopy existed in normal left ventricle. The differential myocyte sound speed and its transmural variation was observed in LV hypertrophic and amyloid myocardium as compared with normal myocardium. High-frequency acoustic microscopy can be a promising technique for myocardial tissue characterization at the myocyte level.

Acoustics↗
PubMed1999

Neurogenic regulation of basal tone of coronary artery with mild atherosclerosis in humans: observation using two-dimensional intravascular ultrasound.

The purpose of this study was to assess the role of the autonomic nervous system in the regulation of basal coronary artery tone in normal and atherosclerotic plaque segments by using intravascular ultrasound in humans. In each of 21 patients, a short-axis image at one site of coronary artery was imaged by means of a 3.2F, 30-MHz intravascular ultrasound before and after intracoronary administration of 2 mg isosorbide dinitrate (ISDN). The authors identified the perimeters of the vessel wall segments with normal or atherosclerotic plaque on ultrasound images and evaluated the basal tone in each segment as a percent increase in each perimeter produced by ISDN. Using heart rate variability analysis for 512 seconds recorded immediately before ISDN administration, they evaluated cardiac sympathetic and vagal activities at rest as the integrated power of fast Fourier transform (FFT) spectrum for the low-frequency (LF: 0.04 to 0.15 Hz), and high-frequency (HF: 0.15 to 0.4 Hz) components, respectively. Of 29 segments examined by ultrasound, 16 were normal and 13 were atherosclerotic plaque. In all 29 segments, ISDN produced an increase in the perimeter of the vessel wall. At the normal 16 segments, the increase in perimeter by ISDN exhibited a significant correlation to the power of HF (r = 0.749, p = 0.0008) but no significant correlation to LF. At 13 plaque segments, however, no significant correlation between the response to ISDN and autonomic nerve activity was observed. In conclusion, the basal tone of normal coronary arterial wall segment is closely related to parasympathetic nerve, whereas the relation is impaired in mild atherosclerotic segments.

Aged↗
PubMed1999

An imbalance in plasma prostanoids in patients with Raynaud's phenomenon and pulmonary vasospasm.

Raynaud's phenomenon has been suggested as a predisposing factor for pulmonary vasospasm which may lead to pulmonary hypertension, but the occurrence of cold stimulus-induced pulmonary vasospasm has been inconsistent. Such inconsistent pulmonary vascular responses may be caused by differences in the production of endogenous vasodilators and vasoconstrictors among patients. Fourteen patients with Raynaud's phenomenon associated with mixed connective tissue disease (n=10) or systemic sclerosis (n=4) participated in the study. Right heart catheterization was performed before and after a cold pressor test, immersing a hand in cold water (15 degrees C) for 5 min. Plasma levels of 6-keto prostaglandin (PG)F1alpha, thromboxane (TX)B2 and endothelin (ET)-1 in the mixed venous blood were measured. Mean pulmonary artery pressure increased after the cold pressor test in five of 14 patients, and the patients were divided into those with pulmonary vasospasm (responders) and those without vasospasm (nonresponders). After the cold pressor test, levels of 6-keto PGF1alpha increased significantly in nonresponders (p<0.01) and decreased significantly in responders (p<0.05). The ratios of 6-keto PGF1alpha to TXB2 significantly increased in nonresponders (p<0.01) but not in responders and the difference between responders and nonresponders after the cold pressor test was also statistically significant (p<0.05). No significant change in plasma ET-1 levels occurred in either responders or nonresponders. The results suggest that an impaired production of prostaglandin I2 and an imbalance between prostaglandin I2 and thromboxane A2 are associated with the occurrence of pulmonary vasospasm induced by Raynaud's phenomenon.

6-Ketoprostaglandin F1 alpha↗
PubMed1999

Choline uptake by mouse brain capillary endothelial cells in culture.

Choline, a precursor of the neurotransmitter acetylcholine, is synthesized in only small amounts in the brain, so the choline concentration in the brain may vary depending on the plasma concentration and the transport rate across the blood-brain barrier. To elucidate the transport mechanism of choline, we carried out uptake experiments with mouse brain capillary endothelial cells in culture (MBEC4). [3H]Choline uptake was linear for up to 5 min. An examination of the concentration dependence of [3H]choline uptake revealed the operation of both saturable (Jmax = 423+/-27 pmol min(-1) (mg protein)(-1) and Kt = 20.0+/-3.1 microM) and non-saturable (kd = 1.23+/-0.045 microL min(-1)(mgprotein)-1) processes. The saturable process was independent of Na+ and pH, but was dependent on membrane potential as a driving force. Various basic drugs and endogenous substances, including substrates and inhibitors of the organic cation transporter, significantly inhibited the [3H]choline uptake. These data suggest that choline was taken up into the endothelial cells via two routes and that a membrane potential-dependent carrier-mediated transport system may participate in choline transport across the blood-brain barrier.

Adenosine Triphosphate↗
PubMed1999

Histological observations and the process of ultrasound contrast agent enhancement of tissue plasminogen activator thrombolysis with ultrasound exposure.

Although the enhancement of tissue plasminogen activator (tPA) induced thrombolysis by ultrasound has been reported to be augmented by ultrasound contrast agents (UCA), few data exist regarding its process. The present study evaluated the effect of a galactose based UCA on the efficacy of ultrasonic enhancement of tPA thrombolysis and observed the serial changes in the acoustic property and histopathology. A catheter-type transducer capable of ultrasound emission in both continuous (CW) and pulsed wave (PW) was used. The tPA thrombolysis was studied in 30 artificial white thrombi, which were assigned to 4 study groups based on insonation modes and with and without UCA. Each sample was suspended in 100ml saline in a beaker. Five minutes after tPA (8000U) administration, ultrasound was applied for 10min. For the UCA-treated groups, UCA (0.25g) was added 5 min after the start of ultrasound exposure. The alteration of the thrombus was monitored with echography. Weight reduction of the thrombus was -25+/-6% in PW and -30+/-7% in CW, which was significantly enhanced by UCA treatment, 40+/-3% (p<0.005) in PW+UCA and -43+/-7% (p<0.005) in CW+UCA. The area of thrombus echo image minimally decreased with ultrasound alone (-12+/-6%: PW, -23+/-11%: CW). In the UCA groups, UCA induced a remarkable reduction of size (-36+/-3%: PW+UCA, -43+/-7%: CW+UCA) with a high-echo intensity in the superficial layer of the thrombus, where multiple cavity formation was observed by light microscope. UCA markedly enhanced the effect of ultrasound on tPA thrombolysis. The altered acoustic property and corresponding histological microcavity formation in the shallow layer within the thrombus suggests that UCA augmented infiltration of tPA into the thrombus.

Adult↗
PubMed1999

Alteration in aortic wall stiffness and accumulation of collagen during the prediabetic stage of type II diabetes mellitus in rats.

Aortic damage during the prediabetic stage of diabetes mellitus (DM) was investigated in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, as an animal model of type II DM. In 30 OLETF and 30 nonDM rats, an oral glucose tolerance test was performed at 10, 20 and 30 weeks of age. At 15 and 30 weeks, intravascular ultrasound images and aortic pressure were recorded and the stiffness parameter beta was calculated. The aortic walls were excised at 5, 15 and 30 weeks for histopathology and the measurement of hydroxyproline. At 10 weeks, blood glucose (mg/dl) and insulin concentrations (ng/ml) of the OLETF rats (2h; 168+/-30 and 0.82+/-0.15) were significantly high (nonDM: 118+/-15; p = 0.02 and 0.16+/-0.64; p = 0.003). At the prediabetic stage (15 weeks), beta in the OLETF rats (2.5+/-0.9) was larger than in nonDM rats (1.4+/-0.4; p = 0.0006), and the collagen (hydroxyproline) content/dry weight (mg/g) of the aortic wall was significantly higher in OLETF (33.5+/-3.1) than in nonDM rats (28.7+/-3.5; p<.05). Histopathological examination showed that from 15 weeks of age the medial wall thickness increased gradually. In the prediabetic stage, collagen accumulation may contribute to impairment of aortic wall stiffness in the OLETF rats, which would accelerate the aging process in the aortic wall.

Animals↗
PubMed1999

Effect of histamine H2-receptor antagonist on the phosphorus-binding abilities of calcium carbonate and calcium lactate in hemodialysis patients.

The effect of histamine H2-receptor antagonist (famotidine) on the phosphorus-binding abilities of calcium carbonate and calcium lactate were examined in 13 chronic hemodialysis patients. In seven patients receiving calcium carbonate, famotidine (20 mg/d) was given because of gastroduodenal disorders, and calcium carbonate was replaced with calcium lactate as a phosphorus binder after 4 wk of treatment with famotidine. With the 4-wk administration of famotidine accompanied by calcium carbonate, the serum phosphorus level increased from 6.3+/-0.9 to 7.1+/-0.5 mg/dl (P<0.05). However, with the substitution of calcium lactate, the serum phosphorus level decreased significantly when compared to that before substitution (6.3+/-0.2 and 6.0+/-0.9 mg/dl after 4 and 8 wk of substitution, respectively), despite continued administration of famotidine. Serum calcium, creatinine, alkaline phosphatase, high sensitive parathyroid hormone, blood urea nitrogen, arterial blood pH, and bicarbonate were not significantly altered during the trial period. In six control patients treated with calcium carbonate alone, there were no statistical changes in serum calcium and phosphorus levels after substitution of calcium lactate for calcium carbonate. These results suggest that famotidine significantly affects the phosphorus-binding ability of calcium carbonate, but not that of calcium lactate. A careful observation of changes in the serum phosphorus level should be required in hemodialysis patients receiving calcium carbonate and histamine H2-receptor antagonists. Calcium lactate may be useful as a phosphorus binder in such hemodialysis patients.

Adult↗
PubMed1999

Elevated plasma levels of adrenomedullin in congenital cyanotic heart disease.

Adrenomedullin is a novel hypotensive peptide originally isolated from human pheochromocytoma. Accumulating evidence suggests the possible involvement of adrenomedullin in the physiology of the pulmonary circulation and the pathophysiology of hypoxaemia. The aim of the present study was to investigate the pathophysiological significance of adrenomedullin in hypoxaemia caused by congenital cyanotic heart disease. Subjects were 16 patients with congenital cyanotic heart disease aged 0.8-10 years (Group C) and 12 age-matched control subjects (patients with coronary artery dilatation after Kawasaki disease; Group N). Plasma adrenomedullin concentrations were measured, using radioimmunoassay, in femoral venous, pulmonary arterial and pulmonary venous blood obtained during cardiac catheterization. Plasma adrenomedullin concentrations in Group C were significantly (3-fold) higher than those in Group N at all sampling sites. In Group C, plasma adrenomedullin concentrations in pulmonary venous blood were significantly lower than those in pulmonary arterial blood. Pulmonary uptake of adrenomedullin in Group C was significantly greater than that in Group N. Patients with congenital cyanotic heart disease showed elevated plasma adrenomedullin concentrations and an increased uptake of adrenomedullin in the pulmonary circulation, which may act to dilate pulmonary vessels and increase pulmonary blood flow to alleviate hypoxaemia. Intrinsically increased adrenomedullin levels may function as a compensatory mechanism for hypoxaemia in congenital cyanotic heart disease.

Adrenomedullin↗