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Biomedical subjects

T Kashima

Publications and source records attributed to T Kashima.

At least 73 records · Page 4Linked to original sources

Influences of localized aortic valve damage on coronary artery blood flow in acute aortic regurgitation: an experimental study.

We examined the influences of localized aortic valve damage on coronary artery blood flow and the prognosis in acute aortic regurgitation. Aortic regurgitation was produced in 18 open-chest dogs by extensively cutting one of the three aortic cusps with a nerve knife introduced via the cardiac apex. The dogs were separated into three groups of six dogs each. In each group the noncoronary cusp (NCC), the right coronary cusp (RCC), or the left coronary cusp (LCC) was cut. Aortic and left ventricular pressures; the phasic aortic, left anterior descending (LAD), and right coronary artery (RCA) blood flows; and electrocardiograms were simultaneously recorded before and after production of acute AR. All dogs in the NCC and RCC groups survived for at least 30 to 60 min, but all dogs in the LCC group died after 5 to 9 min of production of acute AR due to left ventricular failure. After 2 min of aortic regurgitation, the total, systolic, and diastolic LAD flows were 39 +/- 14, 19 +/- 9, and 20 +/- 8 ml/min (mean +/- SD) in the NCC group, 41 +/- 15, 31 +/- 9, and 10 +/- 6 ml/min in the RCC group, and 9 +/- 5, 19 +/- 5, and -10 +/- 2 ml/min in the LCC group, respectively. The corresponding RCA flows were 19 +/- 9, 15 +/- 6, and 4 +/- 3 ml/min in the NCC group, 13 +/- 8, 21 +/- 12, and -8 +/- 4 ml/min in the RCC group, and 14 +/- 4, 19 +/- 4, and -5 +/- 1 ml/min in the LCC group, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

[Exercise capacity in ischemic heart disease evaluated by continuous wave Doppler echocardiography].

To evaluate exercise capacity in ischemic heart disease, we measured the peak aortic flow velocity by continuous wave Doppler (CWD) echo from the suprasternal notch at rest and during multiple load ergometer testing in the supine position. The study subjects consisted of 14 normal controls, 10 patients with effort angina and 21 patients with old myocardial infarction (OMI). In all the patients and in five normal subjects, thallium-201 emission CT (SPECT) was also performed immediately after exercise and four hours subsequently. Change in the peak aortic flow velocity during exercise was compared with the extent of perfusion defects and the presence or absence of redistribution images on SPECT. At rest, the peak aortic flow velocity was not different from that of the other three groups. During exercise, it increased progressively (crescendo type) as the exercise was increased in normal subjects. In patients with angina pectoris it increased at the initial stage of exercise, but was unchanged (crescendo-plateau type) or decreased (crescendo-decrescendo type) at the maximum exercise stage. Redistribution images on SPECT were seen in nine of 10 patients with angina pectoris. In patients with OMI, change in the peak aortic flow velocity was of the crescendo type in 14, crescendo-decrescendo in three and crescendo-plateau in one. In the remaining three it decreased from the beginning of exercise (decrescendo type). Redistribution images were seen in all patients with the crescendo-decrescendo, crescendo-plateau or decrescendo types. Furthermore, myocardial damage was much more extensive in the decrescendo type. We conclude that exercise continuous wave Doppler echocardiography is a useful means of evaluating exercise capacity in ischemic heart disease.

Adult↗

Effects of tolbutamide on cultured heart cells of mice.

To investigate the direct effects of tolbutamide on the myocardium, we studied the ultrastructure, direct effects of tolbutamide on the myocardium, we studied the ultrastructure, beating rhythm, cytotoxicity determining the 51Cr release from damaged cells and the 45Ca activity in the cultured heart cells of mice. After 48 h of cultivation, tolbutamide was added to give a final concentration of 0.37, 0.93, 1.85, and 3.7 nM. The addition of high dose of tolbutamide (greater than 1 mM) to the culture medium produced irregular beating after 1 min and cessation of beating after 20 h. The cultured heart cells incubated with control solution or low concentrations of tolbutamide (less than 1 mM) showed little change in the beating rhythm and frequency. Cytotoxicity of tolbutamide on the cultured heart cells was observed only in high concentrations (greater than 1 mM): the 51Cr release index was 23% at 1.85 mM and 40% at 3.7 mM. On electron microscopy, the heart cells cultured with high concentration of tolbutamide (greater than 1 mM) showed electron-dense bodies in the mitochondria and shortened Z-Z intervals. However, these ultrastructural alterations were not observed in the cultured heart cells incubated with low concentration of tolbutamide (less than 1 mM). The 45Ca activity of cultured heart cells, after the incubation for 24 h in medium containing 45Ca, was significantly increased only with high concentrations of tolbutamide (greater than 1 mM). We conclude that tolbutamide in dose of less than 1 mM had no cytotoxicity and had little effect on the beating rhythm, ultrastructure and intracellular calcium concentration of the cultured heart cells of mice.

Animals↗

Cultured heart cells from the spontaneously diabetic KK mouse.

In order to clarify the mechanism of myocardial changes in KK mice, cultured heart cells from both normal and spontaneously diabetic KK mice were studied by electron microscopy, photoelectric recording, and 45Ca activity. Compared with cultured heart cells from normal mice, those from KK mice showed a decrease in beating frequency and ceased beating more rapidly. The rhythm of the beating cells from KK mice became irregular, while that of the heart cells from normal mice was not changed significantly over a period of 10 days. Electron micrographs of cultured heart cells from KK mice showed an increased number of mitochondria, an intricate arrangement of myofibrils, poorly formed Z bands, and a lipidlike substance. The 45Ca activity of heart cells from KK mice, after incubation for 24 h in a medium containing 45Ca, was increased compared with heart cells from normal mice. Based on these findings, we conclude that ultrastructural alterations exist in cultured heart cells from KK mice and we suggest that an increase of intracellular Ca might play an important role in the pathogenesis.

Animals↗

Chlorpromazine-induced cardiomyopathy in rats.

We studied the chronic effects of chlorpromazine (CPZ) on the myocardium of rats using light and electron microscopy. Wistar strain rats were divided into two groups and given either normal saline or CPZ intraperitoneally at a dose of 5 mg/kg body weight/day for 30 consecutive days. Myocardial degeneration, atrophic muscle fiber, and myocardial fibrosis were observed by light microscopy in all CPZ-treated rats. Ultrastructural alterations of the myocardium were also found in all CPZ-treated rats. They consisted of contracted myofibers, mitochondriosis, degenerated mitochondria, dilated sarcoplasmic reticulum, and increased collagen fibers. However, no abnormal histologic or ultrastructural changes were observed in the normal saline-treated rats. We therefore conclude that a chronic administration of a sedative dose of CPZ causes myocardial damage in rats.

Animals↗

Cardiac involvement in congenital myopathy.

We examined cardiac changes in 8 patients (4 men and 4 women, age 21-43 years) with congenital myopathy proven by skeletal muscle biopsy. Of 8 patients, 4 showed cardiac changes, including 1 with cytoplasmic body myopathy (patient 1), 2 with minimal change myopathy (patients 2 and 3) and 1 with nemaline myopathy (patient 4). Patients 1 and 2 showed left ventricular dilatation with severe global hypokinesis of left ventricular wall. These clinical features were quite similar to those of dilated cardiomyopathy and the patients were in NYHA class 3 or 4. Patient 3 had severe mitral regurgitation with mitral valve prolapse. This patient also had a persistent left superior vena cava and hypoplasia of the aorta, and her cardiac function was in NYHA class 3. Patient 4 showed moderate global left ventricular hypokinesis but the left ventricle was not dilated. This patient also had sino-atrial block and type A Wolff-Parkinson-White syndrome. His cardiac function was NYHA class 1. In conclusion, various types of congenital myopathy are associated with cardiac changes which can result in severe congestive heart failure.

Adult↗

Noninvasive pulsed Doppler echocardiographic detection of the direction of shunt flow in patients with atrial septal defect: usefulness of the right parasternal approach.

Noninvasive pulsed Doppler echocardiography combined with two-dimensional echocardiography by the right parasternal approach was performed to detect the shunt flow through the defect in 31 patients with suspected secundum atrial septal defect (ASD). A defect of the interatrial septum was seen on the two-dimensional echocardiograms of 30 of 31 patients. In all the 30 patients, Doppler signals of shunt flow could be recorded by placing the sample volume in the center of the defect on the two-dimensional echocardiogram. Neither a defect nor Doppler signal indicating shunt flow were demonstrated in any of 15 normal control subjects. Cardiac catheterization indicated significant shunt flow in all the 31 patients with suspected ASD. Doppler signals obtained from the center of the defect showed left-to-right and/or right-to-left shunt flow patterns. The direction of the shunt flow was mainly left to right, with its peak in late systole and atrial systole in 28 of 30 patients; mainly right-to-left flow was present in the remaining two patients, who had Eisenmenger's syndrome. The direction of flow as predicted by the Doppler signal was confirmed by the coincidence of direction of flow as seen on the contrast two-dimensional echocardiogram. In 22 patients for whom the measurement of the pulmonary-to-systemic flow ratio by oximetry was believed to be reasonably accurate, the ratio was fairly well correlated with Doppler-determined left-to-right shunt flow velocity (r = .71, SEE = 6.7 cm/sec).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

[Mechanism of systolic anterior motion of the mitral valve in dogs].

The mechanism of systolic anterior motion (SAM) of the mitral valve remains somewhat controversial. We previously reported that SAM can be produced in dogs using dobutamine infusion. In the present study, dobutamine infusion, dextran infusion and venesection were performed in 13 anesthetized closed-chest dogs to study the mechanism of SAM. The degree of SAM was determined by M-mode echocardiography. End-systolic and end-diastolic short-axis areas of the left ventricle at the level of the chordae tendineae and the fractional area changes were measured by two-dimensional echocardiography. SAM was produced in six of the 13 dogs during dobutamine infusions (Group 1), but not in the other seven dogs (Group 2). During dobutamine infusions, % fractional area changes were greater in Group 1 (85 +/- 5; mean +/- standard deviation) than in Group 2 (65 +/- 15) (p less than 0.01), and the end-systolic short-axis area of the left ventricle was smaller in Group 1 (0.7 +/- 0.4 cm2) than in Group 2 (1.9 +/- 0.3 cm2) (p less than 0.01), although no significant change was observed between Groups 1 and 2 in the end-diastolic short-axis area of the left ventricle. Subsequent injections of dextran (mean 340 ml) in Group 1, decreased the degree of SAM and increased the end-diastolic and end-systolic short-axis areas of the left ventricle. Subsequently, venesections (mean 400 ml) in Group 1 resulted in increases in the degrees of SAM and decreases in the end-diastolic and end-systolic short-axis areas of the left ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

[Continuous wave Doppler echocardiographic assessment of aortic stenosis and aortic regurgitation].

Twenty-four patients with aortic stenosis and 22 with aortic insufficiency were evaluated using continuous wave Doppler echocardiography (echo). Doppler echo studies were performed 48 hours before cardiac catheterization. Fifteen normal subjects served as controls. Peak velocity in the ascending aorta in aortic stenosis ranged from 2.0 to 6.0 m/sec with a mean of 3.7 m/sec, and this was significantly increased over the normal controls (mean 1.1 m/sec: 0.7-1.4 m/sec). Using the simplified Bernoulli equation (P = 4 V2, P: peak pressure gradient, V: peak flow velocity), the peak pressure gradient across the aortic valve was measured from the peak velocity in patients with aortic stenosis. The results (Y) correlated well with the peak-to-peak pressure gradient (X) between the left ventricular pressure and aortic pressure as obtained by cardiac catheterization (Y = 1.1 X +2.5, r = 0.83). Aortic regurgitation was detected by continuous wave Doppler echo in all patients with aortic insufficiency, but in only half of the patients the peak velocity could be measured (3.8 +/- 0.3 m/sec, mean +/- SD). In the remaining patients, it was difficult to measure the peak velocity, but it seemed to be greater than 3.0 m/sec. On the simultaneous recordings of the gradient between aortic and left ventricular pressures and continuous wave Doppler echo in patients with aortic regurgitation, the shape and pattern of the pressure gradient during diastole were similar to those of continuous wave Doppler echo. We conclude that continuous wave Doppler echo is a very sensitive method for diagnosing aortic stenosis and regurgitation, and it provides a quantitative assessment of the severity of aortic stenosis.

Adult↗

Histologic and ultrastructural studies on the myocardium in spontaneously diabetic KK mice: a new animal model of cardiomyopathy.

The hearts from spontaneously diabetic KK mice and control mice were examined by light and electron microscopy. Myocardial degeneration, myocardial fibrosis and calcium deposits in the myocardium were extensive in KK mice aged 8 weeks. In myocytes of newborn KK mice, an irregular arrangement of myofibrils and poorly formed Z bands were found. Ultrastructural changes in myocytes of KK mice aged 4 weeks consisted of destruction of mitochondria, degenerated myofibrils and abnormalities of Z bands. However, increased mucopolysaccharides in interstitium and thickened basement membranes of capillaries were not found in KK mice, in contrast to the previous reports of myocardial changes in diabetic C57BL/KsJ mice, alloxan-diabetic dogs and hypertensive-diabetic rats. These observations suggest that the cardiomyopathy found in KK mice is not secondary to diabetes mellitus but is caused by other factors. In conclusion, myocardial ultrastructural abnormalities are present in newborn KK mice. Thus, this animal can be used as a model of cardiomyopathy.

Animals↗

Relation between QT interval and heart rate. applications and limitations of Bazett's formula.

We studied the relationship between QT interval and RR interval when the heart rate was changed by atrial pacing, atropine, isoproterenol, and exercise in nine healthy adult males. The following results were obtained: (1) QT shortening with an increase in heart rate was minimal in atrial pacing and an equation QT = k4 square root RR was obtained from the QT-RR relationship during atrial pacing (r = 0.64, p less than 0.001); (2) shortening of QT with shortening of RR was least in atrial pacing; (3) during recovery from exercise it was largest and almost coincident with Bazett's formula; (4) Bazett's formula, therefore, is clearly applicable in the evaluation of ECGs recorded at rest or after exercise; (5) Bazett's formula can not be applied in the evaluation of an effect of some drug or maneuver on the QT when such a drug or maneuver can affect both the QT and the RR directly. The RR-dependent QT change can be estimated from the equation QT = k4 square root RR and the difference between a measured QT and the estimated RR-corrected QT would be a genuine effect of the drug or maneuver on the QT at that heart rate. We conclude that atropine, isoproterenol and exercise actually shorten the QT interval.

Adolescent↗

Enhanced sensitivity to digoxin in dystrophic mice.

We estimated the effect of digoxin on the myocardial potassium content and the action potentials of the left ventricular papillary muscles in dystrophic mice (C57BL/6JCL dy X dy). All of 10 dystrophic mice died following ip injection of digoxin at a dose of one quarter of the iv LD50 for normal mice. The myocardial digoxin concentration and the myocardial potassium content in dystrophic mice were similar to those in normal mice before and 60 min after the ip injection of digoxin. The action potential durations (APD) in dystrophic mice were significantly longer than those in normal mice. Perfusion of digoxin (2 micrograms/ml) for 30 min reduced the APD significantly and induced arrhythmias in dystrophic mice, but it did not bring about any significant change in normal mice. These data suggest that dystrophic mice have increased sensitivity to digitalis. This hypersensitivity to digitalis is not due to increased myocardial digoxin uptake or decreased myocardial potassium content.

Action Potentials↗

[Detection of a shunt flow through a defect in secundum atrial septal defect by right parasternal approach using pulsed Doppler echocardiography].

Pulsed Doppler echocardiography combined with two-dimensional echocardiographic (2-DE) system was performed to detect a shunt flow through a defect in the interatrial septum (IAS) in patients with secundum atrial septal defect (ASD) utilizing right parasternal approach (RPA). RPA is a method which provides an accurate evaluation of a defect in the IAS on a 2-DE image by placing a transducer on the right of the sternum because the ultrasonic beam passes in a plane almost perpendicular to the IAS. The subjects consisted of 20 patients with ASD (25 +/- 22 yrs) diagnosed by cardiac catheterization or 2-DE with peripheral contrast material injection, and 10 cases of healthy subjects (34 +/- 18 yrs). Defects in the IAS were clearly visible in 19 patients with ASD on 2-DE images by RPA. By placing the sample volume in the center of the defect, Doppler flows could be obtained in 17 of them. In 13 with sinus rhythm, except a case of Eisenmenger syndrome, Doppler signals showed mainly a laminar flow toward the transducer (positive flow), but a transient flow of low velocity away from the transducer (negative flow) was also observed. The positive flow had its peaks in late systole and atrial systole and occasionally in mid-systole, early diastole and mid-diastole. The negative flow occurred in early systole, mid-diastole and late diastole. In a patient with Eisenmenger syndrome and tricuspid regurgitation (TR), a negative turbulent flow was observed from early systole to mid-diastole. In three patients with atrial fibrillation, Doppler signals were variable. The Doppler echogram of a patient with atrial fibrillation but no complication showed a laminar positive flow with its peaks in late systole and mid-diastole, and a negative flow in early systole. One patient with atrial fibrillation and TR had a systolic negative turbulent flow and a mid-diastolic laminar positive flow. In a patient with TR and mitral regurgitation, the Doppler echocardiogram showed a laminar positive flow throughout the entire cardiac cycle with its peaks in early diastole and mid-diastole. Doppler signals from the left atrium (LA) to the right atrium (RA) through a defect coincided in timing with the appearance of negative contrast echo from the defect to the RA on 2-DE image and signals from the RA to the LA coincided with the appearance of the contrast echo into the LA from the RA through the defect. Doppler signals disappeared after the closure of the defect in all six patients examined.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗