[Deterioration and improvement of cardiac hypertrophy].
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Adenosine Triphosphatases↗
Biomedical subjects
Y Yazaki
Publications and source records attributed to Y Yazaki.
The elevation of the cytoplasmic calcium ions in vascular smooth muscle cells in SHR--measurement of the free calcium ions in single living cells by lasermicrofluorospectrometry.
We have developed an accurate and sensitive system for the measurement of cytoplasmic free calcium concentrations ([Ca++]i) of a single cell by using UV-laser and Indo-1. By this method, we made the first successful measurement of [Ca++]i of single living vascular smooth muscle cells. [Ca++]i in spontaneously hypertensive rats was elevated and maintained after the 6th passage culture. However, [Ca++]i in Goldblatt hypertensive rats was not elevated. Thus, these results suggest that the maintenance of high [Ca++]i levels of vascular smooth muscle cells in spontaneously hypertensive rats is genetically regulated and that it is one of the mechanisms for hypertension.
Aging↗
Isolation and characterization of two isozymes of myosin heavy chain from canine atrium.
To clarify the characteristics of myosin isozymes in the atrium, we fractionated two isoforms of myosin heavy chain (HC), atrial HC alpha (A-HC alpha) and HC beta (A-HC beta), from the canine heart by affinity chromatography, using monoclonal antibodies specific for HC alpha (CMA19) and HC beta (HMC50), respectively, and then compared their peptide composition and enzymatic properties with those of ventricular HC alpha (V-HC alpha) and HC beta (V-HC beta). The reactivity of these isozymes with three monoclonal antibodies revealed that there are at least three different epitopes between A-HC alpha and A-HC beta. Differences in the primary structure of A-HC alpha and A-HC beta were confirmed by one- and two-dimensional gel electrophoretic analyses of these peptides, produced by digestion with alpha-chymotrypsin and cyanogen bromide (CNBr). A-HC alpha and V-HC alpha were indistinguishable proteins, and A-HC beta was also very similar to V-HC beta. Furthermore, there were differences between A-HC alpha and A-HC beta in their Ca2+-activated ATPase activities. The ATPase activity of A-HC beta was lower than that of A-HC alpha and was similar to that of V-HC beta. We concluded that there are two different isozymes of myosin heavy chain in the atrium (A-HC alpha and A-HC beta), as well as in the ventricle (V-HC alpha and V-HC beta), and that A-HC beta is very similar to V-HC beta, the predominant form of ventricular myosin, in its molecular structure and enzymatic activity.
Adenosine Triphosphatases↗
Prediction of pulmonary arterial pressure in adults by pulsed Doppler echocardiography.
Doppler echocardiography was used to estimate pulmonary artery (PA) pressure in 45 adult patients with various kinds of heart disease and the patterns were compared with those of 32 normal control subjects. Doppler signals obtained in the right ventricular (RV) outflow tract just proximal to the pulmonary valve and electrocardiogram were recorded simultaneously. Doppler velocity time intervals were measured as follows: RV preejection period, acceleration time from the onset of the RV ejection flow velocity to the peak, and RV ejection time. Thirty patients had PA hypertension and 16 patients had a low cardiac index. The best correlation with PA pressure was achieved by the RV preejection period/acceleration time index (r = 0.89 vs mean pressure). Sensitivity and specificity for predicting PA hypertension were 93% and 97%, respectively. Acceleration time correlated best with the logarithm of PA mean pressure (r = 0.88). Patients were separated into 2 groups according to cardiac index. In those patients with a cardiac index of less than 2.5 liters/min/m2, both RV preejection period/acceleration time and acceleration time were significantly correlated with PA mean pressure (r = 0.87) and log (PA mean pressure) (r = -0.87), respectively. However, the slope of the regression line for acceleration time and log (PA mean pressure) was significantly steeper than that for patients with a cardiac index of greater than or equal to 2.5 liters/min/m2 (p less than 0.05), whereas the relation between RV preejection period/acceleration time and PA mean pressure in the 2 groups could not be differentiated statistically from each other. Other intervals and ratios were less quantitative because of late systolic turbulent flow and individual variability.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Transmitral reversed blood flow during mid- and end diastole in constrictive pericarditis.
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Adult↗
Distribution of cardiac myosin isozymes in human conduction system. Immunohistochemical study using monoclonal antibodies.
To determine the presence and distribution of cardiac myosin isozymes in the human conduction system, we performed an immunohistochemical study using monoclonal antibodies CMA19 and HMC14, which are specific for myosin heavy chains of human atrial type (alpha-type) and ventricular type (beta-type), respectively. Serial frozen sections of human hearts were obtained from autopsy samples and examined by indirect immunofluorescence. Alpha-type was found in all myofibers of sinus node and atrio-ventricular node, and in 55.2 +/- 10.2% (mean +/- SD, n = 5) of the myofibers of ventricular conduction tissue, which consists of the bundle of His, bundle branches, and the Purkinje network. In contrast, beta-type was found in all myofibers of the atrio-ventricular node and ventricular conduction tissue, whereas almost all myofibers of the sinus node were unlabeled by HMC14. Although the number of ventricular myofibers labeled by CMA19 was small, the labeled myofibers were more numerous in the subepicardial region than in the subendocardial region. These findings show that the gene coding for alpha-type is expressed predominantly in specialized myocardium compared with the adjacent ordinary working myocardium.
Antibodies, Monoclonal↗
Expression of myosin isozymes during the developmental stage and their redistribution induced by pressure overload.
Cardiac muscles contain at least two isozymes--referred to as alpha(HC alpha) and beta(HC beta)--of the myosin heavy chain. The proportional ratio of these isozymes varies depending upon the developmental stage and the physiological and/or the hormonal milieu of the cell. Using monoclonal antibodies (MoAb) specific for human cardiac HC alpha and HC beta, we have examined the expression of these isozymes in fetal through adult cardiac tissues and investigated whether isozymic redistribution occurs in pressure overloaded human ventricles. We found that although HC alpha was expressed in the atrium from the early embryonic stage, in embryonic ventricular myofibers, only HC beta was expressed without expression of HC alpha, but some myofibers replace HC beta by HC alpha after birth, and these HC alpha containing ventricular myofibers were found to be decreased by pressure overload, which suggested that isozymic redistribution from HC alpha to HC beta also occurred in the ventricles, as well as the atrium. In addition, we also found two subtypes of HC beta (beta 1, beta 2) in the human heart. In the ventricle, both beta 1 and beta 2 was present in all myofibers; in contrast, some myofibers contained beta 1 or beta 2 or both with or without expression of HC alpha in the atrium. beta 1 and beta 2 were distinctive in their expression during the developmental stage, since beta 1 was present in the embryonic heart from the early developmental stage, whereas beta 2 was not present in the early embryonic heart, but began to be expressed in the late embryonic stage.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
A case of Takayasu's disease with ruptured carotid aneurysm.
Recently, a number of cases of Takayasu's disease having dilatative or aneurysmal lesions have been reported. Such lesions have come to be considered important manifestations of Takayasu's disease. A case, whose right common carotid artery perforated spontaneously and became a pseudoaneurysm, without any other stenotic lesion is presented with a review of the literature. Surgical treatment was performed successfully.
Adult↗
[Biochemical assessment of the effects of coronary thrombolysis by serum cardiac myosin light chain levels].
To establish the method of biochemical assessment of effects of intracoronary thrombolysis after acute myocardial infarction (MI), the relationships between plasma creatine kinase (CK) or serum cardiac myosin light chain (LC) I levels and changes in left ventricular (LV) wall motion were evaluated. Twenty-seven cases with acute MI without previous infarction were included in this study. Intracoronary thrombolysis was successful within seven hours after onset of MI in 13 patients (reperfusion group), and 14 patients were treated in a conventional manner (control group). Peak levels of CK reached earlier in the reperfusion group (11.3 +/- 2.9 hours) than in the control group (20.9 +/- 5.3 hours). The peak appearance time of CK in the reperfusion group was significantly related to the time between the onset of MI and achievement of coronary reperfusion (r = 0.76). The relationship between total CK release and LV ejection fraction determined by cineangiography one month after onset was not good (r = -0.42). Peak levels of CK were not related to LV ejection fraction. Peak levels of LC appeared about four days after onset in both groups. Peak levels of LC were closely related to LV ejection fraction (r = -0.72). Twenty-four-hour and four-day levels of LC were also related to LV ejection fraction (r = -0.62 and -0.73, respectively). Peak levels of LC were related to asynergic area determined by biplane cineangiography.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
[Hepatic GOT and GPT activities in patients with various liver diseases--especially alcoholic liver disease].
GOT and GPT activities were measured in percutaneous needle biopsy specimens of human liver tissue from 98 cases including normal subjects and patients with various liver diseases. Hepatic GOT activity was markedly decreased in liver tissue of patients with nonalcoholic liver cirrhosis. Hepatic GPT activity was markedly decreased in liver tissue of patients with alcoholic liver cirrhosis. The GOT/GPT ratio in liver tissue was increased in patients with alcoholic liver cirrhosis (5.32 +/- 2.03) and alcoholic liver disease (4.78 +/- 2.43). The increased SGOT/SGPT ratio in patients with alcoholic liver disease is due to primarily to the increased LGOT/LGPT ratio.
Alanine Transaminase↗
Change in concentrations of myogenic components of serum during 93 h of strenuous physical exercise.
Effects of 93 h of long, strenuous ranger training on activities of creatine kinase (CK) and lactate dehydrogenase (LD), along with their isoenzymes, and on concentration of myosin light chain were examined in sera of young soldiers. Total CK activity in serum was measured before, during, and after the training. Throughout, total CK activity in serum increased steadily. At the end of the training, activity of CK-MB was increased but its activity ratio to total CK remained unchanged; the activity ratio of LD1/LD2 also was not increased, although total LD activity was increased. Myosin light chain was increased by about fourfold at the end of the training and remained high for three days thereafter. However, its concentration was much lower than in myopathies such as polymyositis and Duchenne muscle dystrophy. The increased activities in serum of total CK and CK-MB isoenzyme on strenuous physical exercise evidently were of noncardiac origin. Although CK activity was comparable with that seen in myopathies accompanied by disintegration of skeletal muscle, the relatively low concentration of myosin light chain in serum suggests minimal skeletal muscle damage.
Adult↗
Noninvasive assessment of left and right ventricular filling in myocardial infarction with a two-dimensional Doppler echocardiographic method.
Inflow characteristics of left and right ventricular filling were assessed in 40 patients with myocardial infarction and in 10 normal subjects by pulsed Doppler echocardiography. Patients with myocardial infarction were subdivided into four groups, focusing on the involvement of right ventricular and septal branches of the coronary arteries. Group I consisted of 11 patients with anterior infarction who showed an obstructive lesion of the proximal left anterior descending branch involving the first septal perforator with a patent right coronary artery. Group II consisted of 10 patients with inferior infarction who showed an obstructive lesion of the proximal right coronary artery involving the right ventricular branch. Group III consisted of 12 patients with both anterior and inferior infarction who showed obstructive lesions of both the proximal left anterior descending branch and the right coronary artery involving the right ventricular branch. Group IV consisted of seven patients with lateral infarction who showed an obstructive lesion of the diagonal branch or branches of the circumflex coronary artery with a patent left anterior descending branch and right coronary artery. Three measurements were performed from the transmitral and transtricuspidal inflow velocity patterns to assess the left and right ventricular diastolic behaviors. These measurements were: acceleration half-time, deceleration half-time of early diastolic rapid inflow, and the ratio of the peak velocity of early diastolic rapid inflow to that of the late diastolic inflow due to the atrial contraction. Impaired diastolic filling of the left ventricle compensated by enhanced left atrial contraction was observed in patients with myocardial infarction from groups I, II, III and IV.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Applications of anticardiac myosin monoclonal antibodies in the diagnosis of heart disease.
We have developed anticardiac myosin antibodies, especially monoclonal antibodies, for helping in the diagnosis of heart disease. Our investigations were divided into three research projects. We visualized the distribution of myosin isozymes in human atrial and ventricular myocardium by an immunofluorescence staining method using monoclonal antibodies specific for individual human cardiac myosin isozymes. We also revealed the redistribution of these cardiac myosin isozymes in an overloaded condition. The isozymic pattern of cardiac myosin was changed from the atrial type to the ventricular type in the overloaded atrium. This isozymic redistribution can be considered as physiological adaptive mechanism to meet increased cardiac work during overload. We developed a new method of imaging for myocardial infarction by single photon emission tomography using labelled monoclonal antibody specific for cardiac myosin heavy chain. Specific localization of the labelled antibody was demonstrated in the infarcted area and no accumulation of radioactivity was shown in the bone matrix as observed in 99mTc pyrophosphate images. We developed a sensitive radioimmunoassay of cardiac myosin light chain I (LCI) and demonstrated that peak serum levels of LCI in the patients with acute myocardial infarction correlated well with the left ventricular ejection fraction. Furthermore, LCI release from the infarcted myocardium was not affected by coronary reperfusion due to intracoronary thrombolysis. Thus, serial determinations of serum LCI better quantify the extent of myocardial damage even after coronary reperfusion in acute myocardial infarction.
Antibodies, Monoclonal↗
[Application of dipole analysis for the diagnosis of myocardial infarction in the presence of left bundle branch block].
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Aged↗
Effects of steroid treatment on release of cardiac myosin light chain II in acute myocardial infarction in dogs.
The effect of methylprednisolone sodium succinate (MP) on release of myosin light chain II (LCII) from the myocardium was studied in experimental myocardial infarction (MI). Acute MI was produced in conscious, closed-chest dogs by ligating the left anterior descending coronary artery beyond the first diagonal branch. MP, 30 mg/kg, was administered intravenously just before and 24 hours after MI. After MI, LCII levels in the serum were determined serially up to 240 hours. MI size was determined histologically 10 days after MI. In the MP group, LCII levels in the serum within 72 hours were lower than in the control, and cumulative LCII release for 3 days decreased from 530 +/- 159 to 310 +/- 101 ng/ml (mean +/- standard deviation) (p less than 0.001). However, the peak LCII level appeared later (control vs MP, 63 +/- 27 vs 122 +/- 25 hours, p less than 0.001), and the peak LCII level and cumulative LCII release for 10 days were not decreased by MP treatment. MI size also was not reduced by MP (11.0 +/- 4.4% vs 11.8% +/- 4.5% of the left ventricle, difference not significant). Since the rate of disappearance of LCII is rapid and was not affected by MP, these results suggest that MP treatment early after acute MI delays breakdown of myosin filaments, but cannot prevent it.
Acetylglucosaminidase↗
Distribution of myosin isozymes in human atrial and ventricular myocardium: comparison in normal and overloaded heart.
We have prepared monoclonal antibodies specific for either atrial or ventricular myosin and defined the isomyosin composition of myocardium in normal and overloaded human hearts. In the atrial myocardium, normal isozymic pattern was V1 dominant which converted to being V3 dominant in an overloaded condition. In contrast, normal isomyosin pattern of the ventricular myocardium was exclusively V3 dominant, and only a small change in the proportion of isomyosin was observed in an overloaded condition. From this, we conclude that isozymic changes in cardiac myosin could occur in the human heart to meet increased work induced by cardiac overload. However, the physiological importance of these isomyosin redistributions in human myocardium seems to be much greater in the atrium than in the ventricle, since larger amounts of V1 isomyosin which could be transformed to V3 isomyosin were present in the atrial myocardium.
Adenosine Triphosphatases↗
Isozymic changes in myosin of human atrial myocardium induced by overload. Immunohistochemical study using monoclonal antibodies.
An immunohistochemical study using monoclonal antibodies specific for the heavy chains of either human atrial (HC alpha) or ventricular (HC beta) myosin was performed to clarify the distribution of each isozyme in normal as well as pressure-overloaded human hearts. In normal human ventricles, all muscle fibers were stained by a monoclonal antibody (HMC14) specific for HC beta, whereas a small number of fibers reacted with a monoclonal antibody (CMA19) specific for HC alpha. In contrast, in normal human atria, almost all muscle fibers were stained by CMA19, and a relatively larger number of muscle fibers also reacted with HMC14. Furthermore, in pressure-overloaded atria, muscle fibers reactive with HMC14 were strikingly increased while those reactive with CMA19 showed a corresponding decrease. The extent of this isozymic redistribution was in good correlation with atrial pressure. These results not only confirmed the existence of isoforms of myosin heavy chain in human hearts, but also demonstrated that redistribution of iso-myosins could occur as an adaptation to pressure overload.
Animals↗
Vasopressin as a possible contributor to hypertension.
The role of vasopressin as a pressor agent to the hypertensive process was examined. Vasopressin plays a major role in the pathogenesis of DOCA-salt hypertension, since the elevation of blood pressure was not substantial in the rats with lithium-treated diabetes insipidus after DOCA-salt treatment. Administration of DDAVP which has antidiuretic action but minimal vasopressor effect failed to increase blood pressure to the levels observed after administration of AVP. Furthermore, the pressor action of vasopressin appears to be important in the development of this model of hypertension, since the enhanced pressor responsiveness to the hormone was observed in the initial stage of hypertension. Increased secretion of vasopressin from neurohypophysis also promotes the function of the hormone as a pathogenetic factor in hypertension. An unproportional release of vasopressin compared to plasma osmolality may be induced by the absence of an adjusting control of angiotensin II forming and receptor binding capacity for sodium balance in the brain. However, the role of vasopressin remains to be determined in human essential hypertension.
Animals↗