Late diastolic whoop in severe aortic regurgitation.
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Adult↗
Biomedical subjects
M Kino
Publications and source records attributed to M Kino.
Sodium 22+ washout from cultured rat cells.
The washout of Na+ isotopes from tissues and cells is quite complex and not well defined. To further gain insight into this process, we have studied 22Na+ washout from cultured Wistar rat skin fibroblasts and vascular smooth muscle cells (VSMCs). In these preparations, 22Na+ washout is described by a general three-exponential function. The exponential factor of the fastest component (k1) and the initial exchange rate constant (kie) of cultured fibroblasts decrease in magnitude in response to incubation in K+-deficient medium or in the presence of ouabain and increase in magnitude when the cells are incubated in a Ca++-deficient medium. As the magnitude of the kie declines (in the presence of ouabain) to the level of the exponential factor of the middle component (k2), 22Na+ washout is adequately described by a two-exponential function. When the kie is further diminished (in the presence of both ouabain and phloretin) to the range of the exponential factor of the slowest component (k3), the washout of 22Na+ is apparently monoexponential. Calculations of the cellular Na+ concentrations, based on the 22Na+ activity in the cells at the initiation of the washout experiments, and the medium specific activity agree with atomic absorption spectrometry measurements of the cellular concentration of this ion. Thus, all three components of 22Na+ washout from cultured rat cells are of cellular origin. Using the exponential parameters, compartmental analyses of two models (in parallel and in series) with three cellular Na+ pools were performed. The results indicate that, independent of the model chosen, the relative size of the largest Na+ pool is 92-93% in fibroblasts and approximately 96% in VSMCs. This pool is most likely to represent the cytosol.
Amiloride↗
Na+-K+ regulation in cultured vascular smooth muscle cell of the spontaneously hypertensive rat.
Na+-K+ passive transport and activity of the Na+ pump were examined in serially passed cultured vascular smooth muscle cells originating from spontaneously hypertensive (SH), Wistar-Kyoto (WKY), and Wistar (W) rats. Measurements included 22Na+ and 86Rb+ (K+ analogue) uptake and washout rate constants as well as intracellular Na+ and K+ levels. The aforementioned variables were studied in cells subjected to either 2 mM Ca2+ or Ca2+-deficient media. In 2 mM Ca2+ medium, SH rat cells demonstrated the highest exchange (uptake and washout) rate constants for Na+ and Rb+ (K+) among cells of the three rat strains. At this extracellular Ca2+ concentration, the Na+ pump activity of SH rat cells was higher than that of WKY rat cells and was not different from that of W rat cells. Incubation in Ca2+-deficient medium resulted in increased magnitudes of Rb+ washout and Na+ uptake rate constants in all cell preparations associated with elevated intracellular Na+ concentrations and augmented activity of the Na+ pump. Under this condition, cells derived from SH rats showed the highest Na+ uptake and Rb+ washout rate constants associated with the highest Na+ pump activity. The increase in intracellular Na+ level in Ca2+-deficient medium was the highest in SH rat cells. These findings show that innate membrane defects and the response of the Na+ pump to these abnormalities can be demonstrated in in vitro-grown vascular smooth muscle cells of the SH rat.
Animals↗
Ouabain binding to cultured vascular smooth muscle cells of the spontaneously hypertensive rat.
The binding of ouabain and K+ to the Na+ pump were analyzed in serially passed cultured vascular smooth muscle cells (VSMCs) originating from spontaneously hypertensive (SH), Wistar-Kyoto (WKY), and American Wistar (W) rats. Our techniques have utilized analyses of displacement of [3H]ouabain by both unlabeled ouabain and K+ from specific binding sites on the VSMCs. We have found that each of the VSMC preparations from the three rat strains appeared to demonstrate one population of specific ouabain receptors (Na+ pumps); the number of Na+ pump units (mean +/- SE, expressed as 10(5) units/cell; number of observations indicated in parentheses) of both the SH and WKY rats was significantly lower than the number of Na+ pump units of W rat VSMCs [SH: 3.00 +/- 0.02 (231), WKY: 2.87 +/- 0.05 (245), and W: 3.62 +/- 0.04 (225)]; the equilibrium dissociation constant values (microM) for ouabain in VSMCs of SH and WKY rats were similar but were significantly higher than that of VSMCs derived from W rats [SH: 4.69 +/- 0.09 (231), WKY: 4.57 +/- 0.12 (245), and W: 3.69 +/- 0.17 (225)]; and among the VSMCs originating from the three rat strains, the apparent equilibrium dissociation constant value for K+ (mM) was the lowest in those of the SH rat [1.04 +/- 0.003 (143), compared with VSMCs of the WKY rat [1.54 +/- 0.006 (135)] and W rat [1.19 +/- 0.003 (136)]. Our previous studies have demonstrated increased passive Na+ and K+ transport rate constants of SH rat VSMCs compared with either W or WKY rat cells. These findings suggest the possibility of higher permeabilities of the SH cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Bumetanide-sensitive sodium-22 transport in vascular smooth muscle cell of the spontaneously hypertensive rat.
The effect of bumetanide, a known probe of Na+, K+ cotransport, on 22Na+ uptake and washout was examined in serially passed cultured vascular smooth muscle cells of spontaneously hypertensive rats (SHR), Wistar-Kyoto rats (WKY), and Wistar rats. In Ca2+-deficient medium, the drug exerted the greatest effect on 22Na+ washout in vascular smooth muscle cells from SHR and the least effect on cells from WKY. The respective mean values for the apparent bumetanide-sensitive 22Na+ washout rate constants (Ke; X 10(-2)/min) were 7.2, 4.3, and 1.7 for cells from SHR, WKY, and Wistar rats. In both 1 mM Ca2+ and Ca2+-deficient medium, in the presence of 1 mM ouabain, vascular smooth muscle cells from SHR had the highest plateau phase of 22Na+ uptake among the three cell preparations. All cells exhibited higher 22Na+ uptake in Ca2+-deficient medium than in 1 mM Ca2+ medium. Under this condition, bumetanide caused an additional rise in steady state 22Na+ uptake that was most pronounced in cells from SHR (21.3% versus 16.6% for Wistar rats and 4.8% for WKY). This finding indicates that a quantitatively greater inhibition of washout than of the uptake component of the bumetanide-sensitive 22Na+ transport occurs in Ca2+-deficient medium. It is concluded that, in Ca2+-deficient medium, the bumetanide-sensitive 22Na+ washout is higher in vascular smooth muscle cells of SHR than in those of normotensive controls and that this phenomenon reflects a higher Na+ turnover in vascular smooth muscle cell in the hypertensive rat strain.
Animals↗
Histological findings of the right and left ventricular myocardium and clinical follow up in idiopathic ventricular tachycardia.
In order to evaluate the etiology of so-called idiopathic ventricular tachycardia, endomyocardial biopsies were performed in four patients with electrocardiographically documented recurrent and sustained ventricular tachycardia. During the episodes of ventricular tachycardia, standard ECG showed a QRS pattern of right bundle branch block with left axis deviation in two patients and left bundle branch block in two patients. The episodes were associated with palpitation, dyspnea and hypotension in all cases. No organic heart disease was detected by physical examination, chest X-ray films, echocardiograms, left ventriculograms or coronary cineangiograms. His bundle electrograms showed blocks at various sites in the atrioventricular conduction system. The biopsy specimens revealed nonspecific myocardial degeneration in the right and left ventricles. These findings suggest mild but wide-spread myocardial damage in both the working myocardium and the conduction system. The clinical course of these patients appeared benign according to follow-up data of one to nine years' duration. None developed overt clinical signs of dilated, hypertrophic or restrictive cardiomyopathy.
Adult↗
Cardiovascular effects of a new inotropic agent, denopamine (TA-064); with reference to it's effects on cardiac hemodynamics and metabolism.
A new inotropic agent, denopamine (TA-064) was shown to have a strong positive inotropic effect. Its effect on cardiac hemodynamics and metabolism was evaluated by using wall stress and direct measurement of myocardial oxygen consumption. With plasma concentration of denopamine (21-29 ng/ml on average), attainable by one single oral dose (10 mg), the positive inotropic effect was evident by the significant increase in peak (+)dp/dt (+15% increase from control), and shortening velocity of the left ventricle (+39%), when heart rate or blood pressure was not altered significantly. End diastolic stress and end systolic stress of the left ventricle, defined as indices of preload and afterload, respectively, were reduced significantly. The reduction of preload (-51%) was the result of improved left ventricular filling, and the reduction of afterload (-23%) was due to the increased contractility. Neither coronary sinus blood flow not aortocoronary AV O2 defference was changed. Consequently, myocardial oxygen consumption remained unaltered. When the dose is chosen properly, denopamine is able to exert salutary effects in patients with severe heart failure.
Administration, Oral↗
[The natural history of dilated cardiomyopathy and pathophysiology of congestive heart failure].
To clarify the natural history and mechanisms of compensation and decompensation in dilated cardiomyopathy (DCM), the hemodynamic and follow-up data of 52 patients who underwent cardiac catheterization between April 1976 and July 1984 were evaluated. The symptoms of the majority of 42 patients who were in severe congestive heart failure (CHF) (New York Heart Association Functional Class IV) on admission were improved. Two were in Class I, 22 in Class I, 22 in Class III, only six remaining in Class IV at the times of their catheterizations one to two months post admission. The patients were categorized as compensated (Class I and II) and decompensated (Class III and IV), and their data were compared with those of 30 normal subjects. Cardiac status was evaluated at the end of August 1984, and the mean follow-up period was 44 months. The hemodynamic and angiographic characteristics of DCM consisted of an enlarged and poorly contracting left ventricle, with an increased left ventricular (LV) muscle mass, low LV systolic pressure, reduced cardiac output, and elevated systemic vascular resistance. LV volume was larger, and the ejection fraction (EF) was more reduced in the decompensated group in association with elevated preload and afterload. Preload and afterload were within the normal range in the compensated group. LV wall thickness tended to decrease in the decompensated group, and the LV muscle masses did not differ between these two groups. There was a significant inverse correlation between afterload and EF (r = -0.57, p less than 0.01) in DCM. There were five sudden deaths and five CHF deaths, and cardiac symptoms improved in the majority of the survivors. One, two and five year survival rates were 91.2%, 79.8%, and 72.5%, respectively. No hemodynamic variables could be available to predict the prognosis except for the LV end-diastolic pressure and stress. It is concluded that the absence of adequate compensatory hypertrophy and the inappropriate elevation of afterload, or so-called "afterload mismatch" plays an important role in the development of CHF, in addition to depressed contractility in DCM. Persistent elevation of preload despite vigorous medical treatment indicates a poor prognosis. No other hemodynamic variables were good indicators of prognosis.
Blood Pressure↗
Hashimoto's thyroiditis and ulcerative colitis in a patient with Turner's syndrome.
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Adult↗
Electron-microscopic and immunohistochemical studies on endomyocardial biopsies from a patient with eosinophilic endomyocardial disease.
Light- and electron-microscopic studies and immunohistochemical procedures were carried out on blood eosinophils and left ventricular endomyocardial biopsies from a 68-year-old man with an eosinophilia of 8.2 X 10(9)/l and congestive cardiac failure due to eosinophilic endomyocardial disease. Some blood eosinophils were vacuolated and degranulated, and reversal of the normal staining pattern of eosinophil granules was seen by means of electron microscopy. The biopsies showed degenerative changes in the cardiac myocytes, with interstitial fibrosis and infiltration by numerous eosinophils, mast cells, and macrophages. Eosinophils infiltrating the myocardium showed a decrease in the number of granules, many of which were indistinct or contained dissolving crystalloids, which occasionally were seen to be discharged onto the surface of adjacent cardiac myocytes. Immunohistochemical studies of the endomyocardial biopsies with a monoclonal antibody, which is specific for activated eosinophils and binds to the secreted forms of eosinophil cationic protein (ECP) and eosinophil protein-X (EP-X), demonstrated that the lesions contained numerous activated eosinophils and secreted ECP and EP-X. These findings support the concept that in eosinophilic endomyocardial disease, activated eosinophils infiltrate and degranulate in the myocardium, releasing eosinophil cationic proteins which then damage adjacent myocardial cells.
Aged↗
Factors discriminating survivors and nonsurvivors in alcoholic heart disease.
Eighteen patients with dilated cardiomyopathy and a history of excessive ethanol intake were monitored for 3-98 months (mean 23 months). Six patients died (mean age 43.7 +/- 9.2 years) and 12 patients survived (mean age 48.8 +/- 9.5 years). Of the echocardiographic findings taken during heart failure, only the relative wall thickness to the internal dimension of the left ventricle (t/r ratio) differed significantly (survivors 0.33 +/- 0.77 vs. nonsurvivors 0.25 +/- 0.04, P less than 0.05). Of the hemodynamic data obtained after treatment of heart failure, left ventricular end-diastolic pressure differed significantly (survivors 6 +/- 2 vs. nonsurvivors 12 +/- 4 mmHg, P less than 0.001). The two groups could not be differentiated by ejection fraction, cardiac output, end-diastolic or end-systolic volumes, or semi-quantitative analysis of histologic findings obtained by right ventricular endomyocardial biopsy (light microscopy). Only two of six nonsurvivors (33%) succeeded in abstaining from alcohol, while eight of twelve survivors (67%) became teetotalers (P less than 0.05). Total abstinence from alcohol seems to be essential but was not necessarily followed by recovery in the most severe cases. Thus, the absence of adequate hypertrophy and high left ventricular filling pressure may predict the prognosis in alcoholic heart disease.
Adult↗
Cultured rat vascular smooth muscle cells: extracellular calcium and Na+-K+ regulation.
This study explores the relationship between extracellular calcium (Cao) and Na+-K+ regulation as it particularly pertains to the activity of the Na+ pump in cultured vascular smooth muscle cells (VSMCs) originating from Sprague-Dawley rats. As compared with cells incubated in media containing 0.5, 2.0, or 4.0 mM calcium, when the Na pump is active, VSMCs incubated in a Ca-deficient medium show a marked increase in intracellular sodium and no significant change in intracellular potassium. Associated with the rise in intracellular sodium there is an augmented activity of the Na pump. When the Na pump is inhibited, VSMCs incubated in either high-Ca medium (Cao = 4.0 mM) or Ca-deficient medium manifest a greater decline in intracellular potassium than cells incubated in media containing 0.5 or 2.0 mM calcium. Furthermore, when the Na pump is inhibited, VSMCs incubated in a Ca-deficient medium exhibit higher intracellular sodium levels in comparison with their counterparts incubated in media containing calcium. Flux experiments indicate that the aforementioned changes reflect increased membrane permeabilities to Na+ and K+. It is concluded that by regulating the permeability of the VSMC membrane, Cao plays an important role in the intracellular Na+-K+ homeostasis and that its effect on the Na pump is mediated via perturbations in the intracellular Na+ and K+ concentrations.
Animals↗
The effect of melittin on Na+ and Rb+ transport in cultured skin fibroblasts of the spontaneously hypertensive rat.
Melittin effect on transport of Na+ and Rb+(K+ analog) was examined in cultured skin fibroblasts originating from the Spontaneously Hypertensive, Wistar Kyoto and Wistar rats. Melittin increased both Na+ (22Na+) uptake and 86Rb+ efflux as well as the activity of the Na+-pump (ouabain sensitive 86Rb+ uptake) in all three preparations. The effect of the toxin was maximal at a dose of 160-240ng/10(5) cells/ml. At this dose, fibroblasts of the Spontaneously Hypertensive rat demonstrated the greatest response to melittin with respect to the increase in Na+ and Rb+ fluxes and increase in the intracellular Na+ concentrations. It is concluded that melittin can be utilized as a probe to delineate subtle differences in the cellular regulation of Na+ and K+ in the Spontaneously Hypertensive rat as compared with its normotensive controls.
Animals↗
Mechanisms of compensation and decompensation in dilated cardiomyopathy.
Left ventricular (LV) function was evaluated in 32 patients with dilated cardiomyopathy (DC) who underwent cardiac catheterization during the past 6 years (group 4), and the results were compared with the data of 30 normal subjects (group 1). The patients were divided into mildly (group 2, 12 patients) and severely symptomatic subgroups (group 3, 20 patients). DC was characterized by dilated and poorly contracting left ventricle with increased muscle mass, reduced cardiac output and elevated systemic vascular resistance. LV volume was larger, ejection fraction was lower, and end-diastolic and end-systolic stresses were higher in group 3 than in groups 1 and 2. No significant differences were seen in LV muscle mass and wall thickness between groups 2 and 3. A significant inverse correlation was seen between ejection fraction and end-systolic stress in patients with DC (Y = -0.05x + 48.7, r = 0.57, p less than 0.01). The slope of the correlation line between end-systolic stress and volume in DC (Y = 1.20x + 135, r = 0.52, p less than 0.02) was less steep than that of normal subjects (Y = 3.68x + 40, r = 0.64, p less than 0.001). These observations indicate that the primary problem of DC is depressed contractility.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Tricuspid regurgitation-like murmur due to mitral regurgitation with left phrenic nerve paralysis.
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Adolescent↗
Two-dimensional echocardiography of ruptured pulmonic valve with infective endocarditis.
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Adult↗
[3H]ouabain binding to cultured rat vascular smooth muscle cells.
The number of Na+ pump units (Bmax) and the equilibrium dissociation constant (Kd) for ouabain as well as parameters of K+ binding to the Na+ pump were examined in in vitro-grown vascular smooth muscle cells ( VSMC ) derived from Sprague-Dawley rats. The technique to measure these variables utilizes analyses of [3H]ouabain displacement from its VSMC receptors by nonlabeled ouabain and K+. The mean values for Bmax and Kd in the cultured VSMCs were 1.95 X 10(5) receptor sites per single VSMC and 2.68 X 10(-6) M, respectively. The equilibrium dissociation constant for K+ (Ki) was 0.92 mM. K+ binding to the cultured VSMCs demonstrated positive cooperativity with a Hill coefficient (n) of 1.78.
Animals↗
Incidence of the coexistence of left ventricular false tendons and premature ventricular contractions in apparently healthy subjects.
The incidence of the coexistence of left ventricular false tendons and premature ventricular contractions (PVCs) was evaluated prospectively. Over 14 months, left ventricular false tendons were found in 71 (6.4%) of 1117 consecutive patients examined echocardiographically. Two types of false tendons were observed: longitudinal, from the ventricular septum to the posteroapical wall (n = 62), and transverse, between the septum and the lateral wall (n = 9). Among 62 patients with PVCs and no underlying heart disease, false tendons were detected in 35 (56%); 28 had unifocal and seven had bifocal PVCs. Episodes of ventricular tachycardia were documented in one of the 28 patients with unifocal PVCs and in one of the seven patients with bifocal PVCs. These PVCs were poorly controlled by antiarrhythmic drugs but easily suppressed by exercise. Left ventricular false tendons were detected in 36 patients on routine echocardiographic examinations performed in the other 1055 subjects, and 10 of these patients were judged to have no underlying heart disease. PVCs were detected in two (20%) of these 10 patients. Although a definite conclusion that left ventricular false tendons are arrhythmogenic cannot be derived from these results, the unexpectedly high incidence of the coexistence suggests that left ventricular false tendons may be an etiologic factor in the development of PVCs, especially the rate-dependent and medically uncontrollable PVCs seen in apparently healthy individuals.
Adolescent↗