Search PubMed⌕ Search

Biomedical subjects

M Kino

Publications and source records attributed to M Kino.

At least 73 records · Page 4Linked to original sources
PubMed1983

Cardiovascular effects of a newly synthesized cardiotonic agent (TA-064) on normal and diseased hearts.

A new inotropic agent, TA-064, (-)-alpha-(3,4-dimethoxyphenethylaminomethyl)-4-hydroxybenzylalcohol, was shown to have strong effects in experimental animals. Its effectiveness and associated adverse effects were tested in humans invasively (n = 6) and noninvasively (n = 17). Increasing doses of intravenous infusion (1, 2, and 4 micrograms/kg/min) increased plasma levels to 15, 35, and 82 ng/ml, respectively, resulting in marked increases in the peak rate of left ventricular pressure rise (dP/dt) (1,450 +/- 63 to 3,042 +/- 349 mm Hg/s) (mean +/- standard error of the mean [SEM], p less than 0.01) and the ratio of dP/dt to left ventricular pressure at a developed pressure of 40 mm Hg (25 +/- 3 to 39 +/- 2 s-1) (p less than 0.01), with a reduction in left ventricular end-diastolic pressure (12 +/- 2 to 4 +/- 1 mm Hg) (p less than 0.01). Minimal or no changes were seen in heart rate and left ventricular systolic pressure. After a single oral dose (10 mg), the plasma level reached its peak at 90 minutes (16 +/- 9 ng/ml, n = 17). A positive inotropic effect was confirmed echocardiographically in both healthy volunteers (n = 8) and patients with congestive heart failure (CHF) (n = 9) who were maximally treated with conventional regimens: increase in mean velocity of circumferential fiber shortening (healthy volunteers: 1.29 +/- 0.05 to 1.60 +/- 0.11 circ/s [p less than 0.05]; patients with CHF: 0.69 +/- 0.08 to 0.93 +/- 0.09 circ/s [p less than 0.01]), ejection fraction (healthy volunteers: 68 +/- 2 to 75 +/- 2% [p less than 0.05], patients with CHF: 37 +/- 4 to 45 +/- 5% [p less than 0.01]) without change in heart rate. The cardiac index was increased only in the CHF group (2.71 +/- 0.22 to 3.21 +/- 0.24 liters/min/m2) (p less than 0.05). No significant untoward effects were observed. Thus TA-064 is a potent inotropic agent and can be used either parenterally or orally. Salutary effects can be expected in patients with congestive heart failure who are treated with digitalis and diuretic agents.

Adult↗
PubMed1983

Vanadate effect on the Na,K-ATPase and the Na-K pump in in vitro-grown rat vascular smooth muscle cells.

The impact of vanadate on the Na,K-ATPase system in the vascular smooth muscle cell is poorly understood. The present study describes the kinetics of the effect of vanadate on Na,K-ATPase and the Na-K pump in in vitro grown rat VSMC's. Vanadate interaction with the Na,K-ATPase system in vascular smooth muscle cells was examined by observing its influence on ouabain-sensitive adenosine triphosphate hydrolysis in disrupted cells rendered permeable by osmotic shock, and the uptake of rubidium by intact cells. The I50 for vanadate inhibition of ouabain-sensitive hydrolysis of adenosine triphosphate occurred at vanadate concentrations of 10(-6) to 10(-7) M. This inhibition was potassium dependent. The maximal inhibitory effect of vanadate occurred at potassium concentrations of 10-20 mEq/liter. Sodium exerted a moderate antagonistic influence on vanadate inhibition of ouabain-sensitive adenosine triphosphate hydrolysis. Rubidium uptake by vascular smooth muscle cells was not altered within 120 minutes when 10(-5) M vanadate was added to the medium containing intact vascular smooth muscle cells. Yet, vanadium concentrations in the vascular smooth muscle cells within this incubation period reached levels 1.48-fold higher than the extracellular vanadate concentrations of 10(-5) M. These observations indicate that vanadate is a potent inhibitor of the VSMC Na,K-ATPase in disrupted vascular smooth muscle cells. However, in intact vascular smooth muscle cells vanadium gaining access into the vascular smooth muscle cell's interior does not inhibit the Na-K pump, probably because of its binding to intracellular proteins and/or conversion from the vanadate to the vanadyl ion.

Animals↗
PubMed1983

Coxsackie B5 myopericarditis in a young adult--clinical course and endomyocardial biopsy findings.

An 18-year-old student with recent gastrointestinal symptoms was found to have Stokes-Adams syndrome. A transvenous pacemaker was successfully inserted with clinical improvement. Subsequent viral titer studies and serum enzyme changes supported the diagnosis of coxsackie B5 myopericarditis. The first cardiac catheterization and endomyocardial biopsy of the right ventricle were performed on the 14th hospital day; the former revealed no hemodynamic abnormalities, but the latter showed marked necrosis of the myofibers, disarray of the remaining ones, mononuclear cell infiltration and the appearance of fibroblasts with fine collagen fiber proliferation in the interstitium. A second biopsy of both ventricles, carried out on the 46th hospital day, showed no necrosis of the myofibers or inflammatory cell infiltration but increasing collagen fiber proliferation in the interstitium and disarray of the surviving myofibers. These pathological findings suggest the healing process of the myopericarditis. To the best of our knowledge, reports of viral myopericarditis with serial endomyocardial biopsies have been few.

Adolescent↗
PubMed1982

Phospholipid acyl chain metabolism during the differentiation of murine leukemia cell lines. On the redistribution of polyunsaturated acyl chains among phospholipids.

Phospholipid acyl chain metabolism was investigated during the differentiation of murine myeloid leukemic cells (MI cells). Fatty acid composition of the phosphatidylethanolamine (PE) fraction showed no significant change, while a marked decrease in the polyunsaturated fatty acid content was observed in the phosphatidylcholine (PC) fraction during the course of differentiation. When these cells were incubated with [14C]arachidonate, it was actively incorporated initially into PC, and subsequently, gradually mobilized to PE from PC during the 72 h of culture. This characteristic redistribution was observed specifically with polyunsaturated acyl chains. Thus, the normal metabolic pathway of polyunsaturated fatty acids in these cells appears to consist of two steps: firstly fatty acids are incorporated from the external medium into the form of polyunsaturated PC, and, subsequently, are stored within cells as a metabolically stable pool after the conversion into the form of polyunsaturated PE. In differentiated cells, this redistribution pathway was significantly enhanced, suggesting a change in the activity of the deacylation-reacylation cycle during the course of differentiation,

Animals↗
PubMed1982

Analysis of molecular species of phospholipids by field desorption mass spectrometry.

Various glycerophospholipids including their trimethylsilyl and t-butyldimethylsilyl derivatives and cerebroside were analysed by field desorption mass spectrometry with a silicon emitter. Choline glycerophospholipids with diacyl residues and also alk-1'-enyl and acyl residues gave the readily interpretable field desorption mass spectra in which a sodium cluster ion [M+NA]+ was a base peak. As to phosphatidylethanolamine and cerebroside, a protonated molecular ion [M+H+]+ was a base peak. The TMS and TBDMS derivatives gave a molecular ion [M]+. The field desorption analysis of natural phospholipids from myelin was carried out in comparison with the gas chromatographic mass spectrometric analysis.

Animals↗
PubMed1982

Studies on molecular species of choline and ethanolamine glycerophospholipids obtained from rat brain myelin and synaptosomes by gas-liquid chromatography mass spectrometry.

By converting to t-butyldimethylsilyl derivatives, molecular species of ethanolamine glycerophospholipid including both 1,2-diacyl and 1-alk-1'-enyl-2-acyl (plasmalogen) types were able to be analysed by a gas chromatography mass spectrometry selected ion monitoring technique. The samples analysed were ethanolamine glycerophospholipid and also choline glycerophospholipid obtained from myelin and synaptosomes of rat brain, both of which are characteristic subcellular organella of the nervous system. Main molecular species of ethanolamine glycerophospholipid were as follows: in myelin as 1,2-diacyl type, 36:1 (mainly 18:0/18:1), and as 1-alk-1'-enyl-2-acyl type, 34:2 (mainly vinyl 16:0/18:1), 36:2 (mainly vinyl 18:0/18:1) and 36:3 (mainly vinyl 18:1/18:1), whereas in synaptosomes as 1,2-diacyl type 36:1 (mainly 18:0/18:1), 38:4 (mainly 18:0/20:4) and 40:6 (18:0/22:6), and as 1-alk-1'-enyl-2-acyl type 34:2 (mainly vinyl 16:0/18:1), 36:2 (mainly vinyl 18:0/18:1), and 36:3 (mainly vinyl 18:1/18:1). The molecular species of choline glycerophospholipid consisted almost entirely of 1,2-diacyl type and they were in myelin 34:1 (mainly 16:0/18:1), 36:1 (mainly 18:0/18:1) and 36:2 (mainly 18:1/18:1), whereas in synaptosomes 32:0 (mainly 16:0/16:0), 34:0 (16:0/18:0), 34:1 (mainly 16:0/18:1) and 36:1 (mainly 18:0/18:1). In myelin as 1-alkyl-2-acyl type, 34:1 (1-hexadectl-2-octadecenoyl) was present at about 7%.

Animals↗
PubMed1982

Hypertrophic nonobstructive cardiomyopathy: a precise assessment of hemodynamic characteristics and clinical implications.

A precise assessment of left ventricular function was performed in 20 patients with hypertrophic nonobstructive cardiomyopathy to elucidate the basic pathophysiology, and the data were compared with those in 22 normal subjects. Whereas end-diastolic pressure was high in those with cardiomyopathy, a more accurate index of preload, end-diastolic stress, did not differ from normal value. Afterload was about half the normal value. Both isovolumic indexes [peak positive dP/dt and (dP/dt)/DP40] and ejection phase indexes of contractility (ejection fraction) were in the normal range; however, the end-systolic stress volume ratio was significantly reduced (43% of the normal value). Although the left ventricular minute work index was in the normal range, the unit muscle performance (minute work/mass) was very low (49%). An abnormality of left ventricular relaxation was demonstrated by low peak negative dP/dt (56%) and prolonged time constant T (191%), and a stiff left ventricle was demonstrated by a high diastolic elastic stiffness constant (129%). These observations suggest that the contraction of a unit muscle is inappropriate to produce an adequate contraction of the whole ventricle, and that hypertrophy might be an adaptive process to maintain normal systolic function by increasing mass and reducing afterload.

Adult↗
PubMed1982

[Midsystolic closure of the aortic valve in hypertrophic nonobstructive cardiomyopathy].

Midsystolic cessation of left ventricular contraction was documented in a patient with hypertrophic nonobstructive cardiomyopathy (HCM) associated with Cushing's syndrome (adrenal adenoma) without history of hypertension. The carotid pulse tracing showed a rapid upstroke with a prominent percussion wave which was rapidly decayed at midsystole followed by a tiny tidal wave. The decay of this percussion wave coincided in timing with midsystolic closure of the aortic valve in the echocardiogram. The left ventricle (LV) was symmetrically hypertrophied (wall thickness = 1.8 cm). The motion of the interventricular septum and LV posterior wall appeared trapezoid, and the contraction of these walls was normal in early-systole followed by the sudden cessation at midsystole till end-systole. Systolic anterior motion of the mitral valve was not observed. Cardiac catheterization revealed no pressure gradient in the LV even after the various provocative maneuvers. The left ventriculogram simultaneously recorded with LV pressure showed that LV ejection was completed at midsystole, when LV pressure fell from 98 to 83 mmHg. Mitral regurgitation was not observed. Midsystolic cessation of left ventricular contraction in this case is thought to be the cause of sudden interruption of forward aortic flow, resulting in a bifid carotid pulse and midsystolic closure of the aortic valve in the echocardiogram.

Adult↗
PubMed1981

Cardiovascular status in asymptomatic alcoholics, with reference to the level of ethanol consumption.

One hundred and forty-five alcoholics without known causes of heart disease, who were serially admitted to the alcohol detoxification centre, were studied to see the incidence of cardiac abnormalities and dose related effects of ethanol. All patients were divided into heavy (consumed more than the equivalent amount of 125 ml of pure ethanol daily for 10 years or more) and moderate drinkers (consumed 75 to 125 ml of ethanol daily). All of them were ambulatory and free from cardiac symptoms. There was no difference among heavy and moderate drinkers in the incidence of abnormalities detected by the electrocardiograms and chest x-ray films. In the alcoholics, the most frequent finding was a prolonged QTc interval of more than 0.44 s on the electrocardiogram (62 patients, 42.8%), unrelated to serum electrolytes imbalance. Cardiomegaly on chest x-ray film was observed in 25 patients (17.2%). M-mode echocardiogram was recorded in randomly selected patients and compared with age and sex matched controls. The interventricular septum and posterior wall were thicker in alcoholics, while left ventricular volume showed no difference. Left ventricular muscle mass was significantly increased only in heavy drinkers. Left ventricular function at rest was not depressed in these patients at an average of 31 days after the last drink of ethanol. Severe heart failure was not found even among the group of heavy drinkers, of whom more than 90% had liver dysfunction. Cardiac hypertrophy seems to occur in heavy drinkers, but is clinically well compensated in the majority of alcoholics.

Adult↗