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Biomedical subjects

M Arita

Publications and source records attributed to M Arita.

At least 289 records · Page 16Linked to original sources
PubMed1987

Suppression of ventricular premature contractions possibly related to triggered activity by oral diltiazem and atenolol.

The clinical importance of triggered activity as a cause of arrhythmias is uncertain. We assumed that ventricular premature contractions (VPCs) caused by triggered activity could be increased at higher heart rates and be suppressed by calcium channel blockers and beta-adrenoceptor blocker. Thus, we evaluated VPC frequency as a function of underlying heart rate and examined the efficacy of diltiazem and atenolol on VPCs, using 24 hour ECG recording. Plots of VPC frequency vs. heart rate were made at 1-beat/min intervals for all heart rates recorded for at least 5 min during 24 hours. Diltiazem (90-180 mg/day) and atenolol (50 mg/day) were given orally for 4 weeks, respectively in 36 and 16 patients with VPCs of more than 2000/day. Patterns of relationship between VPC frequency and heart rate observed before diltiazem therapy included: an increase of VPCs at higher heart rates (positive correlation) in 16 patients, an increase at low heart rates and a decrease at high heart rates (bidirectional correlation) in 13 patients, an increase at low heart rates and flat curve at high heart rates (positive-flat correlation) in 5 patients, a linear decrease (negative correlation) in 1 patient, and flat curve (flat correlation) in 1 patient. The patterns of correlation in patients treated with atenolol were positive in 6, bidirectional in 7, positive-flat in 2 and negative in 1. Both drugs significantly reduced the VPC frequency per 24 hours for patients with a positive correlation (P group), but induced no significant change for those with the other patterns of correlation (NP group). At the 70% VPC suppression level, diltiazem was effective in 9 of 16 patients of P group and only 1 of 20 patients of NP group (p less than 0.01); atenolol was effective in 5 of 6 patients of P group and only 1 of 10 patients of NP group (p less than 0.05). Both drugs reduced the slope of a positive correlation. These results suggest that: VPCs which increase at higher heart rates may be related to triggered activity, and an evaluation of VPC frequency as a function of heart rate predicts the response of VPCs to diltiazem and atenolol, and probably to other calcium antagonists and beta blockers.

Administration, Oral↗
PubMed1987

The cause of death, risk factors and long-term prognosis of acute myocardial infarction.

Three hundred and eighty-six patients with acute myocardial infarction in the past 11 years between 1975 and 1985 were investigated retrospectively to clarify fatality, cause of death and long-term prognosis in relation to their risk factors and age. The average number of patients admitted in each year was 24.4 for the first 5 years and 44.0 cases per year in the last 5 years. The fatality decreased from 20.3% in the first 5 years to 15.7% in the last 5 years. A major cause of hospital death was cardiogenic shock and congestive heart failure. One hundred and thirty-six patients had coronary arteriography within 2 months after admission. They were divided into three groups; the young (less than or equal to 40 year old)-, middle (41-50 year old)-, and old (greater than or equal to 51-year old)-aged groups. Among the young-aged group, serum cholesterol levels at admission were significantly higher in patients with multi-vessel lesions than those in patients without multi-vessel lesions, while there were many heavy smokers who did not show a significant lesion of the coronary artery. These observations suggest that hypercholesterolemia may act as an important risk factor for coronary arteriosclerosis in young patients, and also that a heavy smoking may promote an initiation of myocardial infarction in young patients without severe coronary artery stenosis. The cumulative 5 and 10 year survival rate for all groups was 84% and 61%, respectively. Fifty-seven patients had reinfarctions, and thirty patients died. The survivors were younger and had a good tolerance to treadmill exercise test at discharge.

Age Factors↗
PubMed1987

Histopathological study of acute myocardial infarction and pathoetiology of coronary thrombosis: a comparative study in four districts in Japan.

To clarify the patho-etiologic factors of Japanese myocardial infarction, a comparative pathological study of myocardial infarction in the Osaka, Akita, Wakayama, and Hokkaido districts, and an extensive histopathological study of 94 autopsy cases with acute myocardial infarct (AMI) in less than 4 weeks at Osaka were carried out. Although AMI in Akita was highly complicated by hypertension, AMI in Osaka was associated with a history of diabetes mellitus and hypercholesterolemia, especially in the young generation (under 59 years of age); hypercholesterolemia was related to the occurrence of AMI. Moreover, in spite of increases in transmural myocardial infarct (TMI) in Osaka, Hokkaido and Wakayama, Akita showed an equal ratio of TMI and subendcardial myocardial infarct. In AMI in Osaka, significant stenosis (more than 75% stenosis) of the coronary artery was of the same grade between the proximal and distal portions in the epicardial coronary artery. AMI in Akita, however, showed more severe stenosis in the proximal than the distal portion. A high incidence (88.3%) of thrombosis formation corresponding to the site of infarction was observed in AMI in Osaka. Moreover, ruptured atheromatous plaques were identified as being responsible for 62.6% of the coronary thrombosis cases, and a high incidence (70.0%) of foamy cell infiltration was disclosed. Thus, it can be concluded that ruptured atheromatous plaque is a major factor in the progression of coronary atherosclerosis and/or thrombosis, which might be due to the process of plaque softening.

Adult↗
PubMed1987

Factors related to the low resting membrane potentials of diseased human atrial muscles.

We studied the ionic mechanism of low resting potential (RP) of quiescent "diseased" human atrial fibers. The RP was -49.7 +/- 0.8 mV (n = 179) in normal Tyrode's solution (5.4 mM [K]o, 36 degrees C). The changes in RP measured at various levels of [K]o appeared to fit the RP-[K]o relationship predicted by the Goldman-Hodgkin-Katz equation, assuming PNa/PK ratio (alpha) to be 0.102 and [K]i to be 131.9 mM. The alpha far exceeded the normal value (about 0.01) by a factor of 10. Acetylcholine (ACh, 10 microM) led to marked increases in the RP. An application of tetrodotoxin (TTX, 6 microM) and perfusion with low [Na]o (10% of the control) media in the presence and absence of ACh produced considerable hyperpolarizations of the RP. These findings indicate that increased alpha value is due to a combination of decreased PK and increased PNa. Applications of ouabain (5 microM) and a cooling procedure (12.3 degrees C) depolarized the membrane, whereas epinephrine (1 microM) hyperpolarized it. Transient hyperpolarization, which exceeded the steady state levels of RP at 5.4 mM [K]o, was observed with perfusing of 5.4 mM [K]o media following perfusion with K-free media. These findings suggest that electrogenic Na pump current plays a significant role in the maintenance of the RP. In conclusion, partial depolarization of "diseased" human atrial fibers was attributed to both decreases in membrane K+ conductance and increases in Na+ conductance. The electrogenic outward pump current seemed to protect the fibers from severe depolarization produced by the conductance abnormality (increased PNa/PK).

Acetylcholine↗
PubMed1987

Inhibition of 22Na influx by tricyclic and tetracyclic antidepressants and binding of [3H]imipramine in bovine adrenal medullary cells.

In bovine adrenal medullary cells we investigated the effects of antidepressants on ionic channels and secretion of catecholamines. Tricyclic (imipramine, amitriptyline and nortriptyline) and tetracyclic (maprotiline and mianserin) antidepressants inhibited carbachol-induced influx of 22Na, 45Ca and secretion of catecholamines (IC50, 14-96 microM). Influx of 22Na, 45Ca and secretion of catecholamines due to veratridine also were inhibited by these drugs (IC50, 10-17 microM). However, antidepressants did not suppress high concentration of K-induced 45Ca influx and catecholamine secretion, suggesting that antidepressants do not inhibit voltage-dependent Ca channels. [3H]Imipramine bound specifically to adrenal medullary cells. Binding was saturable, reversible and with two different equilibrium dissociation constants (13.3 and 165.0 microM). Tricyclic and tetracyclic antidepressants competed for the specific binding of [3H]imipramine at the same concentrations as they inhibited 22Na influx caused by carbachol or veratridine. Carbachol, d-tubocurarine, hexamethonium, tetrodotoxin, veratridine and scorpion venom did not inhibit the specific binding of [3H]imipramine. These results suggest that tricyclic and tetracyclic antidepressants bind to two populations of binding sites which are functionally associated with nicotinic receptor-associated ionic channels and with voltage-dependent Na channels, and inhibit Na influx. Inhibition of Na influx leads to the reduction of Ca influx and catecholamine secretion caused by carbachol or veratridine.

Adrenal Medulla↗
PubMed1987

[ECG-gated magnetic resonance imaging of the left ventricle: visualization of anatomical characteristics and quantification of wall thickness and ventricular volume in left ventricular hypertrophy].

Electrocardiography- and respiration-gated magnetic resonance imaging (MRI) was performed using a 0.15-Tesla resistive magnet system in 54 patients with left ventricular hypertrophy to define the site and extent of abnormal wall thickness and to estimate left ventricular function. Because the major cardiac axes are not orthogonal to the conventional transverse, sagittal or coronal planes, the long-axis and short-axis images of the left ventricle were obtained at the end-diastolic and end-systolic phases. The anatomic characteristics of concentric hypertrophy, asymmetric septal hypertrophy, and asymmetric apical hypertrophy were clearly demonstrated by MRI, even in patients with poor echocardiographic images. Quantitatively, left ventricular wall thicknesses obtained from MR images correlated well with those obtained from echocardiography (r = 0.95), and regression was y = 0.99x + 0.39, and so did the ratios of wall thickness of the interventricular septum to the left ventricular posterior wall (r = 0.91, y = 0.80x + 0.24). Left ventricular volumes calculated by the area-length method from MRI and those from left ventriculography also correlated well (r = 0.98, y = 1.13x + 24.5). In conclusion, using the gated long-axis and short-axis MR images of the left ventricle, the anatomical location and extent of hypertrophy and left ventricular volumes are noninvasively demonstrated.

Aged↗
PubMed1987

Effects of magnesium on transient depolarizations and triggered activity induced by ouabain in guinea pig ventricular muscle.

Effects of Mg on transient depolarization (TD) and triggered activity (TA) induced by ouabain in guinea pig ventricular muscle were studied. Increased Mg concentrations (8-12 mM) suppressed the amplitude of TDs and prolonged the coupling intervals to the preceding action potential. Mg also increased the threshold of excitability for propagated action potentials and promptly terminated the otherwise sustained TA. The Mg-induced TA termination was due to both suppression of TDs and increases in the threshold of excitability, the latter appearing to take precedent.

Action Potentials↗
PubMed1986

Comparison of the inhibitory effects of mexiletine and lidocaine on the calcium current of single ventricular cells.

Effects of mexiletine and lidocaine on inward calcium current (ICa) of single ventricular myocytes from guinea pigs were studied using tight seal whole cell clamp method. Mexiletine at the concentrations of 10, 30 and 100 microM decreased ICa by 23.0, 28.9 and 55.4%, respectively, while lidocaine decreased it by 8.9, 16.8 and 25.2%. At all concentrations tested, a potency for ICa inhibition in mexiletine was significantly greater than that in lidocaine (p less than 0.05). The results suggest that mexiletine has, at therapeutic concentrations, a considerable blocking action on the Ca channels other than well-known action on the Na channels.

Action Potentials↗
PubMed1986

Ketamine inhibits 45Ca influx and catecholamine secretion by inhibiting 22Na influx in cultured bovine adrenal medullary cells.

The effects of ketamine, an intravenous anesthetic, on 22Na influx, 45Ca influx and catecholamine secretion were investigated in cultured bovine adrenal medullary cells. Ketamine inhibited carbachol-induced 45Ca influx and catecholamine secretion in a concentration-dependent manner with a similar potency (IC50 40 microM). Ketamine also reduced veratridine-induced 45Ca influx and catecholamine secretion (IC50 260 microM) but did not affect high K-induced 45Ca influx and catecholamine secretion. The influx of 22Na caused by carbachol or by veratridine was suppressed by ketamine with a concentration-inhibition curve similar to that of 45Ca influx and catecholamine secretion. Inhibition by ketamine of the carbachol-induced influx of 22Na, 45Ca and secretion of catecholamines was not reversed by the increased concentrations of carbachol. These observations indicate that ketamine, at clinical concentrations, can inhibit nicotinic receptor-associated ionic channels and that the inhibition of Na influx via the receptor-associated ionic channels is responsible for the inhibition of carbachol-induced Ca influx and catecholamine secretion. At higher concentrations, the anesthetic also inhibits voltage-dependent Na channels but has no effect on voltage-dependent Ca channels.

Adrenal Medulla↗
PubMed1986

Effects of lysophosphatidylcholine on resting potassium conductance of isolated guinea pig ventricular cells.

We studied the effects of lysophosphatidylcholine (LPC), a toxic metabolite of ischemia, on the inward rectifier potassium channel current in isolated guinea pig ventricular cells. LPC (10-50 microM) added to the external solution decreased the resting membrane potential and occasionally induced repetitive action potential discharges, with or without loss of repolarization. In voltage clamp studies, LPC (20 microM) decreased the conductance at the levels of resting potentials (approximately equal to -80 mV) from 26 +/- 8 nS to 16 +/- 3 nS (mean and SD, n = 4) within 10 min. Prolonged application of LPC (greater than 12 min) produced transient inward currents after depolarizing clamp pulses, thereby suggesting that the LPC elevated intracellular Ca2+ concentrations. The effect of LPC on the single inward rectifier K channel current was examined using the patch clamp technique in a cell-attached mode. LPC decreased the single channel conductance, depending on the concentration (5-100 microM). The slope conductance in the presence of 150 mM K+ in the pipette decreased from 45 +/- 7 pS (control) to 32 +/- 17, 20 +/- 19, and 14 +/- 10 pS for 5, 20 and 100 microM LPC, respectively. LPC induced little change with regard to probability of the channel opening. These results suggest that LPC depolarizes membrane by decreasing single channel conductance of the inward rectifier K channel. This reduction partially contributes to the alleged LPC-induced abnormal automaticities and conduction disturbances in the heart.

Animals↗
PubMed1986

An infectious cDNA clone of the poliovirus Sabin strain could be used as a stable repository and inoculum for the oral polio live vaccine.

Viruses were recovered from HeLa S3 cells and African green monkey kidney (AGMK) cells transfected with an infectious cDNA clone of poliovirus vaccine Sabin 1 strain. The viruses recovered from the different DNA-transfected cells were tested for the biological characteristics of temperature sensitivity (rct marker), plaque size, and bicarbonate concentration dependency (d marker). The results revealed that the above properties were similar to those obtained from tests on the Sabin 1 vaccine reference strain. The recovered viruses and the vaccine reference virus were passaged in AGMK cells at an elevated temperature of 37.5 degrees, and the passaged isolates were tested for the rct marker. The virus recovered from AGMK cells had the most stable rct phenotype while the virus from HeLa S3 cells had a similar stability to that of the reference virus, suggesting that the virus from AGMK cells would be more suitable as a vaccine strain than the other two viruses. Furthermore, an infectious cDNA clone of high specific infectivity, constructed by introducing SV40 large T antigen into the plasmid, was used for production of high titers of virus after transfection. The results of in vitro biological tests on the recovered virus suggested that virus produced in the transfected AGMK cells also had the high quality that is desirable in vaccine stocks. Monkey neurovirulence tests performed with these recovered viruses revealed that the recovered viruses were weakly neurovirulent, similar to the vaccine reference virus. The infectious cDNA clone of the poliovirus vaccine strain could therefore be used to generate a possible inoculum of the oral polio live vaccine. Our findings strongly suggest that an infectious cDNA clone of poliovirus RNA may be used to preserve the constancy and quality of the present seed viruses of the Sabin 1 vaccine strain.

Animals↗
PubMed1986

Effects of oral diltiazem on ventricular premature contractions.

The effects of oral diltiazem (90-180 mg/day for four weeks) on ventricular premature contractions (VPCs) were studied in 16 patients with frequent VPCs using 24-hour ambulatory ECG recordings. VPC frequency was evaluated as a function of underlying heart rate. Plots of VPC frequency vs. heart rate were made at 1-beat/min intervals for all heart rates recorded for at least five minutes during 24 hours. Patterns of correlation between VPC frequency and heart rate observed before diltiazem therapy included: 1) a relatively linear increase in VPCs with heart rate (positive correlation) in ten patients, 2) a linear decrease (negative correlation) in one patient, and 3) an increase at low heart rates and a decrease at high heart rates (bidirectional correlation) in five patients. Diltiazem significantly reduced the mean VPC frequency per 24 hours for patients with a positive correlation, but induced no significant change for patients with a negative or a bidirectional correlation. At the 65% level of VPC reduction, diltiazem was effective in eight of ten patients with a positive correlation but was not effective in the six patients with other correlations (p less than 0.01). These results suggest that an evaluation of VPC frequency as a function of heart rate predicts the response of VPCs to diltiazem.

Administration, Oral↗