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Biomedical subjects

M Arita

Publications and source records attributed to M Arita.

At least 235 records · Page 13Linked to original sources
PubMed1990

Chronic diabetes mellitus prolongs action potential duration of rat ventricular muscles: circumstantial evidence for impaired Ca2+ channel.

STUDY OBJECTIVE: The aim of the study was to investigate the effects of chronic diabetes mellitus on electromechanical properties of ventricular papillary muscles. DESIGN: Conventional glass microelectrodes and tension recording techniques were used in isolated hearts of rats made diabetic for 30-40 weeks by single intravenous injections of streptozotocin. SUBJECTS: Experimental animals were male Wistar rats of 200-250 g. Diabetic rats (n = 14) were given streptozotocin 65 mg.kg-1; controls (n = 15) were given vehicle only. MEASUREMENTS AND MAIN RESULTS: (1) The maximum upstroke velocity of the action potential duration of diabetic muscles was decreased compared to control, with no difference in the resting potential. (2) At all stimulation frequencies (0.2, 1 and 5 Hz), and particularly the lower ones, the action potential duration of diabetic muscles was longer than control. (3) In diabetic muscles, frequency dependent shortening of the late phase of action potential duration (APD75, APD90) was more pronounced, and frequency dependent lengthening of the early phase (APD25, APD50) was less pronounced. (4) A blocker of transient outward current, 4-aminopyridine, lengthened the early phase of action potential durations by the same amount in diabetic and control muscles. (5) A Ca2+ channel blocker, CoCl2, dramatically shortened all levels of action potential duration, with much greater effect on diabetic muscles. (6) Ryanodine lengthened the early phase of action potential duration and shortened the late phase in both diabetic and control muscles. It enhanced the difference between the groups in the early phase. (7) Developed tension in the presence of ryanodine (ryanodine resistant tension component) was greater in diabetic muscles than in control. CONCLUSIONS: The findings suggest that altered Ca2+ current, but not altered Na(+)-Ca2+ exchange current or altered transient outward current, significantly prolongs action potential duration in diabetic rat ventricular muscles.

4-Aminopyridine↗
PubMed1990

Electrophysiological effects of AN-132, a new antiarrhythmic compound, in guinea pig papillary muscles.

We used electrophysiological techniques to examine the effects of AN-132, a new antiarrhythmic agent, on transmembrane action potentials of isolated papillary muscles of guinea pigs. AN-132 (1-90 microM) produced a dose-dependent decrease in the maximum upstroke velocity of the action potential (Vmax). The resting potential and the amplitude, overshoot, and the duration of the action potential were not affected, even at the highest concentration of the drug used (90 microM). In the presence of AN-132, trains of stimuli at a rate of 0.5, 1, 2, and 4 Hz led to an exponential decline in the Vmax, reaching a new steady state (use-dependent block, UDB). The UDB was augmented by higher stimulation frequencies or lower membrane potentials. In the presence of the drug (60 microM), the time constant and the rate of onset of UDB of Vmax were 13.4-4.5 s and 0.141-0.053 AP-1 at stimulation frequencies of 0.5-4.0 Hz, respectively. The time constant for the recovery of Vmax from the UDB was 81.2 +/- 17.2 s. AN-132 (60 microM) only slightly depressed the Vmax of the first action potential elicited after an 8-min quiescent period (tonic block, TB). In papillary muscles depolarized with 8.4 and 10.4 mM [K+]0, both UDB and TB were augmented, but the augmentation was greater with the former. None of the parameters of the slow response elicited in the presence of 27 mM [K+]0 and 0.2 mM Ba2+ were affected by the drug (30-90 microM).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1990

Regression of left ventricular hypertrophy in hypertensive patients: responses to exercise by antihypertensive treatment.

The effects of various antihypertensive treatments on the echocardiographic and electrocardiographic findings of left ventricular (LV) hypertrophy were studied in 75 patients with essential hypertension. The hemodynamic effects of the therapy during exercise were also compared. LV mass by echocardiogram was significantly reduced by beta-blockade and angiotensin converting enzyme inhibition (ACEI), but only slightly reduced by Ca channel blockade. QRS high voltage criteria of LV hypertrophy by electrocardiogram were reduced by all 3 of these antihypertensive treatments. At submaximal exercise, the pressor responses were attenuated by captopril, but not influenced by metoprolol or nifedipine. The increase in plasma norepinephrine by exercise was significantly suppressed after captopril, but was somewhat augmented after metoprolol or nifedipine. These observations indicate that the responses of hemodynamics and sympathetic nervous activity to exercise are different after the treatment by beta-blocker, Ca channel blocker or ACEI, in spite of the equal antihypertensive effect. However, it is suggested that the regression of LV hypertrophy might be induced by antihypertensive therapy, though the different grade by the individual drug.

Adrenergic beta-Antagonists↗
PubMed1990

The making of diabetic guinea pigs by streptozotocin and high incidence of triggered activity in the ventricular muscle.

Myoplasmic Ca2+ metabolism is reported to be impaired in diabetic rat heart. We studied the possibility that the ventricular muscles of diabetic guinea pig are prone to develop delayed afterdepolarizations (DADs) and triggered activity (TA), because DADs and TA are believed to be a possible index of increased level of intracellular Ca2+ concentration. To establish an experimental diabetic model from the guinea pig, male animals were divided into four groups: 1) control group: intracardiac injection of citrate buffer; 2) IP group: intraperitoneal injection of streptozotocin (STZ, 200 mg/kg); 3) IC group: intracardiac injection of STZ; and 4) Ins-IC group: intracardiac injection of STZ after pretreatment with insulin (20 IU/kg). We found that: 1) only in the Ins-IC group was the fasting plasma glucose concentration (determined 40 days after STZ injection) significantly higher than in the control group; 2) oral glucose tolerance test performed 40 days after treatment also showed glucose intolerance in the Ins-IC group. These findings evinced the successful making of diabetic guinea pigs by an intracardiac one-shot injection of STZ during development of insulin-induced hypoglycemia. In vitro electrophysiological experiments were performed on ventricular papillary muscle from diabetic animals (Ins-IC group) by conventional glass microelectrode techniques. Transmembrane action potentials were elicited by pulse trains with various rates (2-5 Hz) and durations (10-30 stimuli) in the presence of ouabain (1 microM) and various Ca2+ concentrations (1.8-7.2 mM). The incidence of TA in the muscles from diabetic animals was significantly higher (chi 2-test, p less than 0.05) than that from controls. The findings gave evidence that Ca2+ homeostasis in the myocardium of diabetic guinea pigs is impaired, and this may be a cause of arrhythmia.

Action Potentials↗
PubMed1990

Increased susceptibility to hypoxia of prolonged action potential duration in ventricular papillary muscles from diabetic rats.

The action potential duration (APD) of ventricular muscles obtained from diabetic animals is reported to be prolonged. We studied the effect of varied periods of diabetes on APD prolongation using isolated ventricular papillary muscles from streptozocin-injected rats. We found that a diabetic period greater than 30 wk was necessary for the evolution of significant prolongation of APD. We then studied the effect of repeated hypoxia (PO2 40 mmHg) and normoxia (PO2 300 mmHg) on prolonged APD of diabetic muscles and compared the findings with those from control rats. Transmembrane potentials were recorded with conventional glass microelectrodes. Under normoxic conditions, the APDs of diabetic muscles were significantly prolonged, the maximum upstroke velocity of action potentials tended to be decreased, and the resting membrane potential was not changed significantly compared with controls. The first hypoxia (20 min) shortened the APD in both diabetic and control rats but more so in diabetic rats, thereby making the APD of diabetic rats virtually identical to the control rat APD during the hypoxia. On subsequent reoxygenation (30 min), these hypoxia-induced changes were almost recovered. The second hypoxia (20 min) produced more severe shortening of the APD in both muscle types, and the effect was again far greater in diabetic rats than controls, ending with a reversed sequence of APDs and the APD of diabetic muscles much shorter than the controls. Excessive shortening of APD in diabetic muscles during hypoxic conditions was speculated to be due to greater increases in the outward K+ current through ATP-regulated K+ channels that may be secondary to the more severe reduction of intracellular ATP concentrations in diabetic versus control hearts.

Action Potentials↗
PubMed1990

[Long-term prognosis related to coronary risk factors, clinical characteristics of acute myocardial infarction and coronary angiographic findings in the elderly].

In order to clarify the characteristics of acute myocardial infarction in the elderly, we investigated the clinical profile and long-term prognosis of patients with myocardial infarction in the past 13 years. The early fatality rate (within 30 days after onset) in the relatively younger patients (less than 65 years old) was 8.8%, and in the older patients (greater than 65 years old) was 29.1%. The fatality rate was significantly higher in older than in younger patients. On coronary and left ventriculography, the older patients showed multi-vessel lesions with decreased ejection fraction and cardiac index. According to the cumulative survival curves related to the coronary risk factors, no significant differences were found with or without smoking or hypertension. However, the long-term prognosis of the patients with controllable hypercholesteremia was better than in uncontrollable patients less than 65 years old. No significant difference was found in patients with hypercholesteremia over age 65. The long-term prognosis of the patients with uncontrollable diabetes mellitus was worse than that of controllable diabetic patients.

Aged↗
PubMed1990

[Effects of calcium antagonists or beta-blockade on left ventricular diastolic function in essential hypertension].

This study was performed to assess the effect of a calcium channel blocker (nifedipine) and beta-blockade (atenolol) on left ventricular early diastolic function and filling in essential hypertension (WHO stage I, II; HT). Twenty-two untreated patients were randomly divided as nifedipine (11 patients) and atenolol (11 patients) treatment groups and both the groups had complete echocardiographic and Doppler studies. Twenty normotensive cases served as controls. Clinical and echo-Doppler data obtained at baseline and four weeks after initiation of each therapy showed no difference between the two HT groups as to mean blood pressure (before therapy, 119 +/- 3 vs 117 +/- 11 mmHg; after therapy, 106 +/- 3 vs 110 +/- 3 mmHg), left ventricular dimension, left atrial dimension, and wall thickness. To evaluate early diastolic function, the interval from the aortic closure sound (IIA, phonocardiography) to the opening of the mitral valve (MVO, echocardiography) and that from MVO to the O point of the apexcardiogram were measured. The IIA-O interval was also calculated. The peak velocities in the rapid filling (R) and atrial contraction phases (A) were measured using pulsed Doppler echocardiography at the center of the mitral orifice. The MVO-O/IIA-MVO and A/R ratios were also calculated. Compared with the controls, the IIA-O interval (143.9 +/- 6.8 msec) and the IIA-MVO interval (81.5 +/- 4.9 msec) were significantly prolonged in HT (p less than 0.01). There was no significant difference between the MVO-O interval and R. Velocity A (54.2 +/- 2.7 cm/sec) and the A/R ratio (1.01 +/- 0.11) increased significantly in HT (p less than 0.05). The IIA-O interval (before therapy, 153.3 +/- 7.6 vs after therapy, 134.3 +/- 6.2 msec) and IIA-MVO interval (87.3 +/- 6.3 vs 77.8 +/- 5.9 msec) decreased and R (43.7 +/- 3.8 vs 49.1 +/- 3.0 cm/sec) increased significantly with nifedipine. The IIA-O interval (135.7 +/- 11.3 vs 150.4 +/- 7.6 msec) and the MVO-O (58.4 +/- 3.9 vs 66.5 +/- 4.7 msec) interval were significantly prolonged with atenolol, however the IIA-MVO interval, R, and A/R did not change. A (57.5 +/- 4.0 vs 50.2 +/- 2.9 cm/sec) was also significantly decreased with atenolol. There was a significant correlation between reduction in velocity A and prolongation in the MVO-O interval (r = -0.62, p less than 0.05) with atenolol. These results suggested that the prolongation of the diastolic closure rate of the mitral valve by atenolol was related to increased ventricular filling and decreased atrial contraction.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1990

[Magnetic resonance imaging of coronary artery lesions using modified spin-echo sequence].

Magnetic resonance imaging of the cardiovascular system has been beset with difficulties in obtaining clear images due to prominent artifacts which course in the direction of the phase encoding axis. These artifacts are commonly believed to derive from blood flow. However, in the ECG-gated spin-echo (SE) sequence using two-dimensional Fourier transform reconstruction, variation in effective repetition time due to physiological changes in the R-R interval of ECG may also result in prominent artifacts. To eliminate these artifacts, we developed a new method, the modified spin-echo (MSE) sequence, by adding a nonselective 90 degree radio-frequency pulse and an optional delay time (Td) prior to the conventional SE sequence. In the MSE sequence, artifacts derived from the cardiovascular system were markedly suppressed. Using the MSE sequence, we attempted direct imaging of the coronary vessels, and obtained very clear images of the coronary arteries and veins. Organic lesions in the coronary arteries were also clearly imaged, including coronary stenosis, dilatation, coronary fistulae, and abnormality of the origin of the right coronary artery. The MSE sequence may offer a clinical advantage in obtaining coronary artery images, and may be used to evaluate coronary artery disease.

Arteries↗
PubMed1989

Inhibition by vecuronium of carbachol-induced influx of 22Na+, 45Ca2+ and secretion of catecholamines in cultured bovine adrenal medullary cells.

In cultured bovine adrenal medullary cells, vecuronium, pancuronium and D-tubocurarine reduced carbachol-induced 45Ca2+ influx and catecholamine secretion by inhibiting 22Na+ influx via nicotinic receptor-ion channel complex with IC50 values of 0.43, 7.6 and 3.9 mumol/l, respectively. IC50 values of pancuronium and D-tubocurarine observed in adrenal medulla were one order of magnitude higher than the plasma concentrations of these muscle relaxants reported to produce 50% neuromuscular blockade, while IC50 of vecuronium was quite close between adrenal medulla and skeletal muscle.

Adrenal Medulla↗
PubMed1989

High-affinity and selectivity of neosurugatoxin for the inhibition of 22Na influx via nicotinic receptor-ion channel in cultured bovine adrenal medullary cells: comparative study with histrionicotoxin.

In cultured bovine adrenal medullary cells, neosurugatoxin and histrionicotoxin inhibited carbachol-induced influx of 22Na, 45Ca and secretion of catecholamines with IC50 of 27 nM and 3 microM, respectively. The inhibitory effects of neosurugatoxin were reversed by the increased concentrations of carbachol, whereas those of histrionicotoxin were not. Histrionicotoxin at concentrations higher than 10 microM also reduced veratridine-induced influx of 22Na, 45Ca and secretion of catecholamines, while neosurugatoxin had no effects. High K-induced 45Ca influx and catecholamine secretion were not altered by either neosurugatoxin or histrionicotoxin. The present findings suggest (1) neosurugatoxin competitively inhibits nicotinic receptor-ion channel complex at nanomolar concentrations, but has no effects on voltage-dependent Na channel and voltage-dependent Ca channel; (2) histrionicotoxin at micromolar concentrations non-competitively suppresses nicotinic receptor-ion channel complex. Higher concentrations of histrionicotoxin also interferes with voltage-dependent Na channel, but has no effect on voltage-dependent Ca channel; (3) neosurugatoxin, due to its high-affinity and selectivity, may be a useful probe for studying nicotinic receptors in nervous tissues.

Adrenal Medulla↗
PubMed1989

Characterization of a pilus produced by Aeromonas hydrophila.

A pilus produced by Aeromonas hydrophila was purified and partially characterized. The pilin monomers had an apparent molecular weight of 17,000. Agglutination studies indicated serological cross-reactivity in the pili of A. hydrophila strains. Presence of pili did not correlate with hydrophobicity or haemagglutinating ability of the bacteria.

Aeromonas↗
PubMed1989

Glucose reverses 2,4-dinitrophenol induced changes in action potentials and membrane currents of guinea pig ventricular cells via enhanced glycolysis.

The precise mechanism involved in the restoration by glucose of action potentials and membrane currents has not been established, so we studied it in single guinea pig ventricular cells under conditions of metabolic inhibition by 2,4-dinitrophenol (DNP). Application of DNP (50 mumol.litre-1) significantly shortened the action potential duration (APD) from 276.3 (SD 47.5) to 43.0(3.9) ms (n = 10). The increase in glucose concentration from 5.5 (control) to 22 mmol.litre-1 significantly restored the APD within 10 min, to 233.2(51.2) ms. In tight seal whole cell clamp studies, we found that DNP increased the steady state outward currents at potentials positive to -60 mV, and that this current was all but suppressed by 22 mmol.litre-1 glucose. The glucose induced recovery in the APD and membrane current was not seen in the presence of 2-deoxyglucose (2 mmol.litre-1), an inhibitor of glycolysis. Insulin (40 mIU.ml-1) reversed the DNP induced shortening of APD and abolished the increase in the outward current in the presence of 11 mmol.litre-1 glucose, though the application of glucose alone at this concentration failed to reverse these changes. Glucose (5.5 to 44 mmol.litre-1) did not directly affect single channel currents of ATP regulated K channels of the excised patch membrane in an outside out mode. These results suggest that the antagonising effects of glucose on the DNP induced alterations in APD and membrane currents are mediated by an increase in intracellular ATP concentration via enhanced glycolysis. Insulin might enhance this effect by facilitating the transport of glucose across the cell membrane.

2,4-Dinitrophenol↗
PubMed1989

Electrophysiologic effects of a short-chain acyl carnitine, L-propionylcarnitine, on isolated canine Purkinje fibers.

The effects of L-propionylcarnitine (PC), a derivative of L-carnitine, on action potentials of canine Purkinje fibers in vitro, were studied under acidic conditions (pH 6.9), using conventional microelectrode techniques. The concentrations of 10(-5) M to 3 X 10(-3) M had no significant effect on action potential amplitude, maximal upstroke velocity of phase 0, and resting potential. However, higher concentrations of PC (10(-2) M and 3 X 10(-2) M) decreased some of these action potential parameters and such high concentrations of PC consistently prolonged the action potential duration (APD), most of which was attributed to the lengthening of phase 3. Under hypoxic conditions (PO2 less than or equal to 40 mm Hg) the drug (10(-2) M) also lengthened the APD with eventual cancellation of the hypoxia-induced shortening in the APD. The drug also prolonged the APD of slow response with a slight decrease in Vmax. In addition, PC significantly (p less than 0.05) depolarized the maximal diastolic potential of the fibers only at low [K+]o (less than or equal to 2.7 mM) and not at high [K+]o (greater than or equal to 5.4 mM). These observations suggest that the PC-induced prolongation of APD is, at least in part, due to a decrease in membrane K+ conductance, an effect partly shared with other amphiphilic intermediates of lipid metabolism, such as palmitylcarnitine or lysophosphatidylcholine.

Action Potentials↗
PubMed1989

Possible increases in potassium conductance by apamin in mammalian ventricular papillary muscles: a comparison with the effects on enzymatically isolated ventricular cells.

Apamin, a bee venom polypeptide, is reported to block the Ca2+-dependent K+ channel in smooth muscle, hepatocyte, and neuroblastoma cells. In embryonic chick hearts, it was found to block the Ca2+ channel. We report here that apamin (10(-9)-10(-7) M) hyperpolarizes the resting membrane potential and shortens the duration of the action potential (AP) in the fast response of adult guinea pig ventricular papillary muscles. This peptide also depresses the isoproterenol or Ba2+-induced slow response APs in the presence of high K+ (21.6 mM) Tyrode solution, without affecting the resting potential. The most striking effect of apamin on the slow response was to shorten the duration of AP with only slight decreases in the maximal rate of increase (Vmax) of the AP, a nonlinear measure of Ca2+ currents. These findings suggest that apamin increases membrane K+ conductance in the mammalian ventricular myocardium. However, in enzymatically isolated single ventricular cells and at wide range of concentrations (10(-7)-10(-11) M), apamin did not affect the AP configuration and did not alter the membrane Ca2+ or K+ current, perhaps because of a loss of apamin sensitivity secondary to enzymatic digestion of the tissue with collagenase.

Action Potentials↗
PubMed1989

Comparative positive inotropic effects of TA-064 (denopamine), a new cardiotonic agent, and isoproterenol and ouabain on guinea pig ventricular muscles.

The effects of TA-064 (TA) on "fast" and "slow" response action potentials and contractile tensions were studied in isolated guinea pig papillary muscles, and the findings were compared with those of isoproterenol (ISP) and ouabain. The results are as follows: (a) TA produced a dose-dependent (10(-7)-10(-5) M) increase in developed tension, with no significant changes in the resting membrane potential (RMP), action potential duration (APD), and maximum rate of rise of action potential (Vmax). (b) The concentration required to increase the developed tension by threefold ("equivalent concentration") were 10(-6) M with both TA and ouabain, while that of ISP was 5 x 10(-8) M. (c) TA increased the maximum rate of rise, dP/dtmax, and the maximum rate of fall, dR/dtmax, of the developed tension to the same extent, unlike those of ISP and ouabain. (d) Positive inotropic effects of TA (10(-7)-10(-5) M) were not completely abolished by atenolol (3.8 x 10(-5) M), a specific beta 1 blocker, whereas those of ISP were completely abolished. (e) The increasing effects of "equivalent concentration" of TA (10(-6) M) on the Vmax of the slow response were less than those of ISP (5 x 10(-8) M). These results suggest that the positive inotropic effects of TA are mainly due to stimulation of beta 1 adrenoceptors, but that the mode of action of the drug differs in several respects from that of ISP or ouabain.

Action Potentials↗