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Biomedical subjects

I Hisatome

Publications and source records attributed to I Hisatome.

At least 109 records · Page 6Linked to original sources
PubMed1990

Inhibitory effect of 9-amino-1,2,3,4-tetrahydroacridine (THA) on the potassium current of rabbit sinoatrial node.

STUDY OBJECTIVE - To examine the effect of 9-amino-1,2,3,4-tetrahydroacridine (THA), a compound similar to the K+ blocker 4-aminopyridine, on potassium channels in the sinoatrial node. DESIGN - The pacemaking portion of rabbit sinoatrial nodes was studied using the double microelectrode voltage clamp method in the presence of THA at various concentrations. MEASUREMENTS AND RESULTS - Above 1 mumol.litre-1, THA prolonged the spontaneous cycle length and the transmembrane action potential duration at 50% repolarisation. Above 10 mumol.litre-1, the compound also decreased the maximum rate of rise, the action potential amplitude, and the rate of diastolic depolarisation. Under voltage clamp conditions, THA reduced the time dependent K+ current (IK) in a dose dependent manner. Neither the decay process of IK nor its activation process were altered by THA. CONCLUSIONS - THA depresses sinoatrial node IK without changing its kinetics. Thus it may inhibit the open state of the potassium channels.

Alzheimer Disease↗
PubMed1990

Use-dependent effects of pirmenol on Vmax and conduction in guinea-pig ventricular myocardium.

1. The use-dependent effects of pirmenol, a new antiarrhythmic drug, on the maximal rate of rise (Vmax) of the action potential, conduction velocity, and their corresponding recovery kinetics were studied in isolated papillary muscles of guinea-pig. Standard microelectrode techniques were used to monitor the conduction and action potential characteristics of the muscles. 2. Pirmenol decreased Vmax and the overshoot of action potentials in a dose-dependent fashion. Also, doses of pirmenol greater than 1 mM abolished the generation of action potentials. Low concentrations of pirmenol (3 and 10 microM) prolonged the action potential duration, while concentrations greater than 0.1 mM shortened it markedly. 3. The resting block of Vmax in the presence of 10 and 30 microM pirmenol was 9.48 +/- 3.12 and 20.36 +/- 3.61%, and that of conduction velocity 2.87 +/- 1.52 and 6.58 +/- 2.09%, respectively. 4. The degree of use-dependent block induced by 10 and 30 microM pirmenol during 0.2, 1, 2 and 3 Hz stimulations was dose- and rate-dependent. 5. In the presence of 30 microM pirmenol, mean values of time constants for the onset of the use-dependent inhibition of Vmax and conduction velocity during a 2 Hz stimulation were 1.32 +/- 0.15 and 1.28 +/- 0.09 s, respectively. The recovery time constants averaged 15.83 +/- 2.14 (for Vmax) and 27.80 +/- 8.74 (for conduction velocity) s in the presence of 30 microM pirmenol. 6. These results showed that the characteristics of the use-dependent inhibition of Vmax and conduction velocity induced by pirmenol are similar to those of slow kinetic drugs such as disopyramide rather than of fast ones.

Action Potentials↗
PubMed1990

Effect of pinacidil on the electrophysiological properties in guinea-pig papillary muscle and rabbit sino-atrial node.

The electrophysiological effect of the antihypertensive drug pinacidil has been examined in preparations of guinea-pig papillary muscle and rabbit sino-atrial node using a standard microelectrode method. In papillary muscle preparations, pinacidil (greater than 30 microM) shortened the action potential duration (APD), whereas it did not affect the maximum rate of rise (Vmax). Pinacidil (greater than 1 microM) also decreased APD of slow action potentials evoked by high K+ (27 mM) solution containing 0.2 mM Ba2+. At 30 microM, the drug reduced the Vmax of slow action potentials. In the spontaneously beating sino-atrial node, pinacidil (greater than 30 microM) shortened APD. At 100 microM, it also decreased the heart rate, Vmax, action potential amplitude and the rate of diastolic depolarization. It is concluded that pinacidil modifies the electrical activity of myocardial cells probably due to an increase in the potassium conductance although in high concentrations the compound might also reduce Ca2+ influx through the cell membrane, which would contribute to an obvious negative chronotropic action.

Action Potentials↗
PubMed1990

Excess purine degradation caused by an imbalance in the supply of adenosine triphosphate in patients with congestive heart failure.

To evaluate purine degradation in patients with congestive heart failure concentrations of serum hypoxanthine, lactate, and noradrenaline were measured before and after submaximal treadmill exercise in 12 patients with chronic congestive heart failure and nine healthy volunteers. In four patients the concentration of hypoxanthine was significantly higher than in the controls or in the remaining eight patients with congestive heart failure. Venous lactate and noradrenaline in the four patients with high concentrations of hypoxanthine were also significantly higher than those in the eight patients with normal concentrations of hypoxanthine. Patients who responded normally were also more likely to have been treated with vasodilators and angiotensin converting enzyme inhibitors. Exercise induced arrhythmias were more common in the patients with high concentrations of hypoxanthine. These results suggest that the excess purine degradation in patients with congestive heart failure might be the result of a "relative" disturbance in the supply of adenosine triphosphate caused by the shift of cellular metabolism from aerobic glycolysis to anaerobic glycolysis during submaximal exercise and that hypoxanthine (a substrate for xanthine oxidase and a source of free radicals) was increased after submaximal exercise in some patients with congestive heart failure.

Adenosine Triphosphate↗
PubMed1990

Acetylcholine-sensitive potassium channels in human atrial myocytes.

Single channel recording techniques were used to study acetylcholine (ACh)-sensitive K+ channel activity in human atrial myocytes isolated from specimens obtained during corrective cardiac surgery. Under conditions of cell-attached patch, the presence of ACh in the patch pipette activated K+ channels. Single channel activity occurred in periodic bursts. The channels exhibited a slope conductance of 46 +/- 2 pS inwardly (means +/- SD, n = 4). During a burst, both open and closed time histograms were fitted by a single exponential curve, suggesting the existence of one open and one closed state during a burst. Open probability increased directly with ACh concentration without affecting open time. The channel could be activated by GTP and guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S) (in the presence and absence of ACh in the pipette, respectively). Slope conductance, the response to GTP and GTP gamma S, and the independence of activation from Ca2+ were similar to those for other species. In contrast, sensitivity to ACh appeared diminished compared with frog atrial myocytes.

Acetylcholine↗
PubMed1989

Hypouricaemia with acute viral hepatitis.

We report five female cases of hypouricaemia accompanied by acute viral hepatitis (serum urate 101 +/- 12 mumol/l, mean +/- SD). Their urate clearance was increased to 14.2 +/- 3.4 ml/min during hyperbilirubinaemia but 24-h urate excretion was not elevated (2.09 +/- 0.64 mmol/24 h). No other renal tubular abnormalities were detected. Comparing urate metabolism with that of four cases of inborn renal hypouricaemia, the degree of uricosuria was lower. One patient showed elevation of serum and urinary oxypurine, which normalized with return of a normal blood uric acid level. In all cases, the serum urate returned to normal after improvement of liver function. We suggest that renal uricosuria due to an isolated renal defect of urate transport might contribute to hypouricaemia in these cases but that inhibition of xanthine oxidase activity might also contribute to this phenomenon.

Acute Disease↗
PubMed1989

Effect of bile acid on electrophysiological properties of rabbit sino-atrial node in vitro.

1 In order to examine the action of bile acid on cardiac pacemaker activity, the effect of sodium taurocholate (NTC) was studied on the membrane potential and current of rabbit sino-atrial node preparations by means of a double microelectrode voltage clamp technique. 2 In spontaneously beating sino-atrial node preparations, NTC (above 30 microM) decreased the maximum rate of rise of the action potential. Above 100 microM, the compound also exerted a bradycardiac effect and decreased the rate of diastolic depolarization significantly. 3 On the current systems, NTC produced dose-related decreases in the slow inward Ca2+ current and the time-dependent outward K+ current. 4 It is concluded that NTC depresses the spontaneous discharge of the sino-atrial node through decreases in both inward and outward current systems.

Animals↗
PubMed1989

Membrane actions of ethanol on rabbit sino-atrial node studied by voltage clamp method.

Electrophysiological effects of ethanol on rabbit sino-atrial node were studied by means of the double-microelectrode voltage clamp method. In spontaneously beating preparations, ethanol (above 1%) decreased the maximum rate of depolarization of the action potential. Furthermore, 3% ethanol produced a significant decrease in the action potential amplitude, the action potential duration at 50% repolarization and the rate of the diastolic depolarization. Of the current systems, voltage clamp studies showed that ethanol reduced the slow inward current, the time-dependent potassium outward current and the hyperpolarization activated inward current. These observations indicate that ethanol does not have an effect on a single current system, but directly modifies the spontaneous discharge of sino-atrial node pacemaker cells due to a reduction of the time-dependent current systems.

Action Potentials↗
PubMed1989

Effects of trimebutine maleate on electrical activities of isolated mammalian cardiac preparations.

The effects of trimebutine maleate on electrical activity in guinea-pig isolated papillary muscles and rabbit sino-atrial nodes have been studied by means of a standard microelectrode method. In papillary muscles, trimebutine (above 10 microM) decreased the maximum rate of rise (Vmax) and the action potential duration at 90% repolarization (APD90), whereas the resting potential was not significantly altered. As to a decrease in Vmax, trimebutine produced a negative shift of the curve relating Vmax to the resting potential along the voltage axis. Trimebutine also depressed the slow action potentials of papillary muscles produced by 27 mM K and 0.2 mM Ba. In spontaneously beating sino-atrial node preparations, trimebutine (above 10 microM) decreased the heart rate, Vmax and the rate of diastolic depolarization. These results indicate that trimebutine maleate possesses a depressant action on the electrical activities of the fast- and slow-response fibres of the heart mainly due to inhibitions of both fast Na+ and slow Ca2+ channels.

Action Potentials↗
PubMed1989

Cause of persistent hypouricemia in outpatients.

We measured serum urate in 3,258 Japanese outpatients. Five of them had persistent hypouricemia. Three also had microhematuria. Four of the five patients were proven to have renal uricosuria with hypouricemia, but otherwise normal tubular function. When tested with both pyrazinamide and benzbromarone, 1 patient had a presecretory reabsorption defect, 2 had postabsorption defects, and 1 an enhanced renal tubular secretion of urate. These results suggest that persistent hypouricemia in outpatients is of very low incidence, is usually caused by an isolated metabolic error of urate transport, and is not related to drug ingestion or systemic disease.

Benzbromarone↗
PubMed1989

Differences in urate metabolism between normouricemia and hyperuricemia in coronary heart disease in man.

We examined hyperuricemia in patients with coronary heart disease. In 85 patients with coronary sclerosis confirmed by coronary angiography, the serum urate level (6.08 +/- 1.60 mg/dL) was not different from that in subjects with normal coronary arteries (6.47 +/- 1.69 mg/dL). The incidence of hyperuricemia in patients with coronary sclerosis was 26%, and was significantly correlated with diuretics, obesity and hypertriglyceridemia, but not with hypertension or hypercholesterolemia. To elucidate the mechanism of urate metabolism in coronary sclerosis, we separated coronary sclerosis patients without complicating factors into hyperuricemics and normouricemics, and studied urate metabolism in comparison with subjects with normal coronary arteries. We found that normouricemics with coronary sclerosis had decreases in the filtered urate load and urate clearance with a normal urate-creatinine clearance ratio. Hyperuricemics with coronary sclerosis had decreases in urate clearance and urate-creatinine clearance ratios, but the filtered urate load was similar to that in normouricemics. It is suggested that in coronary sclerosis patients, normouricemics had a low glomerular filtration of urate with normal tubular urate transport, whereas hyperuricemics had enhanced tubular reabsorption of urate without any difference of urate filtration from normouricemics.

Coronary Disease↗
PubMed1988

Comparative study of the block of Vmax by aprindine and quinidine in the guinea-pig heart muscle.

The depression of Vmax of the action potential in guinea-pig ventricular muscle by aprindine and quanidine was compared. Aprindine caused a more pronounced rate-dependent block (Kd = 10(-6) M at 3.3 Hz) than did quinidine (Kd = 1.6 X 10(-5) M at 3.3 Hz). Aprindine shifted the relationship between Vmax and resting potential to a more negative potential (mean 9.2 mV: 10 microM) than did quinidine (mean 5.7 mV: 10 microM). In addition, aprindine caused a more pronounced resting block (Kd = 1.3 X 10(-5) M) than quinidine (Kd = 8.6 X 10(-5) M). It is concluded that aprindine has a higher affinity for activated and/or inactivated and resting state channels than quinidine, making channels unavailable for conduction upon activation.

Action Potentials↗
PubMed1988

Renal hypouricemia due to an isolated renal defect of urate transport.

A 22-year-old man was found to have low serum urate concentration (1.1-1.7 mg/dl). His urate clearance was markedly increased (26.9-35.5 ml/min) and was not decreased after administration of pyrazinamide, but was even more increased after administration of benzbromarone. No other renal tubular abnormalities were detected. The young man has one sister and two brothers. His sister also has hypouricemia and hyperuricosuria. We suggest that the present case had a genetically determined renal abnormality affecting tubular presecretory reabsorption of urate.

Adult↗
PubMed1988

Inotropic effect of thyrotropin-releasing hormone on the guinea pig myocardium.

The inotropic effect of the physiological level of TRH on isolated guinea pig cardiac muscle was studied using a force transducer and standard microelectrode techniques. TRH increased the contractile force of muscles dose-dependently without changing the time course of contraction in normal Tyrode and a high K+ (27 mM) solution. The positive inotropic effect of TRH was associated with an augmentation of slow action potentials in high K+ solution and was reduced in the presence of diltiazem, verapamil, and manganese. TRH potentiated the response of contractile force to increasing extracellular Ca2+ concentration. The inotropic effect of TRH was suppressed by metoclopramide, phentolamine, and cimetidine, but was not affected by propranolol. TRH increased the contractile force even in the myocardium of reserpinized guinea pig. It is suggested that TRH has a positive inotropic effect at least partly due to an increase in the slow inward Ca2+ current.

Action Potentials↗
PubMed1987

Inhibitory action of 711389-S on the electrical activity of rabbit sinoatrial node.

The effects of 711389-S (0.1-10 mumol.litre-1) on membrane potentials and currents of rabbit sinoatrial node preparations were studied using a conventional double microelectrode voltage-clamp method. The agent 711389-S decreased the heart rate, the maximum rate of depolarisation, and the amplitude of the action potential and increased the action potential duration in a dose dependent manner. The slope of the diastolic depolarisation was also reduced. Of the current systems of sinoatrial node, 711389-S depressed the slow inward current (Isi), the potassium outward current (IK), and the hyperpolarisation activated current (Ih) dose dependently. The kinetics of IK were not altered significantly by the drug. It is concluded that 711389-S does not have an effect on a single current system but that the drug exerts a depressant effect on the electrical activity of the sinoatrial node.

Animals↗
PubMed1987

A case of four coronary artery fistulae originating from three vessels associated with aneurysm.

A case of an aneurysm associated with four coronary artery fistulae originating from three vessels is reported. The patient, a 52-year-old woman, had chest heaviness and palpitations. Coronary arteriography revealed the four fistulae originating from three coronary vessels with an aneurysm draining into the left ventricle and the main pulmonary artery. The patient's symptoms were relieved after fistulectomy and the aneurysmectomy, suggesting that a coronary steal phenomenon through the fistulae was the cause of her symptoms. This case is of interest because of its rarity, since this is the first case report of an aneurysm associated with four coronary artery fistulae from three vessels.

Arterio-Arterial Fistula↗