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Biomedical subjects

I Hisatome

Publications and source records attributed to I Hisatome.

At least 91 records · Page 5Linked to original sources
PubMed1992

Relation between serum uric acid and angiographically defined coronary artery disease in postmenopausal women.

Serum uric acid (UA) levels were studied in 40 postmenopausal women and 57 men, almost matched for age and body mass index (BMI) and undergoing coronary angiography. For women, the mean value of UA increased as the number of coronary arteries with > or = 50% stenosis increased. Its value was significantly higher (p < 0.05) in a three-vessel disease group than that of a group without stenosis. No significant changes were seen in men. However, the increase in UA for postmenopausal women was statistically (p < 0.05) correlated with serum triglyceride levels. Possibly, UA is not an independent coronary risk factor. However, elevated UA levels may suggest the prevalence of severe coronary artery stenosis for postmenopausal women.

Aged↗
PubMed1992

Serum levels of lipids and apolipoproteins in angiographically assessed coronary artery disease in Japanese patients.

Serum total cholesterol (T-CHO), triglyceride (TG), high density lipoprotein cholesterol (HDL-C) and apolipoproteins (apo A-I, A-II, B, C-II, C-III and E) values were determined in 143 Japanese subjects undergoing coronary angiography. Among the factors measured, T-CHO, TG, apo B and C-III levels were significantly higher in patients with coronary artery disease (CAD) than in those without CAD. The HDL-C/T-CHO ratio was also significantly lower in patients with CAD. Although no parameters show differences between the group without CAD and the group of single vessel disease, T-CHO and apo B were significantly higher in the groups with double and triple vessel disease, and TG and apo C-III were also higher in the group with triple vessel disease compared with the normal group. Furthermore, the HDL-C/T-CHO ratio was significantly lower in the double and triple vessel groups, and HDL-C was lower only in the triple vessel group. The results indicate that changes in these parameters suggest a high likelihood of multiple vessel disease, and that an increase in TG and apo C-III levels is also one of the important indicators for CAD even in Japanese patients.

Aged↗
PubMed1992

Disopyramide block of cardiac sodium current after removal of the fast inactivation process in guinea pig ventricular myocytes.

To determine the necessity of sodium channel fast inactivation for the block of sodium current (INa) by disopyramide, we studied the effects of disopyramide on INa in guinea pig ventricular myocytes treated with chloramine-T, which removes the fast component of INa inactivation. After exposure to chloramine-T (2 mM), INa amplitude was reduced at all voltages and INa decay was irreversibly prevented. Disopyramide (20 microM) produced both tonic block and use-dependent block of INa in chloramine-T-treated myocytes. Before treatment with chloramine-T, the time course of both the onset of and recovery from use-dependent block by disopyramide were best fit by the sum of double exponential functions, and the time constant of the slow phase of recovery increased as the membrane was hyperpolarized. After removal of the fast component of INa inactivation by chloramine-T, the fast phase of the onset block and the fast phase of recovery from block were abolished. However, the voltage dependency of the time course of recovery from block was unchanged. Thus, although the fast sodium inactivation process is not required for tonic and use-dependent block of INa by disopyramide, it contributes to the fast phase of block development and unbinding from use-dependent block.

Animals↗
PubMed1992

Cardiac neurosis: interactions between cardiac arrhythmias and symptoms using ambulatory ECG monitoring.

To investigate interactions between cardiac arrhythmias and subjective complaints and the background, ambulatory electrocardiographic (ECG) monitoring and a mental test [Cornell Medical Index (CMI)] were performed on 32 patients who complained of anxiety due to palpitation and/or tachycardic feelings without organic heart disease. The patients were classified into two groups according to the Holter ECG. In one group symptoms corresponded with cardiac arrhythmias (Group C; n = 15); and the other group lacked corresponding arrhythmias in spite of their significant symptoms (Group B; n = 17). From psychological view points, 65% of Group B and 40% of Group C patients showed grades III or IV of CMI tests, whereas only 5% showed grade III in normal volunteers (Group A; n = 20). Patients suffering symptoms without associated cardiac arrhythmias may have psychophysiologic backgrounds, at least in a part. It might be necessary in the treatment of these patients to pay attention to the factor of cardiac neurosis.

Adult↗
PubMed1991

Trimetazidine inhibits Na+,K(+)-ATPase activity, and overdrive hyperpolarization in guinea-pig ventricular muscles.

The effect of trimetazidine on Na+,K(+)-ATPase activity or the Na+,K+ pump was studied in guinea pig ventricular muscles with the use of biochemical and electrophysiological methods. The effect of trimetazidine on enzyme activity was compared with that in the liver, jejunum and kidney obtained from the same species. Na+,K(+)-ATPase activity in the heart and liver was significantly and concentration dependently decreased by trimetazidine (above 1.5 x 10(-5) M). Even the highest concentration (1.5 x 10(-4) M) of trimetazidine failed to decrease the Na+,K(+)-ATPase activity in the jejunum and kidney. The membrane potential was recorded in the ventricular muscle with a microelectrode. The hyperpolarization which followed 1-min overdrive stimulation (3.3 Hz) was decreased by trimetazidine (1.5 x 10(-4) M), but the depolarization during the stimulation was not affected by this drug. Ouabain, a potent Na+,K+ pump inhibitor, markedly decreased the overdrive hyperpolarization and increased the depolarization during the stimulation (10(-7), 5 x 10(-7), 10(-6) M). Therefore, the effect of trimetazidine and ouabain on the Na+,K+ pump-mediated alteration in the resting potential is different, suggesting that trimetazidine has additional direct membrane effects, e.g. a decrease in K+ conductance. In conclusion, trimetazidine inhibits Na+,K(+)-ATPase activity and thus the Na+,K+ pump in the ventricular muscles but with an inhibitory effect about 300 times less than that of ouabain. Trimetazidine inhibited the Na+,K(+)-ATPase in the liver as well, but not that in jejunum and kidney.

Animals↗
PubMed1991

Effects of aprindine on conduction velocity and Vmax in guinea-pig papillary muscles.

One of the effects of antiarrhythmic drugs is the reduction of conduction velocity. Cable theory predicts that there is a nonlinear relationship between conduction velocity and upstroke velocity (Vmax) of action potential. By using conventional microelectrode techniques, aprindine-induced reduction of Vmax of action potential and conduction velocity in guinea-pig papillary muscles were measured. Aprindine-produced, use-dependent, and concentration-dependent changes in conduction velocity and the decline of square of conduction velocity was well fit by a single exponential. Time constants for square of conduction velocity were comparable to simultaneously measured time constants for effects of Vmax. At a concentration of 1 to 10 microM aprindine, onset changes between Vmax and conduction velocity had a log-linear relationship in a predicted fashion. Whereas, in the recovery process from aprindine-induced depression, slow recovery time course of conduction velocity was observed. In conclusion, in the presence of aprindine, only onset block of conduction velocity can be analyzed quantitatively in the relationship to observation on Vmax in vitro. These results suggested that in the presence of aprindine, the recovery of internal conductance may be slower than that of Vmax.

Action Potentials↗
PubMed1991

Effect of urapidil on the action potentials in the guinea-pig ventricular myocardium.

The electrophysiological effects of urapidil, a new alpha 1-adrenoceptor antagonist, were assessed in the reserpinized guinea-pig ventricular myocardium. Urapidil suppressed the maximal rate of rise (Vmax) of steady-state action potentials elicited by the fast responses at high concentrations independently of blockade of myocardial alpha-adrenoceptors, but not the Vmax of Ca(2+)-dependent slow action potentials of partially depolarized muscles in concentrations tested (up to 1.1 mM). Urapidil at high concentrations prolonged the action potential durations of the fast and slow responses in a manner similar to the quinidine-like antiarrhythmic drugs. These results suggest that the inhibitory effect of urapidil on the slow inward Ca2+ current and the Na+ current is in practice negligible.

Action Potentials↗
PubMed1991

Aprindine blocks the sodium current in guinea-pig ventricular myocytes.

Aprindine is a class Ib antiarrhythmic agent. We studied effects of aprindine (3 mumol/l) on the Na+ current using whole cell voltage clamp (tip resistance = 0.5 M omega, [Na]i ando = 10 mmol/l at 18 degrees C). Aprindine revealed tonic block (Kdrest = 37.7 mumol/l, Kdi = 0.74 mumol/l; n = 4). Aprindine, shifted inactivation curve to hyperpolarizing direction by 11.4 +/- 3.5 mV (n = 4) without changes in slope factor. In the presence of 3 mumol/l aprindine, aprindine showed phasic block, i.e., duration-dependent block at 2 Hz (64% +/- 3% at 1.5 ms, 82% +/- 6% at 20 ms, 93% +/- 7% at 200 ms; n = 4). Short single prepulse also produced aprindine-induced phasic block (12% at 1.5 ms, 22% at 100 ms; n = 2). After removal of fast inactivation of Na+ current by 3 mmol/l tosylchloramide sodium, aprindine revealed phasic block, independent of holding potential. The recovery time constant from aprindine-induced phasic block was 4.8 s at holding potential = -100 mV and 5.0 s at holding potential = -140 mV. This use-dependent block of aprindine had pH dependency. Under acidic condition (pH 6.0), 3 mumol/l aprindine showed smaller use-dependent block (14% +/- 7% at 2 Hz; n = 4) comparing with either at pH 7.4 (68% +/- 13%; n = 4) or at pH 8.0 (90% +/- 12%; n = 4). The results suggest that aprindine could bind to the receptor via activation process through channel pore, resulting in decrease of Na+ current, and egress from the receptor through the lipid bilayer. These effects might be attenuated under acidic condition due to changes in intracellular ratio of charged to neutralized form of drug molecule.

Action Potentials↗
PubMed1991

Comparison of Ca2+ channel inhibitory effects of cibenzoline with verapamil on guinea-pig heart.

1. Cibenzoline, a class 1 antiarrhythmic drug, was studied on the effects upon the myocardial slow inward Ca2+ current (ICa) and the contractile force, and was compared with verapamil. 2. In voltage-clamp experiments with guinea-pig ventricular myocytes, cibenzoline caused a concentration-related inhibition of ICa (IC50 = 30 microM), whereas verapamil exerts a stronger effect (IC50 = 0.6 microM). 3. Cibenzoline also produced a concentration-related decrease in contractile force of isolated papillary muscle preparation (IC50 = 30 microM), while IC50 of verapamil was 0.8 microM. 4. Although the myocardial Ca2+ channel blocking effect of cibenzoline is about 1/50 compared to verapamil, cibenzoline possesses an inhibitory action on Ca2+ channel as well as on Na+ channel.

Animals↗
PubMed1991

The effect of TYB-3823, a new antiarrhythmic drug, on sodium current in isolated cardiac cells.

1. Sodium current (INa) blockade by TYB-3823, a newly synthesized antiarrhythmic agent, was investigated in isolated single ventricular myocytes by use of the whole cell patch-clamp technique. 2. TYB-3823 blocked INa under steady-state conditions (Kd,rest = 500 microM, Kd,i = 4.9 microM), findings consistent with a shift in the steady state INa availability curve to more negative potentials. 3. TYB-3823 produced use-dependent block at 2 Hz in conjunction with increase in pulse duration (5-300 ms), that was markedly enhanced at less negative holding potentials. 4. The time course of the onset of block was accelerated and the degree of use-dependent block was decreased at more negative holding potential. The time course of the onset of block was accentuated with enhancing block at more positive holding potentials. 5. The time course of recovery from use-dependent block was accelerated at more negative holding potentials but was accentuated at more positive holding potentials. 6. These results suggest that both tonic block and use-dependent block of sodium channels in cardiac tissue might result from an interaction of TYB-3832 with sodium channels mainly in the inactivated channel states and the kinetics of the interaction between drug and receptor may be modulated by the inactivation gate.

Animals↗
PubMed1991

Bunazosin, an alpha-adrenoceptor antagonist, blocks calcium current in guinea-pig ventricular myocytes.

1. Effect of bunazosin, an alpha 1-adrenoceptor antagonist, upon the slow inward Ca2+ current (ICa) was studied in single ventricular myocytes of the guinea-pig using a whole-cell patch-clamp technique. 2. Bunazosin (10-100 microM) decreased ICa in a concentration-dependent manner with an IC50 of 60 microM during depolarization to + 10 mV from the holding potential of -40 mV. 3. As for the inactivation process of ICa, the steady-state inactivation (f infinity) curve was shifted toward more negative potentials from -12 mV to -17 mV and -21 mV at f infinity = 0.5, by 30 microM and 70 microM bunazosin. 4. Inhibition of ICa by the compound (10 microM) was also dependent on stimulation frequency, with greater block induced at 2 Hz (50%) than at 0.33 Hz (13%). 5. It is concluded that bunazosin possesses a direct Ca2+ channel-blocking (class 4) action in a rate-dependent fashion.

Adrenergic alpha-Antagonists↗
PubMed1991

Clinical significance of hypouricemia in hospitalized patients.

Serum uric acid was measured in 586 normal subjects and 1,220 hospitalized patients. Hypouricemia was noted in 0.34% of the normal subjects and 2.54% of the hospitalized patients. Among hospitalized patients with hypouricemia, 22 were on medication, including allopurinol, anticancer drugs, antibiotics and glucocorticoids. Twenty-one patients had liver disorders and 11 of them had received transfusions. Neoplastic diseases were noted in 14 patients. Thus, hypouricemia was found to be relatively common in hospitalized patients, and seems to be caused mainly by medication, neoplastic diseases, liver disorders and transfusions.

Adolescent↗
PubMed1990

Bunazosin induces use-dependent slowing of conduction in guinea-pig ventricular myocardium.

The use-dependent effects of bunazosin on the maximal rate of rise (Vmax) of the action potential and conduction velocity were studied in isolated papillary muscles of guinea-pig. Standard microelectrode techniques were used to monitor the conduction and action potential of the muscles. In the presence of 30 microM bunazosin, the time constants for the start of the use-dependent inhibition of Vmax during a 0.2, 1, 2 and 3 Hz stimulation were (means +/- S.E.M. in s) 30.9 +/- 8.0, 15.0 +/- 1.6, 7.4 +/- 0.9 and 3.9 +/- 0.7 (n = 4) and those for conduction velocity were 17.3 +/- 2.3, 17.3 +/- 5.2, 6.5 +/- 0.9 and 3.4 +/- 0.2, respectively. These results showed that in the cardiac ventricular muscle of the guinea-pigs, bunazosin produces use-dependent changes in conduction velocity with onset kinetics comparable to those measured simultaneously using Vmax. The characteristics of the use-dependent inhibition of conduction velocity induced by bunazosin are similar to those found with slow kinetic drugs such as disopyramide rather than with fast ones.

Action Potentials↗
PubMed1990

Blocking effect of 1389-S on the sodium current in isolated guinea-pig ventricular myocytes.

Under whole cell patch conditions, 1389-S blocked the INa in guinea-pig ventricular myocytes under steady state conditions (Kdrest = 30 microM, Kdi = 2.4 microM) with a shift of the inactivation curve to the hyperpolarizing direction. Both brief and long conditioning pulses could produce a use-dependent block of 1389-S. These results suggest that 1389-S had a higher affinity to the inactivated than to the rested state under steady state conditions and had a higher affinity to the activated state during train pulses as well as to the inactivated state, making channels unavailable for conduction upon activation.

Animals↗
PubMed1990

An electrophysiological study of 9-amino-1,2,3,4-tetrahydroacridine (THA) on sino-atrial node preparations of rabbits.

1. The electrophysiological effect of 9-amino-1,2,3,4-tetrahydroacridine (THA) on the rabbit sino-atrial node was studied using double-microelectrode voltage clamp methods. 2. THA (above 10 microM) caused statistically significant decreases in the maximum rate of rise, the action potential amplitude, the rate of diastolic depolarization, and increases in the spontaneous cycle length, the action potential duration at 50% repolarization. 3. On the current systems, THA obviously depressed the time-dependent outward K+ current. The compound also decreased the slow inward Ca2+ current and the hyperpolarization-activated inward current. 4. These findings indicate that THA exerts an inhibitory action on the automaticity of sino-atrial node via effects on both outward and inward current systems.

Action Potentials↗