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Biomedical subjects

I Hisatome

Publications and source records attributed to I Hisatome.

115 records · Page 7Linked to original sources
PubMed1987

Estimation of catecholamine potencies on the myocardium by means of a new method.

A simple method is described for evaluating the potencies of catecholamines on the slow response of myocardium. Catecholamines depolarize guinea pig ventricular muscle cells exposed to the high K+ (27 mmol/l) Tyrode's solution containing 0.2 mmol/l Ba through an increase in slow channel conductance. Higher concentrations of catecholamines in addition induce spontaneous action potentials. This model was used to estimate and compare catecholamine potencies on myocardium. Catecholamine concentrations needed for depolarization alone or for depolarization plus automatic activity were taken as basis for comparison. The order of potency obtained by means of this new method was: l-isoproterenol greater than l-adrenaline greater than or equal to dl-noradrenaline greater than or equal to dobutamine greater than or equal to dopamine. This is similar to the order reported with other methods.

Action Potentials↗
PubMed1987

Complete atrioventricular block with a 22-month history of ocular sarcoidosis: a case report.

A 52-year-old woman with acute uveitis associated with ocular sarcoidosis developed complete atrioventricular block 22 months after the initial diagnosis was made. Cardiac sarcoidosis is a serious and, not infrequently, a fatal disease. Although it is difficult to establish the clinical diagnosis of cardiac sarcoidosis, a serial ECG is considered necessary in patients with any kind of sarcoidosis.

Cardiomyopathies↗
PubMed1986

Electrophysiological effect of trapidil on rabbit sinoatrial node cells.

Effects of trapidil on the membrane potentials and currents of rabbit sinoatrial node cells were investigated by means of conventional microelectrode and double microelectrode voltage clamp methods. Trapidil (1 X 10(-4) M) increased the spontaneous firing frequency, the maximum rate of rise, action potential amplitude and the slope of the pacemaker depolarization. Action potential duration was shortened by the drug application. Voltage clamp experiments showed that trapidil increased both the slow inward current (isi) and the potassium outward current (iK). Trapidil fastened the recovery time constant of isi, while the drug did not change the time course of the outward current tail. The hyperpolarization-activated current (ih) was also increased by the drug. The results obtained indicate that at relatively high concentration trapidil produces a positive chronotropic effect on the sinoatrial node cells by mediating an increase in isi, iK and ih.

Animals↗
PubMed1985

Effects of dilazep on the electrophysiological properties of rabbit sinoatrial node cells.

The electrophysiological effect of dilazep (1 X 10(-7) -3 X 10(-6) M), a coronary vasodilator, was examined on rabbit sinoatrial node cells using glass microelectrode and double microelectrode voltage clamp methods. Dilazep exerted a negative chronotropic effect and decreased the maximum rate of depolarization of the upstroke of the action potential and the amplitude of the action potential. The action potential duration at half-amplitude was prolonged after the drug perfusion. The voltage clamp experiment showed that dilazep reduced the slow inward current (Isi), the potassium outward current (IK), and the hyperpolarization-activated current (Ih). The recovery time constant of Isi was also prolonged. In conclusion, it is indicated that dilazep has no specific effect on the current system, but the drug depresses specifically the electrical activity of sinoatrial node cells.

Action Potentials↗
PubMed1985

Isoproterenol inhibits residual fast channel via stimulation of beta-adrenoceptors in guinea-pig ventricular muscle.

When perfused with high K+ (8.1 to 14.9 mM)-Tyrode's solution, the upstroke of action potentials in the isolated guinea-pig ventricular muscle is composed of two components and there are two separable peaks in the first derivative, i.e., Vmax, fast and Vmax, slow. The Vmax, fast was a measure of activation of the residual fast channel, while the Vmax, slow was that of the slow channel. Isoproterenol depressed Vmax, fast with increase in Vmax, slow, in a concentration-dependent manner (10(-8) to 10(-6) M). This depression of Vmax, fast was greater at more depolarized levels of membrane potential. Therefore, the isoproterenol-induced depression of Vmax, fast may be due to a negative shift of the curve relating Vmax, fast to the take-off potential (Em) (Vmax--Em relationship), along the voltage axis. The negative shift of Vmax--Em relationship by isoproterenol was also recognized in small preparations the size of which is well within the space constant. The negative shift was inhibited in the presence of beta-blockers (pindolol 1 microgram/ml or atenolol 10 micrograms/ml) but not by a calcium antagonist, 1-verapamil (1 microgram/ml). These results suggest that isoproterenol blocks sodium channels in the depolarized ventricular muscle via stimulation of the beta-adrenoceptors and that the depression of Vmax, fast is not mediated by the well-known effects of isoproterenol on Vmax, slow, i.e., increased influx of Ca2+ ions.

Action Potentials↗
PubMedDate not supplied

Responses of plasma catecholamines, renin-angiotensin-aldosterone system, and atrial natriuretic peptide to exercise in patients with essential hypertension.

Neurohormonal responses to exercise have not been studied fully in patients with essential hypertension (HT). This study determined if neurohormonal responses to exercise are altered between three subgroups of HT categorized by basal plasma renin activity (PRA). Plasma norepinephrine, epinephrine, atrial natriuretic peptide (ANP), PRA, angiotensin II (AII), and aldosterone were measured at rest and after submaximal treadmill exercise in 39 patients with essential HT (WHO classes I-II) and 13 controls. Patients with HT were divided into three subgroups based on the PRA level [low-renin (< 0.5) HT (n = 14), normal-renin (0.5-2.0) HT (n = 13), and high-renin (> 2.0) HT (n = 12)]. Patients with HT had higher blood pressure during exercise compared to controls, but blood pressure responses were similar among low-, normal-, and high-renin HT. Neurohormonal factors were comparable between all hypertensives and controls, except for higher plasma AII at rest in patients with HT. When neurohormones were compared among three subgroups of HT, plasma norepinephrine and epinephrine responses were similar. Patients with high-renin HT had higher PRA and AII, and lower ANP levels at rest and after exercise. In all hypertensives, negative correlations were observed between resting PRA and resting ANP (r = -0.41, p < 0.01), as well as peak PRA and peak ANP (r = -0.33, p < 0.05). Thus, neurohormonal responses to exercise varied with similar cardiac responses among subgroups of essential HT stratified according to renin levels. Patients with high-renin HT had augmented renin-angiotensin system activity with a decrease in ANP levels both at rest and after exercise. A reciprocal relationship between renin-angiotensin system activity and ANP was observed both at rest and after exercise in HT.

Adult↗