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Biomedical subjects

I Yamaguchi

Publications and source records attributed to I Yamaguchi.

At least 307 records · Page 17Linked to original sources
PubMed1981

Quinacrine-blocked desensitization of adrenoceptors after immobilization stress or repeated injection of isoproterenol in rats.

Repeated forced immobilization or repeated administration of isoproterenol reduces the number of beta adrenoceptors in the heart and spleen of rats. Isoproterenol, but not immobilization, reduced the number of beta receptors in the lung. These changes in beta adrenoceptors were prevented by administration of quinacrine, a phospholipase A2 inhibitor, although the drug had no effect on beta adrenoceptors when given alone. Immobilization, but not isoproterenol, reduced the number of alpha-1 adrenoceptors in the heart but had no effect on the lung. Quinacrine treatment decreased the number of alpha-1 receptors in heart and lung but increased alpha-2 receptors in the spleen. The changes in receptor number attending exposure to agonists are usually consistent with the expected changes. The effects of quinacrine on such changes suggest that phospholipids are involved in modulating the changes in number of receptors or their availability to interact with ligands.

Animals↗
PubMed1980

The electrophysiologic effects of intravenous lidocaine in the Wolff-Parkinson-White syndrome.

Twelve patients with the Wolff-Parkinson-White syndrome underwent electrophysiologic study, before and after the bolus intravenous administration of lidocaine, 1 mg./kg. There was no significant increase in the effective refractory period of the anterograde AV node pathway, the anterograde or retrograde accessory pathway, or the atrial or ventricular muscle; intravenous bolus administration of lidocaine is unlikely to terminate the re-entry tachycardias, or decrease the rate of the ventricular response in atrial fibrillation, in the WPW syndrome. There was no significant increase in the anterograde or retrograde AV conduction times; bolus administration of lidocaine is unlikely to decrease the rates of the re-entry tachycardias. In addition, lidocaine failed to alter significantly features related to tachycardia initiation. Except in isolated, unpredictable cases, intravenous bolus administration of lidocaine is not likely to be of benefit in the supraventricular tachyarrhythmias of the WPW syndrome.

Adolescent↗
PubMed1980

Blood pressure, plasma catecholamines, and sympathetic outflow in pithed SHR and WKY rats.

After destruction, by pithing, of the central nervous system, the blood pressure (BP) of the spontaneously hypertensive (SHR) rat falls, but remains higher than in the pithed normotensive (WKY) rat. At all ages examined, stimulation of the sympathetic outflow evoked greater increases in BP of pithed SHR rats, but the increases in plasma catecholamines were similar in the two strains. The BP increase evoked by administered norepinephrine was greater in old SHR than in old WKY rats, but this increased response was not found in young animals. Both young and old SHR rats, however, were more sensitive than WKY rats to the pressor effects of epinephrine. Results of selective pharmacologic blockade of cardiac or vascular beta-adrenoceptors suggest that a smaller vasodilator response in young SHR rats to the beta-adrenergic effects of epinephrine is responsible for the greater pressor response than in WKY rats. This factor diminishes in older SHR rats in which, as suggested by Folkow, structural changes in the resistance blood vessel diameter may account for the enhanced pressor responsivity of SHR rats.

Animals↗
PubMed1980

Plasma catecholamines in human and experimental hypertension.

Plasma levels of norepinephrine reflect the rate of its release from sympathetic nerves. In patients with hypertension and in spontaneously hypertensive (SHR) rats basal plasma NE levels are normal. SHR rats are abnormally reactive to stress, as are the normotensive (WKY) strain from which they were derived. The amounts of NE released by sympathetic stimulation are similar in pithed SHR and WKY rats, but SHR rats have greater blood pressure responses. This may be due to diminished beta-adrenoceptor-mediated vasodilation in young SHR rats and structural changes in arterioles of older SHR rats. It is concluded that in SHR rats separate abnormalities of centrally-mediated responses to stress and of peripheral sensitivity to catecholamines contribute to the development and maintenance of elevated blood pressure.

Aging↗
PubMed1980

Differential inhibiton of alpha-1 and alpha-2 adrenoceptor-mediated pressor responses in pithed rats.

The relative potencies of alpha adrenoceptor antagonists at pre- and postsynaptic receptors were assessed by comparing their effects on increments in plasma norepinephrine levels and blood pressure during stimulation of the sympathetic outflow from the spinal cord of pithed rats. Since increments in blood pressure are related to the logarithms of increases in plasma norepinephrine, the latter appear to reflect levels of the catecholamine at vascular alpha receptors. Phenoxybenzamine, dibenamine and chlorpromazine were found to block preferentially postsynaptic alpha receptors, phentolamine and tolazoline were nearly equipotent at pre- and postsynaptic receptors and mianserin and piperoxan were more potent inhibitors of presynaptic alpha receptors. Phenoxybenzamine and dibenamine were much more effective in blocking the pressor responses to sympathetic stimulation than administered norepinephrine. The opposite was true of mianserin and piperoxan, whereas phentolamine appeared to be about equipotent in blocking the pressor response to stimulation and norepinephrine. These results suggest that the pressor effects of administered norepinephrine is mediated by different receptors (alpha-2-type) than is the pressor response to stimulation of the sympathetic outflow which appears to be mediated by alpha-1-type adrenoceptors.

Adrenergic alpha-Antagonists↗
PubMed1979

The electrophysiologic effects of intravenous propranolol in the Wolff-Parkinson-White syndrome.

Fourteen patients with the Wolff-Parkinson-White (WPW) syndrome were studied by means of intracardiac stimulation techniques, before and after the intravenous administration of propranolol, 0.1 mg./Kg. There were no significant change, or only a slight increase, in the effective refractory periods of all parts of the re-entry tachycardia circuit studied, in either anterograde or retrograde directions. Re-entry tachycardia was initiated in nine patients in the control state, and in 10 patients after propranolol. The rate of re-entry atrioventricular node-accessory pathway tachycardia was decreased, but by only 10 per cent. The duration and outer limit of the tachycardia zone of atrial extrastimuli were not significantly decreased. Propranolol, by rapid intravenous infusion administration, is unlikely to be effective primary therapy for PSVT in the WPW syndrome.

Adolescent↗
PubMed1979

Electrophysiological actions of mexiletine on isolated rabbit atria and canine ventricular muscle and purkinje fibres.

The electrophysiological effects of varying concentrations of mexiletine on isolated rabbit sinus node and atrial preparations. Purkinje fibres, Purkinje-fibre-ventricular muscle junction and distal conduction system ('gate') were studied in oxygenated Tyrode solution at 35 degrees C using standard microelectrode techniques. 'Therapeutic' concentrations of mexiletine (0.5 to 2.0 micrograms.cm-3) had little effect on the atrial action potentials or on sinus node automaticity but sino-atrial conduction was delayed. In Purkinje fibres, these concentrations of the drug depressed the dV/dtmax of phase 0, conduction velocity and membrane responsiveness accompanied by significant shortening of the action potential duration and the effective refractory period, the change in the former always being greater than that in the latter. Mexiletine decreased antegrade as well as retrograde conduction at the Purkinje-fibre-ventricular muscle junction, while producing a uniform shortening of the action potential duration in the distal conduction system without a preferential effect at the 'gate'. The mechanisms of antiarrhythmic actions of mexiletine are thus complex but resemble those of lignocaine in superfused isolated cardiac muscle.

Action Potentials↗
PubMed1979

Plasma catecholamine and blood pressure responses to sympathetic stimulation in pithed rats.

Sympathetic stimulation in pithed rats elicits increases in blood pressure (BP) and plasma levels of catecholamines. The BP is proportional to the logarithm of the plasma norepinephrine (NE) concentration. Adrenal medullectomy diminishes slightly only the initial phase of the BP responses, whereas bretylium blocks completely the BP response and diminishes by about 70% the increase in plasma NE. Adrenal medullectomy completely prevents the increase in plasma epinephrine (Epi) and diminishes by 30% plasma NE. Plasma levels of NE appear to reflect sympathetic neuronal activity, but the NE at sympathetic nerve endings is responsible for the increase in BP. Epi released from the adrenal medulla may enhance and accelerate the initial BP response, but plays only a minor role after the first 15 s.

Adrenal Medulla↗
PubMed1979

[Hypotensive effects of diltiazem hydrochloride in the normotensive, spontaneously hypertensive and renal hypertensive rats (author's transl)].

In conscious and anesthetized normotensive rats, intravenous administration of diltiazem (0.1--3 mg/kg) produced a dose-related decrease in blood pressure. Administration of diltiazem (1--50 mg/kg) into the duodenum of anesthetized rats also reduced the blood pressure in a dose related manner. In parallel with the change in blood pressure, the heart rate increased in conscious rats and decreased in anesthetized animals. Such an increase in the heart rate was suppressed by pretreatment with propranolol. Similarly, in conscious spontaneously hypertensive rats (SHR), diltiazem dose-dependently decreased the blood pressure and increased the heart rate after intravenous administration (0.03--1 mg/kg). Oral administration of diltiazem (100 mg/kg) also reduced the blood pressure of SHR. In addition, the progressive increase in blood pressure in young SHR was significantly suppressed by chronic oral administration of diltiazem (30 mg/kg). The blood pressure in conscious renal hypertensive rats was also decreased with diltiazem (50 mg/kg p.o.). On the other hand, it was demonstrated that the pressor responses to norepinephrine and angiotensin II in the anesthetized normotensive rats were non-competitively inhibited by intravenous administration of diltiazem at a dose which had no effect on the blood pressure.

Angiotensin II↗
PubMed1979

Effect of diltiazem on insulin secretion. II. Experiments on perfused rat pancreas, anesthetized dogs and conscious rats.

Effect of diltiazem on insulin secretion was investigated in the perfused rat pancreas. Experiments were also carried out in anesthetized dogs and conscious rats with and without glucose loading. In the perfused rat pancreas, diltiazem reduced both glucose- and tolbutamide-induced insulin secretion and these effects of diltiazem were reversed with removal of the compound. Inhibition of the glucose-induced insulin secretion caused by diltiazem was counteracted by increasing the concentration of calcium ion. In experiments on intact animals, diltiazem at vasoactive doses produced no significant influence on the basal level of plasma insulin or glucose-induced insulin secretion. These data taken together with findings in previously reported work suggest that diltiazem reduces insulin secretion from pancreatic B-cells in vitro possibly by the calcium-antagonistic property, while the compound exhibits practically no inhibitory action on the insulin secretion in vivo.

Anesthesia↗