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Biomedical subjects

I Yamaguchi

Publications and source records attributed to I Yamaguchi.

At least 289 records · Page 16Linked to original sources
PubMed1983

Hypotensive and diuretic actions of diltiazem in spontaneously hypertensive and Wistar Kyoto rats.

We investigated the hypotensive and diuretic effects of diltiazem and hydralazine in conscious, spontaneously hypertensive rats (SHR) and their counterpart, Wistar Kyoto rats (WKY). Orally administered diltiazem induced dose-dependent hypotension both in SHR (10-60 mg/kg) and in WKY (30-100 mg/kg) and the effects were more pronounced in SHR than in WKY. Diltiazem did not cause tachycardia in either strain. Moreover, hypotensive doses of diltiazem acutely increased urinary excretion of sodium as well as urine volume in saline-loaded SHR and WKY. Chronic administration of diltiazem (30 mg/kg/day for 8 weeks) to young SHR caused no changes in body fluid distribution or in plasma sodium concentration. On the other hand, hydralazine not only showed almost the same hypotensive potency in SHR and WKY but also resulted reflex tachycardia in both strains. In addition, hydralazine (5 mg/kg) decreased urinary sodium excretion in saline-loaded SHR. In conclusion, it was suggested that diltiazem is an antihypertensive agent with an enhanced hypotensive action in the hypertensive state and without tachycardia and sodium retention effects.

Animals↗
PubMed1982

Cardiovascular changes in response to selective monoamine oxidase inhibition in the rat.

Chronic (21 days) treatment with the selective monoamine oxidase (MAO)-A inhibitor clorgyline, but not with the MAO-B inhibitor deprenyl in pithed rats leads to increased blood pressure responses to sympathetic stimulation and intravenous tyramine, and to elevated unstimulated heart rates. No significant changes are observed in plasma catecholamine responses to sympathetic stimulation, nor in beta-adrenoreceptor numbers in heart ventricles. These findings suggest that the hypotensive effects of MAO inhibitors result from central nervous system rather than peripheral nervous system alterations.

Animals↗
PubMed1982

A second zone of compensation during atrial premature stimulation: evidence for decremental conduction in the sinoatrial junction.

125 consecutive patients with premature atrial stimulation were studied. Three demonstrated sinus node return cycles that were fully compensatory following premature atrial stimuli delivered early in diastole. This second zone of compensation was unaccompanied by significant alterations in the post-return cycle lengths or in P-wave morphology of the return cycle. To account for the occurrence of a complete compensatory pause following very early premature atrial depolarizations, we consider the possibility that retrograde conduction of the early atrial premature depolarization (APD) in the sinoatrial junction was delayed for a sufficient length of time to allow the sinus node to depolarize spontaneously on schedule. Collision between the APD and sinus beat would then occur despite the marked prematurity of the APD. Thus, the early APD had encountered the relative refractory period of the sinoatrial junction, suggesting that decremental conduction takes place within the sinoatrial region in man. These findings imply that there is the potential for reentry in the region of the human sinoatrial junction.

Aged↗
PubMed1981

Mepacrine treatment prevents immobilization-induced desensitization of beta-adrenergic receptors in rat hypothalamus and brain stem.

Forced immobilization is a severe stress in rats which diminishes levels of epinephrine in specific nuclei in the hypothalamus and brain stem, suggesting that release of epinephrine is stimulated to a rate which exceeds the rate of its replacement. In the pineal gland, frog erythrocytes, C6 astrocytoma cells and rat brain, beta-adrenoceptor agonists appear to regulate the number of their receptors. Exposure to high concentrations of an agonist leads to apparent decrease in receptors reflected by a decrease in maximal specific binding of antagonists. The apparent decreases in receptors have been shown to be attended by decreases in physiologic responsiveness. In C6 astrocytoma cells, beta-agonists stimulate methylation of phosphatidylethanolamine to increase formation of membrane phosphatidylcholine which in turn appears to enhance activation of adenyl cyclase. Interference with the metabolism of phospholipids by exposure to phospholipase A2 inhibitor, mepacrine (quinacrine), prevents agonist-induced desensitization of beta-adrenoceptors in astrocytoma cells. In the present study repeated immobilization stress has been found to decrease significantly the number of beta-adrenoceptors in hypothalamus and brain stem while increasing the number of alpha 2-adrenoceptors. The desensitization of beta-adrenoceptors was prevented by treatment with mepacrine.

Animals↗
PubMed1981

Electrophysiological factors of left bundle-branch block.

Left bundle-branch block is rarely an isolated disorder of conduction, additional disorders being found in 29 of 30 patients studied by intracardiac stimulation techniques. These included disorders of sinus node function (prolonged maximum sinus node recovery time (corrected) in 23%, prolonged sinuatrial conduction time in three of eight patients), atrioventricular node function (prolonged AH interval in 33%, prolonged effective and functional refractory periods in 37% and 74%, respectively), "His bundle to right bundle branch" conduction (prolonged HV interval in 53%), and ventriculoatrial conduction (absent in 62%). It is postulated that at least half of the cases of left bundle-branch block were incomplete, even though the duration of the QRS complex exceeded 120 ms, because of (further) leftward deviation of the mean frontal QRS axis with sufficiently premature atrial extrastimuli. Block may be complete or incomplete in left bundle-branch block with left axis deviation of -30 degrees or more on the standard electrocardiogram.

Adult↗
PubMed1981

Adrenoceptor desensitization after immobilization stress or repeated injection of isoproterenol.

Immobilization stress (2.5 h daily) or repeated injection of isoproterenol (1 mg/kg, 3 times daily) for 1 wk caused a subsensitivity to the chronotropic and pressor effect of epinephrine in pithed rats. Propranolol (1 mg/kg) inhibited, to a greater extent in control than in immobilized rats, the chronotropic effect of epinephrine. The residual heart rates did not differ significantly among control, immobilized, and isoproterenol-treated rats. Practolol (1 mg/kg) but not butoxamine (5 mg/kg) mimicked the effect of propranolol. The subsensitivity in the blood pressure responses was not abolished by injection of either of the beta-adrenoceptor blockers. Butoxamine or propranolol shifted the epinephrine dose-blood pressure response curves to the left. The degree of shift was similar in control and immobilized or isoproterenol-treated rats. Daily injection of quinacrine (16 mg/kg), an antimalarial agent that inhibits phospholipase A2, blocked the subsensitivity to the chronotropic effect of epinephrine, but not that to the pressor effect of epinephrine. These observations suggest that immobilization stress causes desensitization of alpha- and beta 1-receptors but not beta 2-receptors. The mechanism of desensitization of beta 1-receptors by immobilization appears to be similar to that after isoproterenol treatment, possibly due to increased turnover of phospholipids.

Adrenergic beta-Antagonists↗
PubMed1981

[Effects of diltiazem on catecholamine release from cat adrenal glands (author's transl)].

Effects of diltiazem on catecholamine (CA) release evoked by several secretagogues were investigated in cat adrenal glands perfused in situ with Locke solution. All compounds were introduced into the perfusion medium. It was found that the release of CA stimulated by either acetylcholine (ACh) (10(-4) M) or high K+ (56 mM) was reduced by approximately 50 and 90% in the presence of 10(-5) and 10(-4) M diltiazem respectively, while diltiazem at 10(-6) M exhibited little or no influence on the Ca release. In addition, diltiazem at a concentration of 10(-6) M or higher produced a dose-related decrease in the CA release evoked by introduction of CaCl2 (2.2 mM) into Ca2+-free perfusion medium. On the other hand, removal of Na+ from the perfusion medium (osmolarity was adjusted with osmotically equal amount of sucrose) caused an increase in release of CA from the glands. Diltiazem (10(-5) M or higher) also reduced this CA release, but its activity was weaker than those found in experiments with ACh, high K+, and Ca2+. In all cases, the effects were reversible on washout. On the contrary, diltiazem, even at a higher concentration of 10(-4) M, exhibited no inhibitory effect on the release of CA induced by acetaldehyde (3 X 10(-3) M). It was suggested that diltiazem, through its Ca2+-antagonistic action, may reduce the evoked CA release which depends on extracellular Ca2+.

Acetylcholine↗
PubMed1981

Effect of GABA agonist and antagonists on cardiovascular and sympathetic responses in SHR and WKY rats.

Injection of muscimol (4 mg/kg, i.a.) to unanesthetized SHR rats reduced the arterial blood pressure and heart rate more than in WKY rats. These cardiovascular responses were accompanied by a moderate increase in plasma norepinephrine level and a marked increase in plasma epinephrine level, in the SHR rats. In the WKY rats, only a moderate increase in plasma epinephrine level was seen. Injection of subconvulsive doses of picrotoxin (2 mg/kg, i.a.) or bicuculline (1 mg/kg, i.a.) to SHR rats, elicited a higher and a more prolonged increase of the arterial blood pressure than in WKY rats. Plasma norepinephrine and epinephrine levels increased to the same extent in both the SHR and WKY rats following picrotoxin injection. These results suggest that the SHR rats differ from the WKY rats in the reactivity of GABAergic responses in cardiovascular centers which also modulate the peripheral sympathetic tone.

Animals↗