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Biomedical subjects

Y Abiko

Publications and source records attributed to Y Abiko.

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

Effects of coronary dilators on segmental forces in normal and ischemic regions of the canine left ventricular wall.

Changes in segmental forces of contraction (determined by a strain gauge arch) in non-ischemic (normal) and ischemic regions of the same left ventricular wall were studied in dogs anesthetized with morphine and pentobarbital. A branch of the left anterior descending coronary artery was completely occluded, and 10 min after occlusion coronary dilators were injected intravenously. The results can be summarized as follows. 1) Coronary occlusion markedly reduced the segmental force of contraction in the ischemic region, while it did not affect that in the normal region. Heart rate did not change markedly after coronary occlusion. 2) Either nitroglycerin (100 microgram/kg) or sodium nitrite (2.5 mg/kg) increased heart rate, and it also increased segmental force of contraction in the normal region while it decreased that in the ischemic region. 3) Papaverine (1 mg/kg) increased heart rate and segmental forces of contraction in both normal and ischemic regions. 4) Dipyridamole (250 microgram/kg) slightly increased heart rate, and it also increased segmental force of contraction in the normal region but not in the ischemic region.

Animals↗
PubMed1981

Hypotensive effect of labetalol on intraocular pressure in rabbits: in relation to its alpha- and beta-adrenergic blocking action on the cardiovascular system.

Rabbits anesthetized with urethane were used. Labetalol was found to be about 3.7 times less potent than phentolamine in blocking phenylephrine-induced vasopressor response, and about 7.6 times less potent than propranolol in blocking isoproterenol-induced vasodepressor response. Labetalol (0.3, 1.0 and 2.5 mg/kg, i.v.) decreased both intraocular pressure (IOP) and mean arterial blood pressure (BP) significantly, and also decreased IOP/BP ratio. Propranolol (1.0 and 2.5 mg/kg, i.v.) reduced both IOP and BP slightly without affecting the IOP/BP ratio. Phentolamine (1.0 mg/kg, i.v.) reduced both IOP and BP significantly, but it did not alter the IOP/BP ratio. When both propranolol (1.0 mg/kg, i.v.) and phentolamine (1.0 mg/kg, i.v.) were injected at the same time, IOP and BP were reduced with a decrease in IOP/BP ratio. These findings suggest that labetalol is effective in decreasing the IOP, although the mechanism of the drug action cannot be explained simply by alpha- and beta-adrenergic blockade.

Animals↗
PubMed1981

Effect of dilazep on shape change of human erythrocyte in blood stored over a period of 42 days.

The influence of addition of 1,4-[3,4,5-trimethoxybenzoyl-oxy)-propyl]-perhydro-1,4-diazepine dihydrochloride monohydrate (dilazep) on shape change of erythrocyte that had been stored in CPD-solution for 3--42 days at 4 degrees C, was studied by the use of a scanning electron microscope. The results obtained are as follows: 1. The discocyte-echinocyte transformation of erythrocyte occurred in blood stored at 4 degrees C for more than 3 days (cold-stored blood). 2. Dilazep (25 and 50 mumol/l) had no remarkable effect on the discocyte-echinocyte transformation of erythrocyte in the cold-stored blood). 3. Dilazep (100--500 mumol/l) slowed down the appearance of echinocyte and inhibited the transformation of erythrocyte in the cold-stored blood.

Azepines↗
PubMed1980

Increase of myocardial pH by 1- and d-propranolol during ischemia of the heart in dogs.

Myocardial pH was measured continuously with a micro pH electrode inserted into the left ventricular wall in dogs. Anterior descending coronary flow was reduced to about 1/3 of the original flow by partial occlusion of the coronary artery. Myocardial pH decreased from 7.50--7.60 to 7.06--7.24 after partial occlusion. Drugs were injected intravenously during ischemia of the heart caused by partial occlusion. l-Propranolol (1 mg/kg) reduced heart rate and increased the pH from 7.06 +/- 0.04 to 7.48 +/- 0.04 (P less than 0.01). d-Propranolol (1 mg/kg) reduced heart non-significantly and increased the pH from 7.24 +/- 0.05 TO 7.56 +/- 0.05 significantly (P less than 0.05). In other studies, the effect of l- and d-propranolol on both heart rate and metabolic responses to isoproterenol (500 micrograms/kg i.p.) was studied. Isoproterenol increased heart rate and also elevated the blood levels of glucose and lactate. l-Propranolol inhibited these responses to isoproterenol. d-Propranolol did not inhibit the heart rate response but inhibited the blood lactate response to isoproterenol significantly. The blood glucose response to isoproterenol was inhibited by d-propranolol non-significantly. The action of both l- and d-propranolol on ischemic myocardial pH may be related to their action on cardiac metabolism as well as to their local anesthetic action.

Anesthesia, Local↗
PubMed1980

[Effects of labetalol on the circulatory system (author's transl)].

Effects of labetalol on the cardiovascular system were studied in dogs, guinea pigs, rats, rabbits, and bullfrogs. In dogs anesthetized with pentobarbital, labetalol decreased heart rate, arterial blood pressure, and myocardial contractile force, and inhibited carotid sinus reflex, without affecting pO2 and pH of circulating blood, urine volume, and urinary excretion of sodium and potassium. Alpha- and beta-adrenergic blocking action of labetalol was demonstrated in dog hearts, arterial preparations of guinea pigs and rats, isolated rabbit hearts, and bullfrog hind limb and rabbit ear preparations. In bullfrog hind limb and rabbit ear preparations, labetalol dilated blood vessels in concentrations larger than those which produced alpha- and beta-adrenergic blockade. The dilatation of blood vessels was observed only when labetalol was added to the perfusate, whereas alpha- and beta-adrenergic blockade continued even after removal of labetalol from the perfusate. It is concluded that labetalol blocks alpha- and beta-adrenergic receptors in the heart and blood vessels of the species used herein, and that this compound inhibits carotid sinus reflex in dogs. In addition, the dilatation of the blood vessels of the bullfrog hind limb and rabbit ear as evoked by labetalol probably involves a mechanism different from that of adrenergic blockade.

Adrenergic alpha-Antagonists↗
PubMed1980

[The effect of atenolol on the cardiovascular system (author's transl)].

Effects of atenolol on the cardiovascular system were studied in rats and dogs. Atenolol (10 microgram/kg - 3 mg/kg) did not increase heart rate significantly in rats pretreated with reserpine (5 mg/kg), while a significant increase occurred with practolol (30 microgram/kg - 3 mg/kg). Atenolol (100 microgram/kg) inhibited the response of canine heart (heart rate and myocardial contractile force) to isoproterenol to a similar degree as seen with propranolol (100 microgram/kg) did. The ability of atenolol to inhibit vasodilating action of isoproterenol, however, was about 1/12 of that of propranolol. Atenolol (0.5 mg/kg) did not inhibit hemodynamic responses to ouabain and CaCl2 in dogs, while this drug inhibited these responses to isoproterenol. Atenolol decreased heart rate, myocardial contractile force, left ventricular pressure, and rate of rise of the left ventricular pressure (dp/dt LV max) dose-dependently. Atenolol (1 mg/kg) decreased coronary venous outflow and myocardial oxygen consumption in dogs, but did not alter the myocardium to a more reduced state, as determined by coronary arterial and venous lactate and pyruvate levels. These results confirmed that atenolol is a potent cardioselective beta-blocker devoid of intrinsic sympathomimetic action. The results also suggest that atenolol inhibits cardiac function without disturbing the intracellular redox state of the myocardium.

Adrenergic beta-Antagonists↗
PubMed1980

[Atenolol, its cardioselective property for adrenergic beta-receptor blocking action and effect on the cardiac function (author's transl)].

Cardioselective property of the beta-adrenoceptor blocking action of atenolol and its effect on the AV conduction, the atrial muscle refractory period and the cardiac contractility were studied in comparison with these of propranolol. A ratio of pA2 values obtained in the isolated right-atrial preparations and the isolated tracheal preparations of guinea pigs demonstrated that atenolol was highly cardioselective, while propranolol was non-selective. This cardioselective property of atenolol was confirmed in in vivo experiments using guinea pigs. Atenolol increased the AV conduction time and decreased the cardiac contractility dose-dependently in anesthetized dogs of which the heart was electrically driven at fixed rates. At 140 beats/min, AV block was observed at 10 mg/kg, i.v. in 3 of 8 dogs, and further increase in a dose ti 30 mg/kg resulted in acute heart failure in one of remaining 5 dogs, while propranolol, though showing a tendency to be less potent in depressing AV conduction in a dose range less than 0.3 mg/kg, produced a state of heart failure in 2 of 5 dogs at 3 mg/kg, i.v. and AV block in all of the remainder at 10 mg/kg, i.v. Functional refractory period of AV node as well as functional and effective refractory period the the atrial muscle were increased dose-dependently by atenolol and propranolol. There were no significant differences between both drugs regarding these effects. Further increase in a pacing rate to 160 and 180 beats/min augmented the depressing effect of both drugs on the AV conduction.

Adrenergic beta-Antagonists↗
PubMed1980

Effect of niludipine on ischemic myocardial metabolism in the dog.

The effect of pretreatment with 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridine carbonic acid-bis(2-propoxyethyl) ester (niludipine, Bay a 7168) (10 microgram/kg i.v.) on myocardial metabolic response to coronary artery ligation was studied in dogs anesthetized with pentobarbital. The results are summarized as follows: 1. Bay a 7168 lowered systolic and diastolic blood pressures markedly, and decreased heart rate slightly. 2. Bay a 7168 increased the endo- and epicardial phosphorylase activity significantly. 3. Bay a 7168 increased the endo- and epicardial ATP levels significantly. 4. Coronary artery ligation increased the endo- and epicardial activity of phosphorylase and decreased the endo- and epicardial glycogen levels. 5. In the presence of Bay a 7168, acceleration of glycogenolysis being caused by coronary artery ligation, was not detected. 6. Changes in the levels of myocardial carbohydrate intermediates being caused by coronary artery ligation, were not modified by pretreatment with Bay a 7168.

Adenosine Triphosphate↗
PubMed1979

Mode of action of ticlopidine in inhibition of platelet aggregation in the rat.

Ticlopidine, when orally administered to rats, resulted in activation of basal and prostaglandin E1 (PGE1)-stimulated adenylate cylase activity through increase in affinity of the cyclase in platelet membrane to PGE1, although it failed to affect adenosine- or sodium fluoride-stimulated activity of the enzyme. In washed platelets, Ticlopidine also activated basal and PGE1-stimulated activity of the cyclase and prevented reduction in the cyclase activity caused by low concentrations of PGE2. Furthermore, Ticlopidine inhibited malondialdehyde formation in platelets induced by thrombin but failed to inhibit that caused by exogenous arachidonic acid. Adenosine 3',5'-cyclic monophosphate (c-AMP): phosphodiesterase activity of platelet lysate was not significantly affected by Ticlopidine treatment. These findings indicate that Ticlopidine inhibits platelet aggregation and prostaglandin synthesis from endogenous substrate through activating basal and PGE1-stimulated activity of the cyclase, preventing PGE2-induced depression of the cyclase activity and thus increasing platelet c-AMP level.

Adenylyl Cyclases↗
PubMed1979

Inhibition of platelet aggregation by a new agent, Ticlopidine.

Effect of Ticlopidine, 5-(2-chlorobenzyl)-4, 5, 6, 7-tetrahydro[3,2-C]pyridine hydro-chloride, on platelet aggregation was studied in the rat. Ticlopidine was found to be a potent, long-lasting inhibitor of platelet aggregation. It inhibited the aggregation induced by any of ADP, collagen, thrombin, arachidonic acid and prostaglandin endoperoxides and/or thromboxane A2-like substancee. Ticlopidine was effective at doses as low as 30 mg/kg when orally given to rats, and the effect lasted as long as the life span of the circulating platelets (half time: about 48 hours). Ticlopidine inhibited also nucleotide release from and prostaglandin synthesis in the platelets, but did not significantly affect platelet adhesiveness to glass, platelet factor 3 availability and clot retraction.

Adenosine Diphosphate↗