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Biomedical subjects

M Kanno

Publications and source records attributed to M Kanno.

At least 325 records · Page 18Linked to original sources
PubMed1982

Differential influences of several alpha-adrenoceptor antagonists on alpha-adrenoceptor-mediated inotropic responses in the left atria of guinea-pigs.

Influences of several alpha-adrenoceptor antagonists on the triphasic time response curves of phenylephrine, which are characterized by an initial increasing phase followed by a declining phase and then a second increasing phase, were investigated in the guinea pig left atria pretreated with sotalol (5 x 10(-5) M) and driven at 0.2 Hz. Phenoxybenzamine (10(-6) M) blocked both the positive and the negative inotropic effects and resulted in disappearance of the characteristic pattern, although lower concentrations (10(-8)--10(-7) M) preferentially attenuated the positive phase. Phentolamine (10(-7)--6 x 10(-6) M) and yohimbine (10(-6)--10(-5) M) preferentially inhibited the negative phase and potentiated the positive inotropic effect, thus changing the pattern to a biphasic or a monophasic one. Prazosin depressed concentration-dependently the positive inotropic effect and blunted the triphasic pattern (10(-9)--10(-8) M) or altered the pattern to a biphasic one (10(-7) M). In the presence of 10(-6) M prazosin, only the negative inotropic effect was observed to subsist. This negative inotropic effect was antagonized by 3 x 10(-6) M phentolamine. The present results suggest that there may exist two distinct types of postsynaptic alpha-adrenoceptors in the left atria of guinea pigs, one type mediating the positive inotropic effect and the other type mediating the negative inotropic effect.

Adrenergic alpha-Antagonists↗
PubMed1982

Effects of nicardipine, a new dihydropyridine vasodilator, on coronary circulation and ischemia-induced conduction delay in dogs.

The effects of 2,6-dimethyl-4-(3-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylic acid 3-[2-(N-benzyl-N-methylamino)]ethyl ester 5-methyl ester hydrochloride (nicardipine, YC-93), a new potent calcium antagonistic coronary vasodilator, on coronary circulation and ischemia-induced conduction delay were examined in anesthetized open-chest dogs. Nicardipine increased both the coronary flow and regional myocardial blood flow in the pre-ischemic period in a dose-dependent manner. However, nicardipine in a dose of 30 micrograms/kg, which was sufficient to enhance the coronary circulation almost maximally, failed to reduce the conduction delay produced by coronary occlusion under a constant atrial pacing. A high dose of nicardipine (300 micrograms/kg) enough to exert a slow channel blocking action on the cardiac tissue was required to improve the conduction delay. These results suggest that the coronary vasodilating action of the calcium antagonists is unlikely to play an essential role in reducing the conduction delay in the ischemic myocardium.

Animals↗
PubMed1981

Monoclonal antibodies that recognize the product controlled by a gene in the I-J subregion of the mouse H-2 complex.

The B cell hybridomas producing monoclonal antibodies (E10, D7, F4, H6, and D4) were established by the fusion of P3U1 or NS-1 murine myeloma cell lines and spleen cells of B10.A(5R) mice hyperimmunized with mitomycin C-treated B10.A(3R) spleen and thymus cells. Two types of monoclonal antibodies specific for the products controlled by a gene in the I-Jb subregion of the H-2 complex were characterized: one specific for the private type of I-Jb determinant, the other recognizing the cross-reactive determinant between the I-Jb and I-Jd products. By using these monoclonal reagents, the I-J-encoded product on the antigen-specific suppressor T cells was found to be expressed on their soluble suppressor factors. Furthermore, the I-Jb products were successfully detected not only on the T cell hybridoma with suppressor activity specific for keyhole limpet hemocyanin (KLH), but also on KLH-primed suppressor T cells enriched by antigen-coated petri dishes and concanavalin A-induced thymocyte blasts of C57BL/6 mice by complement-dependent cytotoxic assays and membrane fluorescence techniques.

Animals↗
PubMed1981

Influence of stimulation interval on inotropism mediated by alpha-adrenoceptors in the left atria of rabbits.

The inotropic effects induced by alpha-adrenoceptor stimulation were investigated in the left atria of rabbits at various stimulation rates and were compared with those by beta-adrenoceptor stimulation. Phenylephrine at a concentration of 10(-5) M in the presence of 5 X 10(-5) M sotalol more increased the contractile force with decreasing the rate of stimulation from 120 to 30 beats/min, whereas the same procedure resulted in a negative inotropic effect at low stimulation rates such as 1 beat/min. Inversion from the positive inotropism to the negative one was observed to occur in a range of 3 to 12 beats/min. Rested state contractions obtained by a stimulation rate of 1 beat per 5 min, i.e. a rest period of 300 sec, were significantly decreased by phenylephrine, while increased by 5 X 10(-9) M isoproterenol. This depressive effect of phenylephrine was antagonized by 3 X 10(-6) M phentolamine. Post rest contractions (PRC) which were elicited following a rest period of 300 sec after steady stimulation of 60 beats/min, were inconsistently affected by phenylephrine in contrast with the consistent and significant increase by isoproterenol. Of 17 preparations treated with phenylephrine, 9 showed an increase and others a decrease in PRC. However, reduction of NaCl concentration by 50% resulted in a decrease in PRC in all preparations treated with phenylephrine without affecting the increase produced by isoproterenol. These results indicate that alpha-adrenoceptor-mediated positive inotropic effect inverts to a negative one when the contractions have a long interval of rest.

Action Potentials↗
PubMed1980

Effects of calcium antagonists and lidocaine on conduction delay induced by acute myocardial ischemia in dogs.

Effects of calcium antagonists and lidocaine on the conduction delay observed in the ischemic myocardium were studied in 24 open-chest anesthetized dogs. Acute myocardial ischemia was produced by complete occlusion of the left anterior descending coronary artery (LAD) for 5 to 10 minutes. The conduction time was measured from the initial deflection of V waves on the His bundle electrograms to the major deflection of the bipolar electrograms recorded from the ischemic and non-ischemic subepicardium under a constant atrial pacing. LAD occlusion produced conduction delay in the ischemic zone (14.3 +/- 2.3 msec, p less than 0.001) with no effect on the normal zone. This ischemia-induced conduction delay was reversible and rate-dependently increased. Administration of lidocaine (2 mg/kg bolus, 4.3 mg/kg/hr constant infusion) prior to the second occlusion increased conduction delay by 12.9 +/- 1.9 msec (p less than 0.001) whereas diltiazem (0.4 mg/kg i.v.) and verapamil (0.3 mg/kg i.v.) reduced the ischemia-induced conduction delay by 12.7 +/- 4.9 msec (p less than 0.05) and 8.4 +/- 1.8 msec (p less than 0.001), respectively. These results indicate that slow channel blocking agents reduce the conduction delay induced by the myocardial ischemia, in contrast with the prolonging effect of lidocaine.

Animals↗
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

[Electrophysiologic effects of calcium channel blocking agents on the sinus node function in anesthetized dogs (author's transl)].

The electrophysiologic effects of calcium channel blocking agents, diltiazem, verapamil and nifedipine, on the sinus node function were examined in 43 anesthetized closed-chest dogs in comparison with the effects of propranolol. The parameters of sinus node function, i.e. sinus cycle length (SCL), sinus node recovery time determined by overdrive suppression (SRT), both of which are thought to reflect sinus node automaticity, and sinoatrial conduction time estimated by Strauss method (SACT), were evaluated. Intravenously administered diltiazem (0.2 mg/kg), verapamil (0.1 mg/kg) and propranolol (0.1 approximately 0.2 mg/kg) increased SCL and SRT significantly although the increase of these parameters induced by nifedipine (0.03 mg/kg) was not statistically significant. The calcium channel blocking agents did not significantly affect SACT in contrast with propranolol which showed a prolonging effect. Thus calcium channel blocking agents suppressed sinus node automaticity yet had little effect on sinoatrial conduction.

Animals↗
PubMed1979

Antiallergic action of 6-ethyl-3-(1h-tetrazol-5-YL) chromone (AA-344) on immediate hypersensitivity reaction in rats.

A newly synthesized compound, 6-ethyl-3-(1H-tetrazol-5-yl)chromone (AA-344) given intravenously or orally inhibited considerably the 72-hr passive cutaneous anaphylaxis (72-hr PCA) induced by IgE in rats. The antiallergic action of AA-344 was neither due to the antihistamine or antiserotonin effect nor was it mediated via adrenergic mechanisms. The results obtained in a double sensitization with two IgE antibodies suggest that AA-344 may not impair antigen-antibody combination but probably prevents the release of chemical mediators including histamine. This assumption was supported by observation that AA-344 inhibited a reduction in the skin histamine content caused by the 72-hr PCA, without effect on the compound 48/80-induced histamine reduction. AA-344 also partially inhibited the IgGa-mediated 3-hr PCA in rats. These results indicate that the inhibitory action of AA-344 on the immediate hypersensitivity reactions is due to prevention of the release of chemical mediators from the mast cells, by acting on some process in sequential events leading to the mediator release following antigen-antibody combination.

Adrenalectomy↗