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Biomedical subjects

N Taira

Publications and source records attributed to N Taira.

At least 235 records · Page 13Linked to original sources
PubMed1978

Vasodilatation by prostaglandin F2alpha in the canine tongue through a parasympathetic mechanism.

1 The vascular bed of the tongue in situ was perfused with blood through the lingual arteries at a constant pressure in anaesthetized dogs. All drugs except for SQ 14,225 were administered intra-arterially.2 Prostaglandin F(2alpha) (PGF(2alpha)) produced a dose-dependent increase in blood flow through the lingual arteries (vasodilatation).3 Marked desensitization was observed on the vasodilator responses to repeated administration of PGF(2alpha).4 The vasodilator response to PGF(2alpha) was abolished by tetrodotoxin in doses that abolished the vasodilator response to electrical stimulation of the lingual nerve.5 The vasodilator response to PGF(2alpha) was not affected by hexamethonium in doses that almost abolished the vasodilator response to lingual nerve stimulation.6 The vasodilator responses to PGF(2alpha) and to lingual nerve stimulation were scarcely modified by (-)-hyoscyamine in doses that fully antagonized the vasodilator response to acetylcholine.7 Electrical stimulation of the vago-sympathetic trunk and noradrenaline produced a decrease in blood flow through the lingual arteries.8 These results indicate that the vasodilator response of the tongue to PGF(2alpha) is due exclusively to excitation of parasympathetic postganglionic neurones and that neuronal receptors involved are quite distinct from nicotinic receptors.9 Intravenous administration of SQ 14,225, an inhibitor of angiotensin I converting enzyme or kininase II, augmented the vasodilator responses to bradykinin and kallikrein but not that to lingual nerve stimulation.10 The results suggest that neither kallikrein nor*kinin (including bradykinin) is responsible for the parasympathetically induced vasodilatation in the tongue.

Animals↗
PubMed1978

Pharmacological analysis of histamine receptors in musculature and vasculature of the dog trachea in situ.

1 The role of histamine H1- and H2-receptors in the musculature and vasculature of the dog trachea was investigated in the blood-perfused trachea in situ. 2 Histamine and acetylcholine caused increases in blood flow (tracheal, vasodilatation) and in intraluminal pressure (tracheal constriction) in a dose-dependent manner. Histamine was almost equipotent to acetylcholine in causing tracheal vasodilatation but was about 30 times less potent in causing tracheal constriction. 3 The histamine H2-receptor agonist, dimaprit, caused a dose-dependent increase in tracheal blood flow but failed to cause tracheal constriction. 4 The tracheal constriction produced by histamine was inhibited strongly by diphenhydramine but not modifed by metiamide. The tracheal vasodilatation produced by histamine was antagonized by both diphenhydramine and metiamide; diphenhydramine was more effective than metiamide. 5 It is concluded that in the tracheal musculature, histamine receptors are exclusively of the H1-type and mediate constriction, whereas in the tracheal vasculature, both histamine H1- and H2-receptors mediate vasodilatation but histamine H1-receptors are predominant.

Acetylcholine↗
PubMed1978

Role of the peripheral vasculature in changes in venous return caused by isoproterenol, norepinephrine, and methoxamine in anesthetized dogs.

We studied effects on venous return of alpha- and beta-adrenergic agonists in anesthetized dogs. Blood from the superior and inferior venae cavae (venous return) was drained at the level of the tricuspid valve into a reservoir, from which blood was pumped into the right atrium at a constant rate. Isoproterenol infused into the ascending aorta or the right atrium increased the venous return and heart rate and decreased systemic blood pressure. The increase in venous return produced by isoproterenol given into the right atrium was not significantly different from that produced by isoproterenol administered into the ascending aorta, although the increase in heart rate was more marked with the latter route of administration. Norepinephrine infused into the ascending aorta increased the systemic blood pressure, venous return, and heart rate. Methoxamine infused into the ascending aorta increased the systemic blood pressure and decreased the venous return but produced no change in heart rate. Isoproterenol increased the venous return even when the sinoaortic baroreceptor reflex was eliminated. Propranolol abolished the increase in venous return caused by isoproterenol and reversed the increase in venous return caused by norepinephrine. The results suggest that a decrease in venous resistance mediated through a beta-adrenergic mechanism is important in increasing venous return, whereas an increase in venous resistance mediated through an alpha-adrenergic mechanism is responsible for a decrease in venous return.

Animals↗
PubMed1978

Effects on atrio-ventricular conduction of propranolol, pindolol and carteolol in the dog heart in situ as assessed by automated devices.

In open-chest dogs the heart rate was controlled at 150 beats/min and drugs were given intravenously. Propranolol (30 microgram/kg--1 mg/kg) prolonged the atrioventricular (A-V) conduction time and functional refractory period of the A-V conduction system (FRP) by blockade of the existing tone of the sympathetic nerves to the heart. The prolongation of the two parameters by the non-specific depressant action of propranolol was evident only at 3 mg/kg. Propranolol (3--30 microgram/kg) shortened the A-V conduction time in the heart deprived of the vagal and sympathetic tone, suggesting some sort of sympathomimetic effect. Pindolol in a wide range of doses (0.3--300 microgram/kg) exerted virtually no effect on the A-V conduction time and FRP, and its non-specific depressant action was apparent only at 3 mg/kg. Carteolol slightly prolonged the A-V conduction time and FRP only in low doses (1--10 microgram/kg), and in high doses (30 microgram/kg--1 mg/kg) it shortened the two parameters, reflecting its predominant sympathomimetic action.

Animals↗
PubMed1978

Differential effects of D 600 on release of catecholamines by acetylcholine, histamine, tyramine and by cyclic AMP from canine adrenal medulla.

The isolated canine adrenal glands were perfused retrogradely with Locke's solution, and the catecholamine contents of the effluents were measured by the trihydroxyindole-fluorimetric method. Stimulation of the glands by acetylcholine, histamine, tyramine and cyclic AMP caused an increase in release of catecholamines from the glands. Introduction of D 600 of the perfusion medium reduced release of catecholamines in response to acetylcholine, and this reduction was overcome by raising calcium ion concentrations of the perfusion medium. Similarly, D 600 reduced release of catecholamines in response to histamine. The release of catecholamines evoked by tyramine was also inhibited by D 600, although to a lesser degree than the release by acetylcholine. In contrast, D 600 was entirely ineffective on the catecholamine release in response to cyclic AMP. D 600 had no effect on the spontaneous catecholamine output. From these results it was concluded that release of catecholamines from adrenal chromaffin cells by acetylcholine and histamine, and by tyramine in part requires the entry of calcium ions across the cell membane, whereas that by cyclic AMP does not.

Acetylcholine↗
PubMed1977

Positive dromotropic effect of dibutyryl cyclic adenosine 3',5'-monophosphate on the atrioventricular node.

The effect of atrioventricular (A-V) conduction of N6-2'-0-dibutyryl cyclic 3',5'-adenosine monophosphate (dibutyryl cyclic AMP) was investigated in comparison with those of norepinephrine, cyclic 3',5'-adenosine monophosphate (cyclic AMP), adenosine-5'-monophosphate (5'-AMP), and adenosine by the use of the isolated, blood-perfused A-V node preparation of the dog. Single injections of dibutyryl cyclic AMP (3-300 micronmol) and norepinephrine (0.1-1 nmol) into the posterior septal artery of the preparation (the upper part of the A-V node is mainly perfused through this artery) produced a dose-dependent decrease in the A-V conduction time. The time to the peak effect and the duration of the effect of dibutyryl cyclic AMP were much longer than with norepinephrine. The positive dromotropic effect of dibutyryl cyclic AMP was resistant to the beta-adrenoceptor blocking action of propranolol. Unlike dibutyryl cyclic AMP, cyclic AMP (above 30 nmol), 5'-AMP and adenosine (above 1 nmol) injected into the posterior septal artery prolonged the A-V conduction time in a dose-dependent manner. The results indicate that dibutyryl cyclic AMP has a mode of action on A-V nodal cells which differs distinctly from that of either norepinephrine or cyclic AMP, 5'-AMP, and adenosine.

Adenosine↗
PubMed1977

Profile of beta-adrenoceptors in femoral, superior mesenteric and renal vascular beds of dogs.

1. The homogeneity of beta-adrenoceptors in femoral, superior mesenteric and renal vascular beds was investigated by the use of the regional perfusion technique in dogs. 2. Isoprenaline and salbutamol produced dose-related increases in femoral and superior mesenteric blood flow. The dose-response curves for the two agonists were parallel, but salbutamol was approximately 1/15 as potent as isoprenaline on a weight basis. 3. Isoprenaline and salbutamol increased renal blood flow in a dose-related manner. However, salbutamol was approximately 1/240 as potent as isoprenaline on a weight basis, and the slope of the dose-response curve for salbutamol was less steep than that for isoprenaline. 4. The dose-response curves to isoprenaline for increase in femoral and superior mesenteric blood flow were shifted to the right by intravenous pindolol but not by intravenous or intra-arterial practolol. 5. The dose-response curves to isoprenaline for increase in renal blood flow were shifted to the right more markedly by intravenous pindolol than by intravenous or intra-arterial practolol. 6. The results indicate that beta-adrenoceptors of the renal vascular bed consist of beta1-type and beta2-type whereas the femoral and superior mesenteric vascular beds contain only beta2-adrenoceptors.

Albuterol↗
PubMed1977

Assessment of the selectivity of OPC-2009, a new beta2-adrenoceptor stimulatn, by the use of the blood-perfused trachea in situ and of the isolated blood-perfused papillary muscle of the dog.

1 The potency and selectivity of 5-(1-hydroxy-2-isopropylamino)butyl-8-hydroxy carbostyril hydrochloride hemihydrate (OPC-2009), a new beta(2)-adrenoceptor stimulant, was compared with those of isoprenaline, trimetoquinol and salbutamol by the use of blood-perfused tracheal preparations in situ and of blood-perfused papillary muscle preparations of the dog. All drugs were injected intra-arterially.2 All the four drugs decreased tracheal intraluminal pressure (tracheal relaxation) and increased tracheal blood flow in a dose-dependent manner. The four drugs produced a dose-dependent increase in developed tension of papillary muscles. In both preparations the duration of action of isoprenaline and salbutamol was short, whereas that of OPC-2009 and trimetoquinol was long. These effects were antagonized by propranolol.3 Dose-response curves to the four drugs for tracheal relaxation were almost parallel. OPC-2009 was 2.4 times more potent, and trimetoquinol and salbutamol were 2.2 and 6.2 times less potent than isoprenaline in causing tracheal relaxation.4 Dose-response curves to the four drugs for tracheal vasodilatation were also parallel. OPC-2009, trimetoquinol and salbutamol were 3.9, 6.7 and 23 times less potent than isoprenaline.5 Slopes of the dose-response curves to the four drugs for increased developed tension were not parallel; that of OPC-2009 was the least steep, whereas that of isoprenaline was the steepest. Trimetoquinol, salbutamol and OPC-2009 were about 18, 570 and 2400 times less potent than isoprenaline.6 Selectivity calculated from relative potencies indicate that OPC-2009 was about 6000 times, salbutamol about 92 times and trimetoquinol about 8.2 times more selective than isoprenaline for tracheal smooth muscle as compared to ventricular muscle.7 The high potency and selectivity of OPC-2009 for tracheal smooth muscle and its long duration of action suggest its potential usefulness for treatment of bronchial asthma.8 The present results are also compatible with the concept that beta(1)-adrenoceptors in cardiac muscle and beta(2)-adrenoceptors in tracheal and vascular smooth muscle can be distinguished. Furthermore, the results revealed that the beta-adrenoceptors mediating tracheal relaxation and vasodilatation may also be different.

Adrenergic beta-Agonists↗
PubMed1977

Cardiohemodynamic effects of SK&F 24260, D 600, diltiazem, dilazep, and trimetazidine in the dog.

The cardiohemodynamic effects of a hypotensive agent, SK&F 24260, and coronary vasodilators, diltiazem, dilazep, and trimetazidine, and D 600 were studied in anesthetized open-chest dogs. The systemic blood pressure, cardiac output (pulmonary arterial flow), venous return (sum of the inferior and superior caval flow) right atrial pressure and heart rate were measured. All 5 drugs decreased the systemic blood pressure and heart rate and increased the right atrial pressure. The venous return and the cardiac output were reduced by higher doses of all the 5 drugs. However, SK&F 24260 in a wide range of doses greatly and diltiazem slightly but clearly increased the venous return and cardiac output. It appears that SK&F 24260 afects predominantly blood vessels whereas the other drugs affect rather the heart to produce a negative inotropic action.

Animals↗
PubMed1977

Chronotropic effects of coronary vasodilators as assessed in the isolated, blood-perfused sino-atrial node preparation of the dog.

Chronotropic effects of 6 coronary vasodilators, carbochromen, dilazep, diltiazem, dipyridamole, nifedipine and verapamil, were compared by close-arterial administration to the isolated, blood-perfused sino-atrial node preparation of the dog. All drugs produced a dose-related decrease in sinus rate, and the order of negative chronotropic potency determined on a weight basis was as follows: (formula: see text). Higher doses of these drugs except dipyridamole caused atrial standstill. The order of potency causing atrial standstill determined on a weight basis was as follows: (formula: see text). Dipyridamole in lower doses produced a negative chronotropic effect alone, but with higher doses a positive chronotropic effect preceded a negative one. Carbochromen in a wide range of doses produced a triphasic response consisting of initial brief positive, succeeding main negative and final gradually-developing slight positive components.

Animals↗
PubMed1976

Effects of atrio-ventricular conduction of calcium-antagonistic coronary vasodilators, local anaesthetics and quinidine injected into the posterior and the anterior septal artery of the atrio-ventricular node preparation of the dog.

The effects on atrio-ventricular (A-V) conduction and blood flow of calcium-antagonists (verapamil, nifedipine and diltiazem), local anaesthetics (procaine and lidocaine) and quinidine were investigated in the isolated, cross-circulated A-V node preparation of the dog. The drugs were injected individually into the posterior septal artery (PSA) through which the upper part of the A-V node is mainly perfused or into the anterior septal artery (ASA) through which the lower part of the node and the more distal conduction system are perfused. Single injections into the PSA of nifedipine (0.3-10 mug), verapamil (1-30 mug), diltiazem (1-30 mug), quinidine (30-300 mug), lidocaine (100 mug-1 mg) and procaine (300 mug-3 mg) produced a dose-related increase in the A-V conduction time and with higher doses of these drugs a second or third degree block of A-V conduction occurred. Nifedipine (0.3-30 mug) and verapamil (1-100 mug) injected into the ASA scarcely affected A-V conduction. Quinidine (30 mug-1 mg) and lidocaine (100 mug-3 mg) injected into the ASA prolonged the A-V conduction time in a dose-related manner, although the effects were less prominent than those produced upon injection into the PSA. High doses of quinidine (3 mg) and lidocaine (3-10 mg) injected into the ASA altered the shape of ventricular bipolar electrograms and prolonged the time interval between an electrogram of the right bundle branch and that of the ventricle. The results are consistent with the hypothesis that in excitation of A-V nodal cells a slow calcium current rather than a fast sodium current plays an important role and that in the His-Purkinje-ventricular system the fast sodium current is predominant. Single injections of the 6 drugs into the PSA produced a dose-related increase in blood flow through the PSA. All drugs but nifedipine increased the blood flow in almost the same dose range that caused impairment of A-V conduction. Nifedipine was 10 times more potent in increasing the blood flow than in impairing A-V conduction.

Action Potentials↗
PubMed1976

Release of noradrenaline proposed as a mechanisms for the positive inotropic action of dipyridamole.

In the arterially blood-perfused canine papillary muscle, i.a. injections of dipyridamole (10-300 mug) produced a dose-dependent increase in developed tension amounting to about 45% of the basal developed tension at 300 mug. The positive inotropic response to dipyridamole was greatly reduced by a prior i.a. injection of propranolol (10 mug) or by pretreatment with reserpine (0.2 mg/kg s.c. for 3 consecutive days) but not affected by a prior i.a. injection of tetrodotoxin (1 mug) or desmethylimipramine (3-10 mug). The positive inotropic response to dipyridamole reduced by pretreatment with reserpine was restored by i.a. infusion of noradrenaline (0.03 mug/min). Dipyridamole did not modify the positive inotropic responses to noradrenaline and tyramine. These results suggest that the positive inotropic response to dipyridamole is largely due to noradrenaline released from adrenergic nerve endings by a mechanism that differs from those operative in the action of tyramine or in liberation of noradrenaline upon excitation.

Animals↗
PubMed1976

Modification by manganese ions and verapamil of the responses of the atrioventricular node to norepinephrine.

In isolated and cross-circulated canine A-V node preparations single injections of Mn2+ (1-30 mumol) and verapamil (0.3-10 nmol) into the posterior septal artery (PSA) caused a dose-dependent increase in the A-V conduction time and, in large doses, produced A-V conduction block. The A-V conduction time increased by Mn2+ and verapamil is resotred by 1-norepinephrine (1-NE) injected into the PSA. The A-V nodal tachycardia induced by 1-NE is suppressed by Mn2+ but not by verapamil. These indicate the following: (1) the slow Ca2+ channel plays an important role in A-V conduction; (2) the positive dromotropic response of the A-V node to 1-NE may have some relations to the Ca2+ channel; (3) the A-V nodal tachycardia induced by 1-NE may be mediated by the Ca2+ channel. Possible causes which produced differences between Mn2+ and verapamil in the effects in antagonizing the 1-NE-induced A-V nodal tachycardia are discussed.

Animals↗
PubMed1976

5-Hydroxytryptamine as a sensitizer of somatic nociceptors for pain-producing substances.

Experiments were performed on loosely restrained, conscious dogs in the femoral artery of which a chronic catheter was implanted. All substances were administered through the catheter and vocalization responses to them were used as a principal measure of nociception. In 10 experiments done on 7 dogs, after a single injection of 3 or 10 mumol of 5-hydroxytryptamine, threshold doses (about 0.5 mumol) of acetylcholine for vocalization produced vocalization responses comparable with those to about 3 times threshold doses. In 5 experiments on 5 dogs, after 10 mumol of 5-hydroxytryptamine, threshold doses (about 0.3 nmol) of bradykinin for vocalization produced vocalization responses comparable with those to about twice threshold doses. These doses of 5-hydroxytryptamine produced small vocalization responses in only 3 of the 12 dogs. These results indicate that 5-hydroxytryptamine, although almost devoid of the activity producing noceceptive responses, sensitizes somatic nociceptors for pain-producing substances.

Acetylcholine↗
PubMed1976

A method for recording smooth muscle and vascular responses of the blood-perfused dog trachea in situ.

1 A method is described for measuring responses of dog tracheal musculature and vasculature in situ. 2 The upper two thirds of the trachea was perfused with blood through both cranial thyroid arteries at a constant pressure. The blood flow through the arteries was measured with an electromagnetic flowmeter. The response of the tracheal musculature was measured as a change in pressure in a water-filled cuff inserted into the trachea via the mouth. Drugs were injected close-arterially. 3 Acetylcholine produced dose-dependent increases in blood flow rate (vasodilatation) and in tracheal intraluminal pressure (tracheal constriction). These responses were antagonized by atropine. 4 Isoprenaline produced vasodilatation which was blocked by propranolol. Adrenaline and noradrenaline caused vasocontriction which was blocked by phentolamine. 5 All three catecholamines produced a decrease in tracheal intraluminal pressure (tracheal dilatation). The tracheal dilatation in response to adrenaline and noradrenaline was converted to constriction by propranolol. The tracheal constriction thus unmasked was abolished specifically by phentolamine. 6 From these results it is concluded that the tracheal musculature and vasculature contain muscarinic receptors, and excitatory alpha- and inhibitory beta-adrenoceptors. In the tracheal musculature beta-adrenoceptors predominate over alpha-adrenoceptors; the reverse is true in the tracheal vasculature.

Acetylcholine↗
PubMed1976

Simultaneous assessment of effects of coronary vasodilators on the coronary blood flow and the myocardial contractility by using the blood-perfused canine papillary muscle.

Effects of 6 coronary vasodilators on the coronary blood flow and the contractile force of the ventricular muscle were examined simultaneously by injecting these drugs to the arterially blood-perfused canine papillary muscle preparation. All compounds produced a dose-dependent increase in blood flow rate, and relative potencies determined on the basis of doses producing a 100% increase in blood flow rate, ED100, were in the descending order : nifedipine greater than verapamil greater than diltiazem greater than dilazep greater than dipyridamole greater than carbochromen, and approximately 1 : 1/12 : 1/26 : 1/100 : 1/300 : 1/500. All drugs except for dipyridamole caused a dose-dependent decrease in the developed tension of the papillary muscle, although nifedipine and diltiazem in low doses produced a slight increase. Relative potencies determined on the basis of doses producing a 50% decrease in developed tension, ID50, were as follows: nifedipine (1), verapamil (1/13), diltiazem (1/40), dilazep (1/100), and carbochromen (1/270). Ratios of the ID50 to ED100 were as follows: diltiazem (5.2), nifedipine (3.5), verapamil (3.5), dilazep (2.5), and carbochromen (1.8). The higher the value the more predominant on the coronary vascular bed or the less depressant on the myocardial contractility were their actions.

Animals↗