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Biomedical subjects

N Toda

Publications and source records attributed to N Toda.

At least 307 records · Page 17Linked to original sources
PubMed1982

Effects of elcatonin on plasma and urine electrolytes in infant beagles.

The effects of elcatonin (ECT) on the renal hemodynamics and electrolyte levels in plasma and urine were investigated in anesthetized infant beagles (3 months old) and adult beagles (9-10 months old). Intravenous injections of 50 MRC U/kg ECT did not alter the systemic blood pressure, renal blood flow, glomerular filtration rate, and urine flow in intact puppies as well as in puppies and adult dogs subjected to extirpation of the thyroid and parathyroid glands (TPTX). One hundred and twenty min after ECT injection, the plasma calcium concentration decreased by 1.06 +/- 0.15 mEq/l in intact puppies and 0.94 +/- 0.10 mEq/l in TPTX puppies, but decreased only by 0.38 +/- 0.22 mEq/l in adult TPTX dogs. The urinary calcium excretion decreased in all the puppies. The plasma phosphorus concentration decreased by 1.02 +/- 0.10 mg/dl, and the phosphorus excretion rate increased 63.6 +/- 26.4% in intact puppies; whereas the plasma phosphorus and phosphorus excretion were not altered in TPTX puppies. Diuresis and natriuresis were not obtained. These data suggest that the acute hypocalcemic effect of ECT is dependent on age and is not associated with its action on kidneys.

Animals↗
PubMed1982

Responses of isolated dog coronary arteries to tyramine.

In isolated dog coronary arteries contracted with prostaglandin F2 alpha, tyramine in concentrations of 10(-6) and 5 x 10(-6) M caused relaxations, but it produced contractions at 2 x 10(-5) M or higher. The relaxant response to tyramine was attenuated, but the contractile response was enhanced at the second trial as compared with the responses at the first. Relaxations induced by low concentrations of tyramine were reversed to contractions by treatment with propranolol (10(-6) M) or sotalol (10(-5) M), and were abolished by cocaine (3 x 10(-6) M) or bretylium (2 x 10(-5) M). In coronary arteries isolated from reserpine (0.5 mg/kg)-pretreated dogs, tyramine produced only a contraction. Under resting conditions, contractions induced by tyramine (5 x 10(-6) to 2 x 10(-3) M) were potentiated by cocaine and propranolol, and were inhibited by phentolamine. Norepinephrine produced a dose-dependent relaxation in the arteries contracted with prostaglandin F2 alpha. In the presence of propranolol, the arteries under resting conditions were contracted by norepinephrine, the contraction being suppressed by treatment with phentolamine. It may be concluded that relaxations of dog coronary arteries induced by tyramine are mediated by liberation of norepinephrine from adrenergic nerves which stimulates beta-adrenoceptors in the smooth muscle. It seems likely that the tyramine (2 x 10(-5) M or higher)-induced contraction is not mediated by norepinephrine released, but it is partly due to a direct action on alpha-adrenoceptors.

Animals↗
PubMed1982

Involvement of endogenous prostaglandin I2 in the vascular action of histamine in dogs.

In helical strips of dog mesenteric and gastroepiploic arteries contracted with prostaglandin (PG) F2 alpha, the addition of histamine (10(-6) M) caused a relaxation, which was markedly attenuated by treatment with aspirin, indomethacin or tranylcypromine. Treatment with chlorpheniramine prevented the inhibitory effect of aspirin or tranylcypromine. Combined treatment with chlorpheniramine plus aspirin or tranylcypromine slowed the development of histamine-induced relaxations as did the treatment with chlorpheniramine alone. Relaxations of mesenteric and gastroepiploic arteries induced by histamine were markedly attenuated or abolished by combined treatment with chlorpheniramine and cimetidine. Histamine-induced relaxations of coronary and renal arterial strips were suppressed by cimetidine alone but were unaffected by aspirin. Contractile responses of cerebral arterial strips to histamine were attenuated by chlorpheniramine and potentiated by aspirin. The collagen-induced platelet aggregation was inhibited by treatment with bathing media in which mesenteric arteries were stimulated by histamine; the inhibition was prevented by treatment of the arteries with aspirin. It may be concluded that relaxation of mesenteric and gastroepiploic arteries induced by histamine is mainly associated with the release of prostaglandin I2 from the arterial wall, which results from an activation of histaminergic H1 receptors. Histamine-induced cerebroarterial contractions mediated via H1 receptors appear to be partly counteracted by prostaglandin I2 released.

Animals↗
PubMed1982

Influence of trimetazidine, an antianginal drug, on isolated dog arteries and veins.

In helical strips of dog coronary, mesenteric, renal, femoral and basilar arteries contracted with prostaglandin F2 alpha, trimetazidine produced a dose-related relaxation, which was not influenced by treatment with propranolol, atropine, cimetidine, aminophylline and aspirin. Relaxations induced by trimetazidine of strips of large and small coronary arteries did not differ, while those of large artery strips induced by nitroglycerin were significantly greater. Mesenteric vein strips responded with a greater relaxation to trimetazidine than mesenteric artery strips, while the vein and artery strips relaxed in response to nitroglycerin to a similar extent. Contractile responses to transmural stimulation and norepinephrine of mesenteric vein strips were attenuated by trimetazidine to a greater extent than those of artery strips. However, trimetazidine did not protect alpha-adrenoceptors from persistent blockade by phenoxybenzamine. Treatment with high concentrations of trimetazidine attenuated the relaxant response to isoproterenol of coronary arteries and the contractile response to Ca++ of the arteries exposed to Ca++-free media and depolarized by excess K+. It may be concluded that trimetazidine preferentially relaxes venous muscle and reduces contractile responses of veins to activation of sympathetic nerves, thereby reducing venous return or preload of the heart.

Animals↗
PubMed1982

[Studies of blood flow through the spinal cord of rabbit using the H2 clearance method ].

Using the H2 clearance method, spinal cord blood flow of the rabbit could be steadily measured. This allowed examination of blood flow problems using data analysis to provide informed decisions as to whether or not the blood flow through the gray and white matter was distinguishable. Spinal cord blood flow was also compared through the cervical, thoracic, and lumbar cord regions. The results were as follows: 1. The H2 clearance curves consisted of about 70% monoexponential curve (Mono), and 30% biexponenial curve (Bi), with a tendency toward higher values in the latter. 2. In Bi, a significant positive correlation was noted between the total flow values and the initial slope method values. The initial slope method was therefore used for subsequent data analysis. 3. By using a histogram to evaluate the data on each medullary segment, it was possible to separate a subgroup with a peak around 20 ml/100 g/min and another one with a peak around 40 ml/100 g/min. Based on the microangiographic findings, a more abundant vascular distribution was demonstrated in the gray matter than in the white matter. The first subgroup was noted corresponding to the blood flow through the white matter, and the latter through the gray matter. When the blood flow through the white and gray matter was calculated according to the subgroup data base, the flow ratio through the white and gray matter was 1:2. 4. Comparing the blood flow through each spinal cord segment revealed no significant difference at a p level of 0.01.

Animals↗
PubMed1982

Effects of Mepivacaine on adrenergic neuroeffector junction of the isolated rabbit aorta.

The effect of mepivacaine on adrenergic neuroeffector junction was studied in the isolated rabbit aorta. Mepivacaine, 5 X 10(-5) to 5 X 10(-4) M, attenuated the contractile response to transmural neural stimulation, the attenuation being greater in the response at high frequency stimulations. The attenuation of the responses by mepivacaine was not prevented by prior application of cocaine. The concentration-response curve for norepinephrine was shifted to the right by mepivacaine, 5 X 10(-5) to 2 X 10(-3) M. The attenuation of the response to transmural stimulation was greater than that of the response to an equipotent concentration of exogenous norepinephrine. Pretreatment with mepivacaine, 5 X 10(-5) to 2 X 10(-3) M, protected alpha-adrenoceptors from persistent blockade by phenoxybenzamine in a dose-dependent manner. The contractile response to histamine was not significantly altered by mepivacaine in concentrations up to 5 X 10(-4) M. Mepivacaine, 5 X 10(-4) and 2 X 10(-3) M, decreased the response to high concentrations of KCl. Ca2+-induced contractions in aortic strips previously exposed to Ca2+-free media and depolarized by excess K+ were significantly inhibited by mepivacaine, 5 X 10(-4) and 2 X 10(-3) M. It may be concluded that mepivacaine causes vasodilation through an alpha-adrenoceptor antagonism in addition to a sympathetic nerve conduction blockade. High concentrations of mepivacaine appear to interfere with the transmembrane influx of calcium in the vascular smooth muscle.

Animals↗
PubMed1981

Interaction of sulfated glycosaminoglycans with lectins.

The sulfated glycosaminoglycans, such as keratan sulfate and chitin sulfate having 3-hydroxy free N-acetyl-beta-D-glucosaminyl residues as constituents, reacted with wheat germ agglutinin and Solanum tuberosum agglutinin by sugar-specific interaction. The glycosaminoglycans showed different inhibitory activities to the hemagglutination reaction of these lectins and keratan sulfate and its modified products formed insoluble complexes with both of the lectins at pH 7.0 in physiological saline solutions (0.15 M NaCl). S. tuberosum agglutinin was precipitated within a particularly narrow concentration range of keratan sulfate, and the formation of a soluble complex was observed by gel chromatography. These interactions were specifically inhibited by N,N'-diacetylchitobiose but not by 2 M NaCl. The specific interactions of the glycosaminoglycans with S. tuberosum agglutinin were confirmed by their ultraviolet difference spectra with two peaks at 285 and 298 nm attributable to the tryptophan residues in the binding site of the agglutinin. It was also found that S. tuberosum agglutinin and wheat germ agglutinin have different binding specificities. The presence of sulfate groups in either keratan sulfate or chitin sulfate did not interfere with their specific interactions with S. tuberosum agglutinin as strongly as with wheat germ agglutinin. The N-acetylneuraminic acid residues in keratan sulfate were found to be receptor sites for wheat germ agglutinin but not for S. tuberosum agglutinin.

Animals↗
PubMed1981

Cardiotoxic and inotropic effects of ouabain on atria isolated from rabbits of different ages.

1 In sino-atrial node-right atrial preparations and left atrial preparations obtained from rabbits of different ages (2 to 360 days old), cardiotoxic and inotropic effects of ouabain were compared. Tachyarrhythmias were produced in immature and mature rabbit atria exposed for 6 to 8 min to ouabain (5 x 109(-6) M). The total number of contractions before the arrhythmias developed varied inversely with age (2 to 90 days old). Percentage reductions in the resting membrane potential, overshoot and maximum rate of rise induced by ouabain were greater in mature rabbit atria than in immature rabbit atria. 2 Reduction of Ca2+ in the bathing media suppressed the development of tachyarrhythmias. 3 In electrically-driven left atria isolated from immature and mature rabbits, similar frequency-contractile force curves were obtained, maximum contractions being attained at a frequency of 120/min. Ouabain at 2 x 10(-7) M shifted the curve upward and at 10(-6) M greatly potentiated the contractile force developed at low frequencies (6 to 30/min). Increase in contractions induced by ouabain relative to pre-drug concentrations at a frequency of 60/min were greater in immature rabbit atria (15 days old) but the positive inotropic effect of 2 x 10(-7) M ouabain relative to the effect seen at 10(-6) M was appreciably less. 4 It may be concluded that atria isolated from immature rabbits tolerate higher concentrations of ouabain than those isolated from mature rabbits.

Action Potentials↗
PubMed1981

Non-adrenergic, non-cholinergic innervation in monkey and human cerebral arteries.

1 Transmural electrical stimulation (0.5 to 20 Hz) and nicotine (10(-4) M) produced relaxations of helically-cut strips of monkey and human cerebral arteries, contracted with prostaglandin F2 alpha. 2 The relaxation induced by electrical stimulation was suppressed or abolished by tetrodotoxin, while the nicotine-induced relaxation was abolished by hexamethonium but was unaffected by tetrodotoxin. Both relaxation was abolished by hexamethonium but was unaffected by tetrodotoxin. Both relaxations were not attenuated by beta-adrenoceptor antagonists and atropine. 3 These findings may indicate that large cerebral arteries of the monkey and man are innervated by non-adrenergic, non-cholinergic nerves, excitation of which liberates unknown vasodilator substance(s).

Adult↗
PubMed1981

Different mechanisms of action of histamine in isolated arteries of the dog.

1 In helically-cut strips of dog coronary, superior mesenteric, right gastro-epiploic and renal arteries contracted with prostaglandin F2 alpha (PGF 2 alpha), histamine produced a dose-related relaxation, while, in contrast, the amine caused only a contraction of cerebral arterial strips. 2 The contractile response of cerebral arteries to histamine was attenuated by chlorpheniramine (10(-6)M) but was unaffected by cimetidine (10(-5)M). Relaxant responses to histamine of coronary and renal arteries were significantly attenuated by treatment with cimetidine and to a similar extent by combined treatment with cimetidine and chlorpheniramine. Chlorpheniramine alone was ineffective. 3 In mesenteric and gastro-epiploic arteries, relaxant responses to histamine were attenuated only slightly by cimetidine. Chlorpheniramine slowed the development of histamine-induced relaxations but did not alter the magnitude of the relaxations. Combined treatment with these H1- and H2- antagonists attenuated the histamine-induced relaxations to an appreciably greater extent than treatment with cimetidine alone. 4 It may be concluded that the cerebroarterial contraction induced by histamine is mediated through H1-receptors and the relaxations of coronary and renal arteries induced by histamine are mediated through H2-receptors. It appears that H1- and H2-receptors interact with each other to produce potentiation of histamine-induced relaxations of mesenteric and gastro-epiploic arteries.

Animals↗
PubMed1981

Angiotensin-induced relaxation in isolated dog renal and cerebral arteries.

Helically cut strips of dog renal and cerebral (basilar and middle cerebral) arteries contracted with prostaglandin (PG) F2 alpha relaxed in response to angiotensin II (AII; 10(-9) to 10(-7) M) in a dose-dependent manner. In renal arterial strips, the relaxation was preceded by a transient contraction. Both the relaxation and the contraction induced by AII were suppressed by [Sar1,Ala8]AII or [Sar1,Ile8]AII. Treatment with propranolol, atropine, hexamethonium, cocaine, aminophylline, cimetidine, or ouabain failed to alter the relaxing effect of AII. The peptide-induced relaxation was reversed to a contraction by aspirin or indomethacin. Treatment with tranylcypromine or 15-hydroperoxy arachidonic acid suppressed the relaxation induced by AII in renal and cerebral arteries but did not alter relaxations induced by PGI2 or K+ (5 mM). In experiments with superfused dog renal and coronary arteries and rat stomach strips, the renal arteries in response to AII released a prostaglandin like substance; the release was suppressed by [Sar1,Ala8]AII or indomethacin. It appears that the relaxation of isolated dog renal and cerebral arteries induced by AII is mediated by the release of PGI2, which is associated with stimulation of AII receptors.

Aminophylline↗
PubMed1981

Response of isolated monkey coronary arteries to catecholamines and to transmural electrical stimulation.

In helically cut stripes of monkey coronary arteries of different sizes, contracted with prostaglandin F2 alpha or K+, responses to norepinephrine, epinephrine, isoproterenol, and transmural electrical stimulation were compared. In response to norepinephrine, only contractions were induced in large arteries, contractions at low concentrations and relaxations at high concentrations in medium-size arteries, and only relaxations in small arteries. Epinephrine produced a greater contraction than norepinephrine in the arteries. Relaxant effects of isoproterenol were greater in small and medium-size arteries than in large arteries. Transmural electrical stimulation applied at frequencies of 2,5, and 20 Hz to strips of medium-size arteries produced a frequency-dependent contraction that was reversed to a relaxation following treatment with phentolamine. Propranolol abolished the relaxation. In strips of dog coronary arteries of medium size, transmural stimulation elicited only a relaxation which was suppressed or reversed to a contraction by propranolol. Dog arteries of this size responded to norepinephrine and epinephrine with only a relaxation. It may be concluded that the quantity or the susceptibility of alpha-adrenoceptors is in the order of large greater than or equal to medium greater than small-size arteries from monkeys, whereas that of beta-adrenoceptors is in the order of medium = small greater than large arteries. Monkey coronary arteries appear to respond to endogenous and exogenous norepinephrine with a contraction more consistently than dog coronary arteries.

Animals↗
PubMed1981

Effect of intra-aortic balloon pumping and calcium antagonist for reducing coronary reperfusion injury.

Open heart surgery under aortic cross-clamping is often required, but coronary reperfusion injury after release of aortic cross-clamping is unavoidable irrespective of applications of various protective methods to the myocardium. The anterior descending branch of the left coronary artery of mongrel adult dogs was occluded for 2 hours and then reperfused. The protective effects of intra-aortic balloon pumping (IABP) and of a calcium antagonist "diltiazem hydrochloride" (diltiazem) on the decreased reperfusion of ischemic, border and normal areas were examined by measuring the regional myocardial blood flow (RMBF) using a radioactive microsphere method. Diltiazem could increase significantly the RMBF in the border area. IABP induced a significant increase in the RMBF of the same area more than Diltiazem, with the increase in the endocardial layer tending to be superior to that in the epicardial layer. The results suggested that diltiazem is very effective for reducing the coronary reperfusion injury. It is also suggested that IABP is even more effective than diltiazem because it increases the RMBF significantly and, moreover, has a tendency to increase the blood flow in the endocardial layer which is poor in collateral vessels and thus vulnerable to ischemia.

Animals↗
PubMed1981

Mechanism of the excitatory action of motilin on isolated rabbit intestine.

Synthetic motilin caused a dose-dependent contraction on isolated rabbit intestinal segments, including the duodenum, ileum, and rectum. The contraction of duodenum was significantly greater than that in the ileum or rectum. In the duodenum, motilin was approximately 100 times as potent as acetylcholine on molar basis. The motilin-induced contractions were not influenced by atropine, chlorpheniramine, cimetidine, phentolamine, propranolol, cinanserin, 1-sar-8-ala-angiotensin II, or aspirin. Motilin did not affect the contraction induced by transmural electrical stimulation or acetylcholine. The response to motilin was unaffected by acetylcholine. Removal of Ca++ from bathing media or verapamil suppressed the motilin-induced contractions to a significantly greater extent than the contractions induced by acetylcholine. Thus, it may be concluded that motilin produces intestinal contractions by acting directly on smooth muscles, but not by acting on pharmacologically known drug receptors nor by releasing neurotransmitters such as endogenous acetylcholine. Motilin does not appear to modify autonomic nerve functions.

Acetylcholine↗
PubMed1980

Age-related changes in the transmembrane potential of isolated rabbit sino-atrial nodes and atria.

Transmembrane potentials were recorded from single cells of the sino-atrial (S-A) node and right atrium isolated from rabbits of different ages (2 to 360 days old). In neonatal rabbit atria, the shape of pacemaker action potentials recorded from same S-A nodal cells were not regular, and action potentials showing a slow depolarisation during diastole were frequently recorded from the right atrium close to the crista terminalis. The atrial rate decreased, the maximal diastolic potential or resting potential and the size of the overshoot increased, and action potential durations were prolonged with age. Such alterations in the membrane potential related to age were not associated with changes in the atrial rate. The maximum rate of rise did not significantly differ in S-A nodes and right atria from rabbits of different ages. It may be concluded that the membrane permeability for K+ is increased and/or the permeability for Na+ is decreased during early postnatal period, resulting in alterations in the automaticity and parameters of the membrane potential. The relationship between maximum rate of rise and maximal diastolic potential or resting potential appears to be altered with age.

Action Potentials↗
PubMed1980

Modifications by lidocaine and its N-dealkylated metabolites of the response of the isolated rabbit aorta to transmural electrical stimulation.

Contractile responses of rabbit aortic strips to transmural stimulation and to exogenously applied norepinephrine (NE), potassium chloride (KCl), and histamine were studied in the presence of lidocaine or its metabolites, monoethylglycinexylidide (MEGX) and glycinexylidide (GX). Lidocaine, 10(-4) and 5 x 10(-4) M, attenuated the contractile response to transmural stimulation, whereas MEGX, 2 x 10(-5) and 10(-4) M, potentiated, but 10(-4) M, potentiated the response to transmural stimulation. The suppression induced by lidocaine and MEGX was not reversed by excess calcium, 2.2 and 4.4 mM, but was partially reversed by cocaine, 3 x 10(-6) M. Lidoncaine, 5 x 10(-4) M, and MEGX, 2 x 10(-3) M, shifted the dose-response curve of NE to the right, whereas GX, 5 x 10(-4) M, shifted the curve to the left. The maximum tension developed by K+ was attenuated by lidocaine, 5 x 10(-4) M, MEGX, 5 x 10(-4) and 2 x 10(-3) M, and GX, 2 x 10(-3) M. It may be concluded that lidocaine attenuates the response to stimulation of sympathetic nerves innervating the arterial wall by interfering with the release of NE. In contrast, the metabolites, MEGX and GX, potentiate the response, possibly by increasing the release of NE. MEGX in high concentrations appears to have the same mechanism of inhibitory action as does lidocaine.

Alkylation↗