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Biomedical subjects

M Sakanashi

Publications and source records attributed to M Sakanashi.

144 records · Page 8Linked to original sources
PubMed1978

Effects of dobutamine on coronary circulation and cardiac metabolism of the dog.

Effects of (+/-)-4-[2-(3-p-hydroxyphenyl-1-methyl-amino)ethyl]pyrocatechol (dobutamine) on coronary circulation and cardiac metabolism were investigated using the heart in vivo and the isolated perfused heart of dogs. In the heart in vivo dobutamine 1--30 microgram/kg i.v. and 1--100 microgram i.c. produced dose-dependent increases in coronary perfusion pressure, coronary blood flow, heart rate and left intraventricular pressure. In the perfused heart dobutamine 10 microgram i.c. increased coronary flow, heart rate, cardiac contractility and myocardial oxygen consumption. Delta redox potentials decreased but did not show negative values. Propranolol 0.1 mg/kg i.v. and 0.1 mg i.c. inhibited these effects of dobutamine. Dobutamine shows basically the same actions as isoproterenol, but does not reduce the coronary perfusion pressure by the relatively high dose applied. The results suggest that dobutamine may have a selective adrenergic beta 1 receptor stimulating action on the heart and have a merit in maintaining the coronary perfusion pressure.

Animals↗
PubMed1978

Effects of 5-([2-(diethylamino)-ethyl]amino)-3-phenyl-1,2,4-oxadiazole dihydrochloride (DEPO) on cardiac functions and myocardial metabolism of the dog.

Effects of 5-([2-(diethylamino)-ethyl]amino)-3-phenyl-1,2,4-oxadiazole (DEPO) on cardiac functions and myocardial metabolism were examined using the heart in vivo and the isolated perfused heart of dogs. In the heart in vivo DEPO i.v. produced dose-dependent decreases in coronary perfusion pressure (PP), heart rate (HR), left ventricular pressure (LVP), dP/dt max of LVP and coronary vascular resistance (VR). DEPO i.c. dose-dependently increased left circumflex coronary flow (LCCF) and decreased PP, LVP and dP/dt max of LVP, but did not change HR. In the isolated perfused heart, DEPO induced a marked increase in coronary blood flow (CBF) and depressed HR and myocardial contractile force. Myocardial oxygen consumption and myocardial redox potential were not significantly changed. DEPO could not modify the effects of isoproterenol, adenosine and reactive hyperaemia on the heart. The results suggest that DEPO may have a coronary vasodilating action and some direct inhibitory actions on the heart.

Adenosine↗
PubMed1977

Activation of afferent cardiac sympathetic nerve fibers of the cat by pain producing substances and by noxious heat.

Afferent discharges of 64 single units were recorded from the left cardiac sympathetic nerve of anesthetized cats. Mechano-sensitive terminals of the afferent fibers were localized in the extrapulmonary part of the pulmonary artery, left atrium, left ventricle and left pericardium, as determined by direct mechanical probing of the heart after death of the animals. Conduction velocity of the fibers ranged from 2.5 to 14.6 m/s. Excitation of these Adelta-fibers with mechanically excitable endings was produced by intravenous injections of acetylcholine, 5-hydroxytryptamine, bradykinin, histamine and veratridine, and/or by topical application of these agents to the receptor region. Noxious heat to the mechanically excitable field in the wall of the pulmonary artery and the left ventricle also activated their afferent fibers. These observations provide evidence for a certain number of afferent units in the cardiac sympathetic nerve with polymodal sensitivity. These afferent fibers can provide the spinal cord with information not only on mechanical changes in cardiac events, but also changes in the chemical environment of the cardiac nerve ending, possibly produced by myocardial ischemia.

Acetylcholine↗
PubMed1977

Effects of dihydroergotamine methanesulfonate on the microcirculation of the rat cremaster muscle.

Effects of dihydroergotamine on the microcirculation of the rat cremaster muscle were investigated microscopically using colour photographic technique. 1. Dihydroergotamine 10(-4) g/ml constricted arterioles of the rat cremaster. 2. Dihydroergotamine 10(-4) g/ml produced a significant contraction of venules. 3. Dihydroergotamine 10(-4) g/ml markedly inhibited the contractile response of noradrenaline 10(-6) g/ml on arterioles of the rat cremaster. The results suggest that dihydroergotamine has an appreciable vasoconstrictive action, especially upon venules, and that dihydroergotamine also has an adrenergic alpha-receptor blocking action. By means of highly sensitive negative colour film we obtained a satisfactory photograph of the rat cremaster's circulation.

Animals↗
PubMed1974

Afferent fibres from pulmonary arterial baroreceptors in the left cardiac sympathetic nerve of the cat.

1. Afferent discharges were recorded from the left cardiac sympathetic nerve or the third sympathetic ramus communicans of anaesthetized cats. Twenty-one single units with baroreceptor activity were obtained.2. The receptors of each unit were localized to the extrapulmonary part of the pulmonary artery, determined by direct mechanical probing of the wall of the pulmonary artery after death of the animals. Conduction velocity of the fibres ranged from 2.5 to 15.7 m/sec.3. Afferent discharges occurred irregularly under artificial ventilation. The impulse activity was increased when pulmonary arterial pressure was raised by an intravenous infusion of Locke solution, or by occlusion of lung roots, and decreased by bleeding the animal from the femoral artery.4. Above a threshold pressure, discharges occurred synchronously with the systolic pressure pulse in the pulmonary artery. A progressive further rise in pressure did not produce an increase in the number of impulses per heart beat. Occlusion of lung roots initially elicited a burst of discharges but the number of impulses for each cardiac cycle gradually decreased.5. The receptors responded to repetitive mechanical stimuli up to a frequency of 10/sec, but failed to respond to stimuli delivered at 20/sec.6. The results provide further evidence for the presence of afferent fibres in the cardiac sympathetic nerve. These afferent fibres are likely to provide the spinal cord with specific information only on transient changes in pulmonary arterial pressure.

Acetylcholine↗
PubMedDate not supplied

Indomethacin-induced contractions of dog coronary arteries.

We investigated the mechanisms responsible for indomethacin-induced contractions of coronary arteries. In isolated dog hearts perfused through the coronary circulation with blood under constant pressure, an intracoronary injection of 1 mg of indomethacin decreased coronary blood flow without significant changes in myocardial contractile force and heart rate. Indomethacin (10(-8)-10(-5) M) caused concentration-dependent contractions of isolated dog coronary arterial strips. These contractions were significantly inhibited by calcium-free solution, diltiazem, nifedipine, prostaglandin E1, arachidonic acid, and phospholipase A2, but not by phenoxybenzamine, atropine, or oleic acid. Propranolol and prostaglandin F2 alpha tended to enhance the contractions. The results indicate that indomethacin contracts dog coronary arteries through inhibition of intramural synthesis of vasodilating prostaglandins.

Animals↗
PubMedDate not supplied

In vitro evidence for dopaminergic receptors in human renal artery.

Effects of dopamine on human renal arteries were pharmacologically investigated in vitro. Norepinephrine (5 X 10(-10)-5 X 10(-5) M) produced concentration-dependent contractions of isolated renal arterial strips, which were significantly depressed by prior administration of phentolamine or phenoxybenzamine. Isoproterenol (4 X 10(-10)-4 X 10(-6) M) concentration dependently relaxed the strips under potassium contracture, but a high dose (4 X 10(-5) M) constricted them. Biphasic responses to isoproterenol were changed to concentration-dependent contractions by prior administration of propranolol, and abolished by propranolol together with phentolamine. Dopamine (5 X 10(-8)-5 X 10(-4) M) produced concentration-dependent contractions of human renal arteries, which were not significantly influenced by propranolol but which were reversed to relaxations by phentolamine. Dopamine-induced relaxations, which were obtained after administration of phentolamine, were not significantly affected by propranolol, but were significantly depressed by combined application of propranolol and haloperidol, or of propranolol and droperidol. Results suggest that isolated human renal arteries have dopaminergic receptors in their smooth muscles which show relaxations of renal arteries after alpha-adrenoceptor blockade.

Adult↗
PubMedDate not supplied

Comparison of haemodynamic responses to cilnidipine and nicardipine in an experimental model of acute congestive heart failure.

1. The haemodynamic effects of cilnidipine, a new calcium channel blocker, were examined in a canine model of acute congestive heart failure and were compared with those of nicardipine at equihypotensive doses. 2. The model was prepared by injections of saponin into coronary arteries of anaesthetized open-chest dogs followed by volume loading and continuous i.v. infusion of methoxamine. After the treatment, aortic blood flow (AoF) and left ventricular dP/dt markedly decreased, while left ventricular end-diastolic pressure (LVEDP), right atrial pressure and systemic vascular resistance (SVR) increased. Cilnidipine (0.3, 1.0 and 3.0 micrograms/kg per min), nicardipine (0.3, 1.0 and 3.0 micrograms/kg per min) or the respective vehicle was given i.v. after accomplishment of heart failure. 3. These drugs both produced a comparable reduction in aortic pressure and an increase in AoF associated with profound decreases in LVEDP, SVR and coronary vascular resistance. In contrast, administration of nicardipine was associated with significant increases in heart rate and cardiac contractility but that of cilnidipine was not. 4. These results indicate that cilnidipine as well as nicardipine can exert beneficial haemodynamic effects in a model of acute heart failure probably through lessening afterload and cilnidipine may moderate reflex-induced sympathetic stimulation.

Acute Disease↗
PubMedDate not supplied

Simultaneous measurement of renal blood flow of the outer and inner cortex by laser-Doppler flowmetry in anesthetized dogs: effect of enalapril diacid.

Renal hemodynamic effects of the angiotensin-converting enzyme inhibitor enalapril diacid (30 micrograms/kg, i.v.; n = 8) were examined using laser-Doppler flowmetry in anesthetized dogs. Two laser-Doppler flowmetry probes were applied simultaneously to measure the renal blood flow of the outer and inner cortex. Changes in cortical renal blood flow, obtained by the laser-Doppler flowmetry method, were intimately related to those in total renal blood flow measured with the electromagnetic flow probe during occlusion of the abdominal aorta or after administration of angiotensin II, norepinephrine, acetylcholine or dopamine. Enalapril diacid produced a significant increase in total renal blood flow, despite moderate hypotension. The blood flow of the inner cortex significantly increased by 21% following enalapril diacid, while that of the outer cortex did not. These data indicate that there may be a regional difference in the intrarenal vasodilating effect of enalapril diacid. These results also demonstrate that the laser-Doppler flowmetry method is suitable for the continuous measurement of directional changes in both outer and inner cortical blood flows.

Acetylcholine↗
PubMedDate not supplied

Regional vasodilating effects of spirapril diacid and enalapril diacid in anesthetized dogs.

The acute regional hemodynamic effects of spirapril diacid, a novel nonsulfhydryl angiotensin-converting enzyme inhibitor, and enalapril diacid at an equidepressor dose were examined in anesthetized dogs by simultaneously measuring renal, coronary, vertebral arterial and aortic blood flow. Spirapril diacid (30 micrograms/kg, i.v.) lowered aortic pressure and increased aortic and renal blood flow associated with no marked change in heart rate, myocardial contractility, vertebral and coronary blood flow in a similar manner to enalapril diacid (30 micrograms/kg, i.v.). Both inhibitors thus produced an increase in stroke volume and a decrease of the rate-pressure product. The decrease of renal vascular resistance after administration of both agents was greater than that in vertebral and coronary vascular beds. A relatively more prolonged renal vasodilatation and a shortened coronary vasodilatation were seen with spirapril diacid as compared with enalapril diacid, despite practically identical reductions in total peripheral resistance. Each of the drugs markedly inhibited the pressor and renal vasoconstrictor responses to angiotensin I. These results indicate that the two inhibitors exhibit a similar profile of regional differences in vasodilatory effects, although they might display different durations of regional vasodilatation.

Anesthesia↗
PubMedDate not supplied

Comparative effects of the calcium antagonist isradipine and some other dihydropyridine derivatives on regional blood flow in anesthetized open-chest dogs.

The effects of isradipine (PN 200-110), isopropyl 4-(2,1,3-benzoxadiazol-4-yl)-1,4-dihydro-5-methoxycarbonyl-2,6-dim ethyl-3- pyridinecarboxylate, on some cardiovascular parameters and regional blood flow were compared with those of other dihydropyridine derivatives in anesthetized open-chest dogs. Intravenous (i.v.) administrations of isradipine 3 and 10 micrograms/kg, nifedipine 10 micrograms/kg, nicardipine 10 micrograms/kg and nisoldipine 10 micrograms/kg, decreased aortic blood pressure and increased aortic (AoF), vertebral (VBF) and coronary blood flow (CBF), but did not affect heart rate and left ventricular end-diastolic pressure. Renal blood flow was reduced by isradipine 10 micrograms/kg and nifedipine 10 micrograms/kg, but was not influenced by isradipine 3 micrograms/kg, nicardipine 10 micrograms/kg and nisoldipine 10 micrograms/kg. Left ventricular dP/dt was increased by isradipine 3 micrograms/kg, nicardipine 10 micrograms/kg and nisoldipine 10 micrograms/kg, but remained essentially unchanged following isradipine 10 micrograms/kg and nifedipine 10 micrograms/kg. The increase in AoF, VBF and CBF lasted 5-9 min following nifedipine 10 micrograms/kg or nicardipine 10 micrograms/kg, 17-30 min following nifedipine 10 micrograms/kg or nicardipine 10 micrograms/kg, 17-30 min following nisoldipine 10 micrograms/kg, and 16-44 min following isradipine 3 micrograms/kg i.v., but persisted for at least 60 min following isradipine 10 micrograms/kg. Under the experimental conditions and at the doses used in this study, all 4 drugs reduced total peripheral resistance as well as resistance in the vertebral, coronary and renal vascular beds. The results suggest that isradipine exerts cardiovascular effects similar to other calcium antagonists of the dihydropyridine group, but possesses a longer duration of action and shows a greater specificity in reducing coronary vascular resistance than nifedipine, nicardipine and nisoldipine.

Anesthesia↗
PubMedDate not supplied

Cardioprotective effects of hydrolyzed bopindolol against contractile dysfunction produced by coronary stenosis and reperfusion in dogs.

The effects of the active metabolite (18-502) of bopindolol, which is a new nonselective beta-adrenoceptor antagonist, were studied on the ischemic changes in myocardial segment shortening, cardiac lactate metabolism and S-T segment of subendocardial electrocardiogram during coronary stenosis and on their recoveries after reperfusion in anesthetized dogs, and were compared with those of propranolol at a dose exhibiting a comparable degree of beta 1-blocking activity. In the presence of coronary stenosis, intravenous administration of 18-502 (5 micrograms/kg) and propranolol (0.2 mg/kg), but not saline, produced significant improvements of regional myocardial dysfunction, lactate production and S-T segment elevations in the ischemic myocardium, which were associated with significant decreases in heart rate and cardiac contractility. After release of the stenosis, administration of 18-502, but not propranolol, resulted in a significantly accelerated recovery of the ischemic segment function as compared with the control group. In rat heart homogenates, 18-502 inhibited the lipid peroxidation approximately 4 times more potently than propranolol. These data show that 18-502 exerts favorable effects during myocardial ischemia produced by coronary stenosis and that it has a cardioprotective action against the contractile dysfunction following reperfusion.

Adrenergic beta-Antagonists↗