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Biomedical subjects

H Ono

Publications and source records attributed to H Ono.

At least 649 records · Page 36Linked to original sources

Isolated, blood-perfused phrenic nerve-diaphragm preparation of the dog: description of a new method and effects of neuromuscular blocking agents on twitch tension and blood flow.

An isolated, blood-perfused phrenic nerve-diaphragm preparation of the dog was developed for pharmacological investigation. A hemi-diaphragm with the ipsi-lateral phrenic nerve intact was excised from a dog anesthetized with pentobarbital sodium and was perfused with arterial blood from a donor dog through the phrenic artery. This preparation maintained its tone and response in good condition for 10 hr without any deterioration of twitch tension. Effects of succinylcholine, d-tubocurarine, decamethonium, and gallamine on twitch tension and blood flow of this preparation were studied. Drugs were injected into the phrenic artery. All four compounds produced a dose-dependent depression of twitch tension elicited by indirect stimulation applied to the phrenic nerve without any depression in the tension elicited by direct stimulation applied to the muscle. The ratios of the potency to produce a 50% depression in twitch tension elicited by indirect stimulation among succinylcholine, decamethonium, d-tubocurarine, and gallamine were roughly 1:1/3:1/3:1/30 on a weight (mg) basis. d-Tubocurarine produced a dose-dependent increase in blood flow. Other compounds did not cause significant changes in blood flow. The increase in blood flow produced by d-tubocurarine was markedly inhibited by diphenhydramine, which suggested histamine release by d-tubocurarine.

Animals↗

Journal of experimental psychology: human perception and performance.

We examined the nonveridicality of visual direction produced by monocular viewing. In Experiment 1, 19 subjects pointed to a small light and moved a small light to their subjective median plane. The extent of constant error under monocular and binocular viewing conditions differed in both tasks (p less than .001). The monocular-binocular difference was larger when the viewing distance was 25 cm than when it was 50 cm (p less than .01). Also, correlations between phoria and monocular-binocular differences ranged from .58 to .77, depending on viewing distances and tasks. The effects of phoria within the context of Hering's .001). The monocular-binocular difference was larger when the viewing distance was 25 cm than when it was 50 cm (p less than .01). Also, correlations between phoria and monocular-binocular differences ranged from .58 to .77, depending on viewing distances and tasks. The effects of phoria within the context of Hering's .001). The monocular-binocular difference was larger when the viewing distance was 25 cm than when it was 50 cm (p less than .01). Also, correlations between phoria and monocular-binocular differences ranged from .58 to .77, depending on viewing distances and tasks. The effects of phoria within the context of Hering's principle of visual direction can account for these results. In Experiment 2, the same subjects adapted to phoria-induced error by placing a finger over a monocularly viewed target. The difference in their pointing responses before and after the task were reliable (p less than .005), and the correlations between phoria and the pre- to posttest differences were .45 and .77, depending on the number of adaptation trials. We argue that all monocular experiments dealing with visual direction should control for these effects.

Discrimination, Psychological↗

Excitation by lyoniol-A of vagal afferent nerves and the reflex autonomic and somatic actions in rats.

Lyoniol-A (2mg/kg, i.v.), a toxic component isolated from the Ericaceous tree, markedly caused the increase in rate of discharges from vagal afferent nerves in the rat. This agent also caused respiratory depression, hypotension and the relief of decerebrate rigidity. These effects of lyoniol-A on the respiration an the rigidity were absent under conditions of bilateral cervical vagotomy, and the hypotension was abolished by sectioning of both vagal and carotid sinus nerves. These results suggest that the excitation by lyoniol-A of the afferent activities reflexly produces respiratory depression, hypotension and the relief of decerebrate rigidity.

Animals↗

Decrease in effects of muscimol on the dorsal root after repeated administration of diazepam in rats.

In in situ experiments on spinal rats transected at the C1 level and on non-spinal rats, muscimol (3 mg/kg, i.v.) depolarized the primary afferent fibers and diazepam (3 mg/kg, i.v.) potentiated this effect of muscimol. When diazepam was given for 14 days, the effect of muscimol was significantly reduced in non-spinal rats. These findings suggest that diazepam probably interacts with GABA-ergic mechanisms more closely in supraspinal regions of the rat.

Animals↗

Analysis of the mechanism of acute decrease of blood pressure induced by captopril (SQ 14,225) in dogs by the use of aprotinin, SAR1-ILE8-angiotensin II and indomethacin.

Acute effects of captopril (SQ 14 225) on blood pressure were investigated in pentobarbital anesthetized dogs. Intravenous captopril (0.1-3 mg/kg) caused reduction of blood pressure dose-independently, while dose-dependent attenuation of exogenous angiotensin I-induced pressor response and potentiation of bradykinin-induced reduction of blood pressure were observed wih the same doses of this agent. This acute decrease in blood pressure was partially inhibited by a pretreatment with any one of aprotinin, Sar1-Ile-8-angiotensin II and indomethacin. More significant inhibition of the blood pressure decrease was observed after the combined pretreatment with Sar1-Ile8-angiotensin II and indomethacin or that with all the three drugs, though no complete abolition of the blood pressure decrease was achieved. These results suggest that captopril may decrease blood pressure in anesthetized dogs through other mechanism(s) in addition to angiotensin converting enzyme inhibition, including the prostaglandin release probably from the kidney.

1-Sarcosine-8-Isoleucine Angiotensin II↗

Effects of perhexiline on hemodynamics in anesthetized open-chest dogs.

Cardiohemodynamic effects of perhexiline were investigated in anesthetized open-chest dogs, measuring blood flow rates of the pulmonary artery (PAF), superior and inferior venae cavae (SVCF and IVCF), right atrial pressure (RAP), systemic blood pressure (SBP), and heart rate (HR). Sum of SVCF and IVCF was interpreted as venous return (VR). Perhexiline, 0.3-3 mg/Kg, injected intravenously over 2 min caused dose-dependent increases in PAF, VR, and RAP, followed by decreases in PAF and VR at higher doses. SBP and HR were depressed with perhexiline dose-dependently. Verapamil, 0.03-0.3 mg/Kg, also increased PAF, VR, and RAP to the lesser extent than perhexiline. Verapamil decreased these variables except RAP more markedly than perhexiline. Treatment with propranolol (1 mg/Kg) and phentolamine (1 mg/Kg) which completely blocked cardiohemodynamic effect of 1 microgram/Kg of norepinephrine, markedly attenuated the effects of perhexiline on VR and PAF but not completely. It is concluded that the effect of perhexiline to increase VR and PAF is in most part mediated through the cardiovascular reflex control for blood pressure reduction by the drug, though a direct effect on capacitance vessels may be included.

Anesthesia↗

Facilitation of Neuromuscular transmission by calcium antagonists, diltiazem, nifedipine and verapamil, in the dog.

Effects of three Ca++-antagonists, diltiazem, nifedipine and verapamil, on the neuromuscular junction were investigated in the in situ canine anterior tibial muscle preparation by close-arterial injections via the femoral artery. All these Ca++-antagonists dose-dependently augmented the twitch tension elicited by indirect stimulation applied to the common fibular nerve at a frequency of 0.1 or 0.2 Hz. The maximum of the twitch tension reached about 130% of the control by 10 mg of nifedipine, or 30 mg of diltiazem or verapamil. Nifedipine was approximately 3 times as potent as diltiazem or verapamil. Nifedipine was approximately 3 times as potent as diltiazem or verapamil in this augmentation. On the other hand, these doses of Ca++-antagonists had little effects on the twitch tension elicited by direct stimulation of the muscle. The tetanic contraction elicited by indirect stimulation of 30 Hz was partially inhibited and the post-tetanic potentiation of the twitch tension was also slightly depressed with diltiazem and verapamil. Nifedipine induced slight increases in the tetanic contraction and the post-tetanic potentiation. In addition it was demonstrated that these Ca++-antagonists depressed the acetylcholine-induced contraction of the skeletal muscle.

Acetylcholine↗

Effect of Ca2+-antagonistic vasodilators, diltiazem, nifedipine, perhexiline and verapamil, on platelet aggregation in vitro.

Ca2+-Antagonistic vasodilators, diltiazem, nifedipine, perhexiline and verapamil, showed inhibitory activity on platelet aggregation in human platelet-rich plasma (PRP) induced with ADP, adrenaline and collagen. Preincubation of PRP with one of the drugs effectively prevented the aggregation induced by ADP, ID50s being 2.1 x 10(-4), 3.5 x 10(-5), 3.4 x 10(-5) and 2.3 x 10(-4) g/ml for diltiazem, nifedipine, perhexiline and verapamil, respectively. Nifedipine and perhexiline were equipotent and about 10 times as potent as diltiazem and verapamil. In addition, PRP maximally aggregated with 9.1 mumol/l ADP was disaggregated by administration of any of these drugs. The mechanism of action was considered to be Ca2+-antagonism because, with the exception of perhexiline, the potency ratio of the anti-aggregating activity had a close resemblance to that of the vasodilator activity of these drugs previously reported in the literature. Perhexiline showed the most potent anti-aggregating activity but has been reported to be the least potent vasodilator among the Ca2+-antagonists studied. This further studies are necessary to elucidate the mechanism of perhexiline's inhibition of platelet aggregation.

Adenosine Diphosphate↗

[Experimental studies on metabolism of iron overload in dogs with carbon tetrachloride induced chronic hepatic injury (author's transl)].

In order to clarify the influence of iron overload in the liver, histological and histochemical examinations were performed on the dogs to which colloidal iron (chondroitin sulfuric iron) as well as inorganic iron (ferrous sulfate) was intravenously administered for a long period. The experimental animals were firstly divided into two groups were respectively subdivided into three groups; the two corresponding to the injected irons and the one with no iron injection. Also the liver iron content was measured by atomic absorption spectrophotometry when the animals were sacrificed. The results were summarized as follows: 1) Even in the group in which only CCl4 was given without any iron solution, positive iron granules were found in Kupffer cells or macrophages at the central necrotic zone of hepatic lobules. The liver iron content was 80.15 +/- 25.74 microgram/100mg wet weight and higher than that of 35.20 +/- 6.13 micro/100mg.w. w. in normal control group, however, there were no significant difference between these two values (Fig. 1). 2) In the group in which only colloidal iron was given, iron deposition was limited to the Kupffer cells and did not appear in hepatocytes unless the liver content reached to 978.0 microgram/100mg.w.w.. On the contrary, in the group in which only inorganic iron was given, positive iron granules were already found in hepatocytes at the peripheral zone of hepatic lobules with liver iron content of 157.7 microgram/100mg.w.w.. 3) In the group in which inorganic iron was administered with CCl4, positive iron granules were found in hepatocytes, even though the level of liver iron content was as low as 81.86 microgram/100mg.w.w. being far lower than that in the group without CCl4. 4) Liver iron content was well correlated with the duration of administration of iron solution, irrespective the kinds of injected iron. And the slope of the regression line in the group in which only colloidal iron was given was steeper than that in the group in which only inorganic iron was administered (Fig. 2). And also the slope of the regression line in the group in which colloidal iron was administered with CCl4 was steeper than that in the group without CCl4 (Fig. 3). 5) In the group in which colloidal iron was administered with CCl4, marked iron deposition was observed in Kupffer cells or macrophages at the central necrotic zone of hepatic lobules, and accompanied by hepatic fibrosis in chronic cases. These results indicate that the long-term administration of colloidal iron may accelerate the hepatic fibrosis when chronic hepatic injury co-existed, even if it seems that it is mostly metabolized in reticuloendothelial system of the liver.

Animals↗

Effects of perhexiline on contractile response of rabbit aorta to norepinephrine and potassium.

Perhexiline (3.2 X 10(-7)-6.4 X 10(-6) M) and verapamil (2 X 10(-8)-2 X 10(-7) M) inhibited the contraction of rabbit aorta induced with 40 mM K+ and with low concentrations (5.9 X 10(-9)-5.9 X 10(-8) M) of norepinephrine more effectively than the contraction induced by higher concentrations of norepinephrine. The tension induced by 1.2 X 10(-6) M norepinephrine was augmented with the above concentrations of perhexiline and verapamil. Higher concentrations (3.2 X 10(-5)-6.4 X 10(-5) M) of perhexiline significantly reduced the peak tension induced by norepinephrine. The results suggest that perhexiline is a Ca2+ antagonist and also has an unspecific spasmolytic action.

Animals↗