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Biomedical subjects

M Oba

Publications and source records attributed to M Oba.

At least 55 records · Page 3Linked to original sources
PubMed1988

Cerebral protective effect of flunarizine in a canine model of cerebral ischaemia.

To test the effect of flunarizine on cerebral ischaemia, 15 dogs were subjected to ischaemia, using the 'canine model of the completely ischaemic brain regulated with a perfusion method' in which the cerebral blood flow (CBF) can be fully regulated. Five animals served as untreated controls, 10 received flunarizine, a calcium antagonist (1 mg/kg in 5 dogs and 3 mg/kg in 5 dogs), before the ischaemic period. After 1 h CBF was restored and recovery of the electrical activity of the brain and the degree of brain swelling were observed for 3 h. At the end of the experiments, the degree of extravasation of Evans blue was examined. Remarkable recovery of EEG was found in the groups given flunarizine when compared with untreated controls. However, no significant difference was found between untreated controls and flunarizine treated groups for the degree of brain swelling and the degree of extravasation of Evans blue. These results suggest that the treatment of flunarizine is of benefit for functional recovery against cerebral ischaemia, but does not suppress ischaemic brain oedema.

Animals↗
PubMed1987

Protective effect of phenytoin and its enhanced action by combined administration with mannitol and vitamin E in cerebral ischaemia.

To study the therapeutic effect of phenytoin on cerebral ischaemia and confirm whether or not the effectiveness of phenytoin could be enhanced by combined administration with free radical scavengers, twenty-five dogs were subjected to ischaemia, using the "canine model of the completely ischaemic brain regulated with a perfusion method". Five animals served as untreated controls, fifteen received treatment with several doses of phenytoin and five were treated with 10 mg/kg phenytoin, 2 g/kg mannitol and 30 mg/kg vitamin E. These drugs were administered prior to the production of ischaemia. After one hour ischaemia, cerebral blood flow was restored and the recovery of electrical activity of the brain and the degree of brain swelling were observed for three hours. With regard to the recovery of the EEG, the higher the administered dosage, the better was the degree of recovery of the EEG. And the group which was treated with a combination of phenytoin, mannitol and vitamin E exhibited remarkable recovery of the EEG. With regard to the degree of brain swelling, a similar dose-related suppressive effect was seen in the phenytoin-treated groups. Furthermore, in the combination therapy group, brain swelling was attenuated significantly. Based on these results, it is concluded that phenytoin has a protective effect in cerebral ischaemia and it shows its most remarkable effect when given together with radical scavengers, such as mannitol and vitamin E.

Animals↗
PubMed1987

Experimental study on the reversibility of cerebral ischemia. Residual blood flow and duration of ischemia.

The flow threshold and time threshold for reversibility of cerebral ischemia were studied using a canine model of cerebral ischemia regulated by controlled perfusion of cerebral blood flow (CBF). CBF was continuously monitored with a laser Doppler flow meter, the brain was brought to a constant level of ischemia for a defined period of time, after which recirculation was instituted. The electroencephalogram (EEG) and somatosensory evoked potentials (SEP) were monitored and used as an index of brain function. No recovery of brain function was found following recirculation if the CBF was reduced to a level below 20% of the normal state for more than one hour. When residual blood flow was 30% of the normal level, however, recirculation after one hour of ischemia resulted in nearly complete recovery of brain function. Significant functional recovery was not seen after two or more hours of such ischemia. Nearly complete recovery was also seen following reperfusion within three hours with 40% of normal CBF. It was demonstrated that the reversibility in the ischemic brain was critically correlated to the level of blood flow and its duration. If these results can be applied to the human brain, emergency cerebral revascularization for ischemic stroke should be attempted when critical flow and time thresholds have not been crossed, namely, in less than 1 hour and 3 hours of insult when the residual blood flow is reduced to 30 and 40% of the normal state, respectively. In clinical situations, this "critical time" may be too short for acute revascularization unless cerebral protective measures are applied pre-operatively to prolong the viability period of ischemic cerebral tissue.

Animals↗
PubMed1987

[Cerebral protective effect of flunarizine in a canine model of cerebral ischemia].

Recently there is the hypothesis proposing that ischemic brain damage is associated with intracellular accumulation of calcium (Ca++). Therefore a variety of experiments have been carried out to investigate whether a Ca++-entry blocker was able to protect against brain damage caused by ischemia. The purpose of the present experiment is to study the protective effects of a Ca++ antagonist, flunarizine, on cerebral ischemia. In this experiment fifteen dogs were subjected to ischemia, using the "canine model of the completely ischemic brain regulated with a perfusion method" in which the cerebral blood flow (CBF) can be fully regulated. Five animals served as untreated controls, ten received treatment with flunarizine (1 mg/kg in five dogs and 3 mg/kg in five dogs, respectively). This agent was administered intravenously 20 minutes prior to the production of ischemia, when cerebral blood flow was reduced to one-tenth its normal value while monitoring CBF by means of a laser-Doppler flow meter. After one hour CBF was restored and the recovery of electrical activity of the brain and the degree of brain swelling were observed for three hours. At the end of the experiments, the degree of extravasation of Evans blue in the excised brain was examined. With regard to the recovery of EEG, no recovery of EEG was seen subsequent to recirculation except one dog in the control group. Whereas in the groups treated with flunarizine, remarkable recovery of EEG was found following recirculation in a dose dependent fasion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Cooperative inhibitory effect of follicular fluid and cAMP on hamster oocyte maturation.

Porcine or human follicular fluid inhibited the spontaneous maturation of isolated hamster oocytes in vitro during the first 1.5 h of culture. Moreover, the presence of 50% follicular fluid combined with 100 microM dbcAMP cooperatively reduced the incidence of germinal vesicle breakdown. The addition of FSH also inhibited the resumption of meiosis, and the presence of LH did not overcome the inhibitory effects of follicular fluid and tended to impede isolated hamster oocyte maturation in vitro.

Animals↗
PubMed1986

[Protective effect of phenytoin and its enhanced action by combined administration of mannitol and vitamin E in cerebral ischemia].

Phenytoin is well known as the anticonvulsant agent and also said to protect the brain against ischemic damage. The purpose of the present experiment is to study the therapeutic effect of phenytoin on cerebral ischemia and confirm whether the effectiveness of phenytoin could be enhanced by combination of free radical scavengers such as mannitol and vitamin E. In this experiment, twenty-five dogs were subjected to ischemia, using the "canine model of complete ischemic brain regulated with a perfusion method" in which it is possible to control the degree of blood flow to a cerebral hemisphere via a perfusion pump at will. Five animals served as untreated control, fifteen received treatment with phenytoin (7 mg/kg in five dogs, 10 mg/kg in five dogs and 30 mg/kg in five dogs) and five treated with 10 mg/kg phenytoin, 2 g/kg of mannitol and 30 mg/kg of vitamin E. These drugs were administered intravenously 20 minutes prior to the production of ischemia, when cerebral blood flow was reduced to one-tenth its normal volume. After one hour, cerebral blood flow was restored and the recovery of electrical activity of the brain and the degree of brain swelling were observed for three hours. With regard to the recovery of EEG, no recovery of EEG was seen subsequent to recirculation except one dog in the control group. Whereas in the group treated with phenytoin, gradual emergence of slow wave ws observed soon after recirculation. The higher the administered dosage is, the better the degree of recovery of EEG was seen. Thus, the dose-related recovery of EEG was observed within the dose ranges tested.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

[Experimental study on reversibility of cerebral ischemia--residual blood flow and duration of ischemia].

This experimental study was designed to estimate the flow thresholds and the time thresholds for reversibility of cerebral ischemia. We used a "canine model of completely ischemic brain regulated with a perfusion method", in which the cerebral blood flow (CBF) could be controlled. The residual blood flow was reduced to 10%, 20%, 30% or 40% of normal CBF, and the recirculation was started after 1, 2, 3 or 4 hours of ischemia. CBF was measured by a laser doppler flow meter. EEG and somatosensory evoked potential (SEP) was monitored and used as a parameter expressing the brain function. In the 10% and 20% ischemia group, functional recovery could not be obtained even if reperfusion was started at 1 hour after the onset of ischemia. On the other hand, in the 30% ischemia group, nearly complete recovery of EEG and SEP could be seen when reperfusion was done at 1 hour from the onset of ischemia. But recirculation after 2 hours of ischemia did not lead to significant functional recovery. In the 40% ischemia group, reperfusion within 3 hours of ischemia allowed full recovery of ischemic brain. On the contrary, reperfusion after 4 hours of ischemia showed a gradual deterioration of EEG and SEP. Accordingly, it was clearly demonstrated that the reversibility of ischemic brain was critically correlated to severity and duration of cerebral ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

[Effects of cerebral protective agents in experimental cerebral ischemia. Relationship between the degree of ischemia and EEG].

We have previously demonstrated that the preischemic administration of perfluorochemicals (PFC) in combination with 20% mannitol, vitamin E and dexamethasone is effective in protecting the brain from cerebral ischemia. This experimental study was designed to evaluate the effect and limitation of the post-ischemic administration of those 4 agents on cerebral ischemia. We used "Canine model of complete ischemic brain regulated with a perfusion method." Using this model we were able to control the amount of blood flow to the left cerebral hemisphere by using an infusion pump. Infusion blood volume was reduced to 30%, 40% or 50% of the normal state, then the combined treatment was started 1,2,3,4,5 or 6 hours after the onset of ischemia in each ischemic group. By monitoring the EEG for 8 hours of ischemic period, we were able to evaluate the effect of the drugs on cerebral ischemia. In untreated groups, electrical activity deteriorated gradually. In the 30% ischemia group, the EEG became isoelectric within 1 hour following ischemia. In half of the 40% ischemia group, the EEG became isoelectric but in the other half low voltage slow wave were seen to last for 6-8 hours. In the 50% group, the EEG deteriorated gradually but did not disappear within 8 hours. The effectiveness of the treatment was judged by the degree of the recovery of electrical activity. The effectiveness of the treatment appeared to depend on the severity and the duration of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

[Experimental study of cerebral protective effect on cerebral ischemia of various antioxidants and other agents. With special reference to the combined treatment of mannitol, vitamin E, dexamethasone and perfluorochemicals].

We have previously reported that the combined administration of mannitol and perfluorochemical blood substitutes is evidently effective in protecting the brain from cerebral ischemia. This experimental study was designed to develop more effective method in suppressing brain infarction than the combined treatment of mannitol and PFC. Using the "Canine model of complete ischemic brain regulated with a perfusion method" in which it is possible to control the degree of blood flow to a cerebral hemisphere via a perfusion pump, the effect of eight agents including six kinds as the free radical scavenger on cerebral ischemia was investigated. Eight agents were mannitol, vitamin E (Vit. E), dimethyl sulfoxide (DMSO), vitamin C, glycerol, nizofenone (Y-9179), dexamethasone (Dexa.) and suloctidil (MY-103). After pretreatment with each agent, blood flow was reduced via the pump to 1/10 of the normal state and 1 hour later, return to the normal state was allowed. Subsequent changes in EEG were observed and the effects of the drugs evaluated. In the control group, no recovery of electrical activity was seen, but in six groups among eight treated groups, i.e., treated with mannitol, Vit. E, DMSO, MY-103, Y-9179 and Dexa, gradual emergence of slow waves was observed. And more favorable effects were found when the combined administration of mannitol, Vit. E and Dexa was made in the same experimental schedule as compared with the single administration of each of these drugs. Furthermore in the animals administered with PFC in combination with mannitol, Vit. E and Dexa, flattening of electrical activity could not be seen throughout the period of severe ischemia. Moreover, the power of electrical activity recovered nearly to the preischemic state immediately after recirculation. Although the possible mechanisms are not yet completely clarified, the present results are thought to indicate that this new combination therapy utilizing PFC with mannitol, Vit. E and Dexa may be useful in the treatment of cerebral ischemia.

Animals↗
PubMed1983

[Villaret's syndrome due to extra-cranial internal carotid aneurysm: a case report].

A 69 year-old male was admitted to our clinic with the chief complaint of hoarseness and difficulty in swallowing. These symptoms occurred about 5 months after penetrating neck injury. Neurological examination revealed right ninth to twelfth cranial nerves palsy and Horner's syndrome. Plain skull X-P demonstrated two broken pieces of glass below the right mastoid processus. The right carotid angiogram showed a 45 x 25 mm aneurysm originated from the right internal carotid artery just below the carotid canal. As the first operation, gradual occlusion of right internal carotid artery combined with the right STA-MCA anastomosis was performed. But two days after complete occlusion, left hemiparesis and pseudobulbar palsy appeared. Two months after such episode, aneurysm and the pieces of glass were removed. He discharged on foot with the improvement of the symptoms of lower cranial nerves. Villaret's syndrome caused by the traumatic aneurysm of extracranial internal carotid artery is rare. This case seems to be the first report in Japan.

Aged↗
PubMed1981

Ultrastructure and some biologic properties of human oocytes and granulosa cells cultured in vitro.

Of follicular oocytes with germinal vesicles, 79% resumed meiosis within 48 hours in modified Ham's F-10 medium for oocyte culture, and 59% of them reached the second-metaphase stage of meiosis. An increase in cortical granules and tubular aggregates and a decrease in the Golgi apparatus were observed during the maturation process. Scanning electron microscopy of the oocyte surface revealed a decrease in number and length of microvilli. Nuclear DNA contents diminished to approximately one-half, but cytoplasmic protein contents measured by cytofluorometry were unchanged after culture in spite of these structural changes. Insemination with washed spermatozoa resulted in fertilization of 5 of 43 zona-intact cultured oocytes. After removal of the zona, 6 of 17 cultured oocytes showed polyspermic penetration, although immature oocytes were not fertilized even after removal of the zona. Cultured granulosa cells secreted progesterone spontaneously, and its amount was correlated with follicular size. Ultrastructurally, mitochondria with laminar cristae, enlarged nuclei, dispersed Golgi apparatus, smooth endoplasmic reticulum, lipid droplets in the ooplasm, and granular cytoplasmic protrusions were observed on the oocyte surface.

Cell Membrane↗
PubMed1980

Acute and chronic cardiocirculatory effects of oral prazosin in chronic refractory heart failure.

The acute hemodynamic effects of oral prazosin were investigated in 7 patients with chronic refractory heart failure. A single dose of 1 to 3 mg prazosin produced a significant increase in cardiac index (+17.6%, p less than 0.01) associated with substantial decreases in pulmonary arterial diastolic pressure (-31.6%, p less than 0.02), systemic vascular resistance (-29.7%, p less than 0.01), and double product (-24.1%, p less than 0.02). Plasma renin activity was significantly elevated (+42.4%, p less than 0.02). These effects were found maximum at 2 hours and persisted for 8 hours. The chronic hemodynamic effects in 5 patients with chronic refractory heart failure were evaluated by administration of 1 to 2 mg prazosin 3 times daily for 8 weeks, and ventricular function was assessed by echocardiography and carotid pulse recording. All the patients showed improvement in the clinical symptoms of heart failure. Peripheral venous pressure decreased slightly (-12.5%). ET/PEP increased (+24.5%) without any significant changes in EF and mVcf. Plasma renin activity also slightly increased (+17.8%). Thus, prazosin possesses sustained nitroprusside-like actions, and is effective in the management of chronic congestive heart failure refractory to conventional therapy. While, further investigation is necessary to define the effect of prazosin on plasma renin activity.

Administration, Oral↗