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Biomedical subjects

T Asano

Publications and source records attributed to T Asano.

At least 847 records · Page 47Linked to original sources
PubMed1982

[The influence of pentobarbital and Y-9179 on regional cerebral blood flow and infarction size in the middle cerebral artery occlusion model in cats (author's transl)].

Following permanent occlusion of the middle cerebral artery (MCA) in cats, the effect of delayed administration of pentobarbital (PBT) and a novel imidazole derivative (Nizofenone or Y-9179) on the regional cerebral blood flow (rCBF) was studied. The rCBF was measured for one week by the hydrogen clearance technique without anesthesia. The overall effects of these drugs on histological changes were also assessed. Twenty-four animals, in which platinum electrodes were chronically implanted in the ten predetermined positions, were divided into following three groups. The control, PBT and Y-9179 groups received the vehicle, PBT (25 mg/kg/day) and Y-9179 (6.25 mg/kg/day), respectively. Drug administration was started 30 min after MCA occlusion and continued for three days. In the affected hemisphere of the animals which survived for one week, histological examination revealed ischemic lesions composed of the marginal, reactive and central zones. The infarction ratio calculated as the ratio of the damaged area to the whole hemispheric area was significantly smaller in the drug treated groups than in the control. In the Y-9179 group, the reduction of the area comprizing the central and reactive zones was particularly prominent. There were no apparent differences in the time-course of the rCBFs between the control and Y-9179 groups. Each channel showed reduction of the rCBF following MCA occlusion. Although slight fluctuations of the rCBF were seen during the first three to four hours, the initially dropped rCBF remained stable in both groups. In the PBT group, on the other hand, an increase of the rCBF took place following the administration of the drug in the area where the rCBF was initially reduced less than about 40 ml/100g/min after MCA occlusion. Most of the electrodes showing such an increase in the rCBF topographically corresponded to the reactive or boundary zone. In the control group, vasogenic edema characterized by the perivascular exudation of plasma fluid was prominent in the periphery of the central zone as well as in the inner layer of the reactive zone. Such changes were almost absent in the Y-9179 group, whereas it was more evident and close to the control in the PBT group. So far as the correlation between the course of the rCBF and the final histological outcome was examined, there was no evidence indicating the beneficial effect of the redistribution of the rCBF by PBT. Y-9179 had no significant action on the course of the rCBF but its anti-edema effect might be related to its cerebral protective action. The mechanism of cerebral protection by PBT or Y-9179 needs further clarification.

Animals↗
PubMed1982

[Relationship between focal cerebral ischemia and cerebral water content (author's transl)].

The correlation between the local cerebral blood flow (lCBF) and the specific gravity (SG) of the topographically corresponding cortical area was examined using a model of regional cerebral ischemia by means of transorbital occlusion of the middle cerebral artery (MCA) in cats. Cats were divided into the following experimental groups. Group A: two hours MCA occlusion followed by two hours recirculation; Group B: two hours MCA occlusion; Group C: four hours MCA occlusion. The lCBF and the SG were measured by the use of hydrogen clearance method and gradient column, respectively. Two hours MCA occlusion resulted in a moderate drop in SG in the cortical areas where the lCBF decreased below 20 ml/100g/min during ischemia (Group B). Four hours MCA occlusion in Group C resulted in a similar drop in SG. Two hours recirculation following two hours MCA occlusion in Group A, however, caused a remarkable drop in SG which was significantly greater than those in Group B and C. There was no correlation between the drop in SG and the level of post-ischemia lCBF (reactive hyperemia) in Group A. Thus, the present study revealed i) that the development of cerebral edema as evidenced by the drop in cortical SG was associated with an extreme reduction in lCBF, ii) that recirculation exerted a detrimental influence on the post-ischemic brain injury and iii) that the edema aggravation during recirculation was not necessarily dependent on the magnitude of reactive hyperemia. Based on the above results, it was suggested that the cause of edema aggravation following recirculation, namely the development of vasogenic edema, might reside in some chemical mechanism such as lipid peroxidation.

Animals↗
PubMed1982

[Cerebral vasospasm and lipid peroxidation--lipid peroxides in the cerebrospinal fluid after subarachnoid hemorrhage].

The relationship between lipid peroxides in cerebrospinal fluid (CSF) and the occurrence of cerebral vasospasm following subarachnoid hemorrhage (SAH) was evaluated by analyzing CSF with high-performance liquid chromatography (HPLC) and gas chromatography mass spectrometry (GC-MS). Hydroperoxy eicosatetraenoic acids (HPETEs) and hydroxy eicosatetraenoic acids (HETEs) were synthesized by the treatment of arachidonic acid with hydrogen peroxide and cupric chloride. The retention time of these HPETEs and HETEs were determined on HPLC. The position of oxydation occurred was determined after methylation, reduction and trimethyl silylation using GC-MS. Thus the elucidation of positional isomers of HPETEs and HETEs was made possible by the retention time on HPLC. The supernant of CSF after SAH was adjusted to pH 3.0 and then absorbed to octadecyl silyl silica column. The eluted fraction with 15% ethanol-water from octadecyl silyl silica column was analyzed by HPLC detecting at 238 nm. No peak was observed on HPLC at the region of HPETEs and HETEs in the CSF obtained from healthy person. In SAH patients, several peaks were recognized in accordance with the occurrence of cerebral vasospasm. One of the peaks was identified as 5-HETE by HPLC and GC-MS. In 10 SAH patients, semi-quantitative analysis of 5-HETE in the CSF was performed by measuring the height of the peak identified as 5-HETE on HPLC. The close correlation was recognized between the occurrence of cerebral vasospasm and the appearance of 5-HETE in the CSF. The results of the present study suggest that lipid peroxidation is involved in the pathogenesis of chronic vasospasm after SAH.

Arachidonic Acids↗
PubMed1981

Stimulation of pre- and postsynaptic dopamine receptors by an ergoline and by partial ergoline.

The capacity of the ergoline, pergolide, and of the partial ergoline, LY 141865, to stimulate pre- and postsynaptic dopamine (DA) receptors was investigated. Binding studies have revealed that pergolide has a high affinity, while the partial ergoline, LY 141865, has a low affinity for the postsynaptic striatal DA receptors in vitro. Two behavioral animal models were used to assess the DA agonist potencies of these compounds for the postsynaptic DA receptors in vivo. Pergolide induced turning behavior in rats with 6-hydroxydopamine (6-OH-DA) lesions, and relief of tremor in monkeys with ventromedial tegmental lesions, at a lower dose and for a longer duration than LY 141865. An in vivo and an in vitro biochemical test was use to measure the ability of these compounds to stimulate presynaptic DA receptors. In the in vitro test, pergolide and LY 141865 were found to have low inhibitory activity for synaptosomal tyrosine hydroxylase, while in the in vivo test, both drugs were effective even in low doses in reversing the gamma-butyrolactone elicited increased accumulation of striatal DOPA. These results suggest that pergolide has a high affinity for pre- and postsynaptic DA receptors, while its partial ergoline analogue has a high affinity for the presynaptic, but not for the postsynaptic DA receptors. The data also suggest that dopamine synthesis in vitro and in vivo may be regulated by different presynaptic DA receptors.

Animals↗
PubMed1981

Chloride-dependent stimulation of GABA and benzodiazepine receptor binding by pentobarbital.

Pentobarbital reversibly increased Na+-dependent GABA binding to bovine cerebral cortex membranes. This effect was chloride-dependent. Kinetic analysis of [3H]GABA binding revealed an increase of the apparent number of binding sites. Pretreatment of the membranes with Triton X-100 extremely diminished the effect of pentobarbital on both [3H]GABA and [3H]flunitrazepam binding.

Animals↗