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B Mihara

Publications and source records attributed to B Mihara.

48 records · Page 3Linked to original sources
PubMed1988

Autoradiographic analysis of second-messenger systems in the gerbil brain.

Quantitative in-vitro autoradiographic study was performed to localize two prominent second-messenger systems (the adenylate cyclase and phosphoinositide systems) in the normal gerbil brain. [3H] Forskolin and [3H] phorbol 12, 13-dibutyrate (PDBu) were used to identify the regional distribution of adenylate cyclase and protein kinase C, respectively. The localization of the forskolin binding was not uniform, being particularly concentrated in the striatum, the accumbens nucleus, the olfactory tubercle, the substantia nigra, the CA3 region of the hippocampus and the molecular layer of the cerebellum. On the other hand, the PDBu binding was rather uniform, although the superficial layer of the cerebral neocortices, the strata oriens of the CA1 region of the hippocampus and the molecular layer of the cerebellum showed relatively dense binding. Quantitative autoradiography of the second-messenger systems in the brain is expected to provide important information concerning the role of neurotransmitters in the pathophysiology of various conditions.

Animals↗
PubMed1988

Comparison between the photoelectric method and H2 clearance method for measuring cerebrocortical blood flow in cats.

The photoelectric method using carbon black as a nondiffusible tracer of blood was compared with the hydrogen clearance (H2) method in nine anesthetized cats. A photoelectric apparatus and H2 electrode were applied to a small region of the cerebral cortex (left ectosylvian gyrus) for simultaneous measurement of the regional CBF. The values of CBF(H2) and CBF(photoelectric) were 50.7 +/- 19.2 and 52.1 +/- 14.5 ml.100 g-1.min-1, respectively. CBF(H2) and CBF(photoelectric) were found to correlate well (r = 0.588, p less than 0.01) when changes in CBF were induced by CO2 inhalation, exsanguination, hyperventilation, and occlusion of the middle cerebral artery. The correlation between CBF(H2) and CBF(photoelectric) was much better in the case of intraindividual comparisons (r = 0.957, p less than 0.01). In addition to its merits in common with the H2 clearance method, such as handiness, low cost, and strict regionality, the photoelectric method displayed the following advantages: time-to-time measurements of CBF (less than 20 s), immediate display of the microcirculatory flow pattern, and simultaneous monitoring of cerebral blood volume. However, measurements from deep structures of the brain are better performed by the H2 method despite the disadvantage of the use of a potentially explosive gas.

Animals↗
PubMed1988

Are blood platelets involved in the pathogenesis of ischemic brain edema in gerbils?

Edema formation following severe permanent or temporary cerebral ischemia in gerbils with an artificially reduced platelet count was investigated. Acute focal cerebral ischemia was produced by extracranial carotid ligation, and the local cerebral blood flow was estimated using the hydrogen clearance method. Brain tissue water and sodium and potassium contents were taken as indexes of brain edema. The platelet count was reduced in some gerbils by intravenous injection of neuraminidase. After 60 minutes of ischemia, a marked increase in tissue water and sodium contents accompanied by a decrease in potassium content was observed in untreated gerbils. However, gerbils with a reduced platelet count revealed similar but significantly smaller changes in all the measured parameters. Restoration of blood flow after 60 minutes of ischemia resulted in further accumulation of water and sodium and in depletion of potassium in both groups. These changes were significantly smaller in the gerbils with a reduced platelet count. It is concluded that platelets, activated by cerebral ischemia, may be involved in the development of ischemic brain edema in gerbils.

Animals↗
PubMed1988

Bilateral hemispheric reduction of cerebral blood volume and blood flow immediately after experimental cerebral hemorrhage in cats.

Acute cerebral circulatory changes following experimental cerebral hemorrhage were investigated in eight cats. The cerebral hemorrhage was produced in the right basal ganglia by introducing arterial blood via a thin catheter, using the systemic arterial blood pressure of the cat as a driving force. Local cerebral blood volume was measured continuously in the bilateral parietotemporal cortexes employing photoelectric apparatuses. Carbon black dilution curves were recorded from the regions, and the mean transit time of blood was calculated. Local cerebral blood flow was estimated from mean transit time and cerebral blood volume. Intracranial pressure was monitored continuously in the right parietal epidural space. Five minutes after cerebral hemorrhage, intracranial pressure increased by 24.0 +/- 6.1 mm Hg, while mean arterial blood pressure increased by only 2.9 +/- 2.0 mm Hg. Cerebral blood volume decreased by 1.60 +/- 0.24 vol% in the hemorrhagic and 1.14 +/- 0.30 vol% in the nonhemorrhagic hemisphere. Cerebral blood flow decreased by 30.0 +/- 4.5 ml/100 g brain/min in the hemorrhagic (initially 64.5 +/- 13.6) and by 30.3 +/- 7.5 ml/100 g brain/min in the nonhemorrhagic (initially 60.9 +/- 6.9) hemisphere. Increased intracranial pressure appeared to be the main cause of the observed cerebral blood volume/flow reduction shortly after experimental hemorrhage in the basal ganglia. Several other factors and mechanisms involved are discussed.

Animals↗
PubMed1986

Dual effect of naloxone on blood platelet aggregation and cerebral blood flow in gerbils.

The effect of naloxone on blood platelet aggregation and cerebral blood flow in gerbils was studied. Administration of naloxone in dose 1 mg/kg to intact gerbils resulted in a marked increase in platelet aggregability accompanied by 27% reduction in cerebral blood flow. Focal cerebral ischemic injury significantly enhanced platelet aggregatory response and treatment with naloxone was without any additional effect on platelet aggregation. Cerebral blood flow in ischemic hemisphere, however, increased following naloxone injection by 46%. In vitro naloxone in millimolar concentrations inhibited platelet aggregation in a dose-dependent way. Apparent decrease in fluorescence of platelet membranes tagged with fluorescence probe due to naloxone suggests conformational changes in platelet membrane as a primary mechanism for the antiaggregatory effect of naloxone in vitro.

Animals↗
PubMed1983

Transfer function through regional cerebral cortex evaluated by a photoelectric method.

A new technique is reported for obtaining the transfer function through the regional cerebral cortex. Tissue carbon-black (CB) dilution curves were recorded with a photoelectric apparatus used as a densitometer head in cat cortex in situ following intracarotid injection of 0.2 ml of 1/40 diluted CB solution. The linearity and stationarity of the vascular system, reproducibility of the curve, and recirculation were tested. The tissue CB dilution curve, a cumulative distribution function, was first differentiated yielding two curves comprising the inlet and outlet curves. The error due to "overlapping" was corrected for by extrapolation using the gamma-density function. The transfer function through the cortex was then calculated by numerical deconvolution of the inlet and outlet curves. The validity of the calculated transfer function was verified by comparison with that obtained from actual CB dilution curves recorded simultaneously from the pial artery and superior sagittal sinus. The transfer function was further subjected to moment analysis for determining the intraparenchymal circulatory parameters of the cerebral cortex. Some examples demonstrating the applicability of technique are given.

Animals↗
PubMedDate not supplied

Three-dimensional analysis of human carotid atherosclerotic ulcer associated with recent thrombotic occlusion.

To clarify the mechanism of ulcer formation of atherosclerotic plaques in human carotid arteries, autopsy investigations were performed on eight patients who had died of cerebral infarction due to recent carotid thrombosis. Eleven control patients who had carotid atherosclerosis without thrombosis were also investigated. Histological changes of the arteries in serial sections were reconstructed three-dimensionally. Each artery with occlusive thrombosis was found to have an intimal ulcer at the head of the thrombus on the proximal slope near the base of the thickened atheromatous plaque at the carotid sinus. Most ulcers formed obliquely or longitudinally, were parallel to the vessel axis, had a fusiform shape, and measured 7 +/- 2 x 3 +/- 1 mm (mean +/- s.d.). The ulcers arose by marginal separation of the innermost layer from the underlying layer of the stratified intima. An underlying atheroma developed along the borders of these intimal layers reaching the subendothelium, with thinning of the intimal cap to less than 150 microns. The process of ulceration may be generated by vessel injury induced by hemodynamic forces, such as tensile forces and shear stress. The ulcer may extend along the fragile region where the wall may exhibit uneven compliance due to differences in the tissue structures of each intimal layer. Furthermore, macrophages may play a key role in ulcer formation.

Adult↗
PubMedDate not supplied

No intracerebral steal phenomenon in the ischemic brain following papaverine administration.

The steal phenomenon due to a vasodilator was investigated in 6 cats in which cerebral ischemia had been produced by left middle cerebral artery (MCA) occlusion. The photoelectric method was employed for continuous recording of the cerebral blood volume together with frequent determinations of the cerebral blood flow (CBF) through the ischemic cerebral tissue at the following four stages: before MCA occlusion, 2 hours after MCA occlusion before the injection of papaverine, after the injection of papaverine, and when the systemic arterial blood pressure (SABP) was adjusted non-pharmacologically to the control level using a "vasculator". The administration of the vasodilator produced conflicting results for the CBF changes in the ischemic area with a decrease in SABP as reported previously in the literature. However, when the SABP was corrected to the control level, the CBF in the ischemic region became increased in all 6 cases to above the control ischemic flow values. It is concluded that the decreased CBF in the ischemic tissue after vasodilator administration was not due to the steal phenomenon, but simply to a fall in SABP.

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