[Recurrent aseptic meningitis following influenza vaccination in a case of systemic lupus erythematosus].
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Biomedical subjects
Publications and source records attributed to K Kogure.
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The regional distribution of substance P-like immunoreactive (SPI) structures in the lower brainstem of the human fetus was investigated using the indirect immunofluorescence technique. SPI cells were found in a number of areas including the inferior colliculus, central gray matter of the midbrain, n. laterodorsalis tegmenti, midbrain and medullary reticular formation, n. vestibularis inferior, and n. prepositus hypoglossi. An extensive network of SPI fibers of varying densities were identified throughout the lower brainstem.
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Post-ischemic changes in energy metabolites and natural antioxidant compounds have been measured in rat brain in vitro concurrent with two different assays for peroxidized lipids. No exogenous free radical initiators were employed. In vitro oxygenation of minced brain preparations for periods of 10 minutes to 4 hours, following 5 minutes of preparatory ischemia, yielded increased levels of lipid conjugated dienes and TBA-reactive material, in contrast to anaerobically incubated preparations. However, either aerobic or anaerobic incubation of brain minces facilitated increased ratios of lactate:pyruvate and glutathione (oxidized):glutathione (reduced), as well as increased total ubiquinone content and loss of alpha-tocopherol. Observation of lipid radical formation in vivo was then attempted using rats given embolic stroke in one hemisphere and left in the post-ischemic condition for times up to 24 hours. Conjugated dienes were found in lipids extracted from the ipsilateral hemisphere but not from the contralateral hemisphere. These observations of conjugated dienes in vivo (formed presumably during post-ischemic reperfusion) and in vitro (facilitated by oxygenation of brain minces), indicate that lipid radical intermediates and associated chain peroxidation processes are potentiated by ischemia and occur during tissue reoxygenation.
Phosphorus nuclear magnetic resonance with surface coils was used to investigate the regional metabolism of the rat brain in vivo under conditions of normoxia, severe hypoxemia, partial necrosis, and partial ischemia. The results show an increase in sugar phosphate and/or inorganic phosphate with injury in accordance with in vivo assays. The technique provides a powerful means of monitoring the metabolism of stroke and its response to therapy in vivo.
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The mechanisms responsible for early prenecrotic ischemic brain edema were investigated in rats by comparing brain metabolism, tissue water (HOH) content, and sodium and potassium ion concentration in brain during ischemia induced by decapitation, by the Pulsinelli-Brierley technique, and by carotid embolization. Although brain metabolic functions were similarly disturbed in all three groups, an increase in brain HOH occurred only in the embolism model, which allowed collateral perfusion. Early ischemic brain edema is therefore dependent upon (1) impaired energy-dependent ion pumps and (2) a hydrostatic pressure gradient from patient vascular lumens. Elevated perfusion pressure increases the extent of this early edema. Induced hypertension causes impairment of blood-brain barrier function, as evidenced by extravasation of Evans blue dye 5 minutes after embolic ischemia, and strikingly increases the extent of macromolecular extravasation 4 hours after ictus. This increased protein leakage is accompanied by elevated HOH content and sodium concentration, as compared to findings in normotensive animals. It is concluded that the use of induced hypertension as a therapeutic modality in patients with acute stroke may be harmful.
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The ability of neutral red to serve as an internal pH indicator in biological systems was tested in the rat brain after parenteral adminstration of the dye. The injected dye is avidly taken up by the brain cells and is distributed mainly in intracellular organelles. The ratio of optical signals recorded from the frozen brain at 445 and 530 nm and compared with calibration curves provides pH values. Color transition of neutral red ranges from 6.0 to 8.0 pH units. Topographic application of this method is particularly useful in studying local pH changes in brains with developing ischemic foci.
Temporal and site correlation of local cerebral blood flow (1-CBF), tissue redox state, energy metabolism, tissue pH, and cerebral electrophysiological activity in induced cerebral ischemia was performed in rats in an effort to obtain helpful clues for the management of occlusive cerebrovascular disease. CBF decreased acutely in both the embolized and nonembolized hemispheres but returned toward normal in 5 minutes. However, total cerebral oxidative metabolism remained depressed throughout the 30-minute observation period despite improved perfusion. The change in CBF correlated with the development and resolution of tissue acidosis, which was maximal 3 minutes after embolization but became alkaline after 30 minutes, possibly due to accumulation of sodium lactate. Oxidized form of nicotinamide-adenine dinucleotide and cytochrome a,a3 quickly became reduced in the ischemic core, but a tardyspontaneous postischemic tissue perfusion resulted in their hyperoxidation. The CBF-metabolism uncoupling as well as postischemic hyperoxidation of the electron transport system, which is associated with accumulation of pyruvate and lactate, probably resulted from stagnation of electron flow at the entrance to the mitochondrial respiratory processes. Seizures could not account for these results, as paroxysmal changes in the EEG usually appeared only in the nonembolized hemisphere and were not dependent upon lack of energy. These studies confirm that metabolic failure may persist in ischemic tissue despite adequate reperfusion, which may, in fact, contribute to tissue damage through hyperoxidation.
Cerebral infarction was produced in rats by internal carotid injection of 35 mu plastic microspheres. Electroencephalograms were recorded through the scalp and from the thalamus. Regional concentration of endogenous brain ATP was studied by the histochemical bioluminescent method. Following embolization, a specific pattern of seizure propagation is noted. Spike activity appears first in the contralateral hemisphere, then the contralateral thalamus, infarcted thalamus, and finally the cortex. The results of these present experiments suggest that seizure activity following an evolving focal ischemic injury in the brain appears in the face of lowered ATP content.
The direct viable court (DVC) method of determining the number of living bacteria in natural seawater was applied to samples collected from areas around Japan ranging from polluted to oligotrophic. In summer, the DVC comprised 1.5-39.8% (mean, 11.2%) of the total direct count (TDC) in Tokyo Bay, which was highly eutrophic. In offshore areas (Sagami Bay and the Kuroshio region), the percentages ranged from 0.7 to 7.9 (mean 2.8%). In winter, slightly higher percentages were observed in Sagami Bay. The majority of DVC cells were free-living. The distruction of bacteria correlated closely with particulate or dissolved organic matter.
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Diffuse leptomeningitis did not occur in healthy adult male Wistar rats with transient candidemia produced by the injection of organisms into the internal carotid artery, even though intraparenchymal microabscesses with yeasts and pseudohyphae were seen throughout the brain. Candida albicans was culturally identified in the brain and kidney. Injecting the organisms into the cisterna magna caused an infection characterized by lymphocytes and histiocytes and was confined to the leptomeninges. In this meningeal model, fungi were recovered only from the CNS. The overwhelming prevalence at autopsy of cerebral candidal microabscesses without diffuse leptomeningitis is apparently due to transient candidemia. Meningitis due to candidemia is rare and seems to require a microabscess that is accessible to the circulating CSF. This latter event is a late and overwhelming feature of cerebral candidiasis.