Changes in cerebrocortical pO2-distribution, rCBF and EEG during hypovolemic shock.
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Biomedical subjects
Publications and source records attributed to W Meier-Ruge.
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The activities of glycolytic enzymes were determined in human autoptic temporal lobes from patients with different forms of dementia. For some enzymes (hexokinase, phosphofructokinase and phosphoglycerate mutase) the effect seen in dementia can be regarded as an intensification of the normal ageing affect. For other enzymes (aldolase, phosphoglucose isomerase, triosephosphate isomerase and lactate dehydrogenase) no changes in enzyme activities corresponding to those found in dementia are observed in the normal ageing process. These effects are most pronounced in the non-vascular Alzheimer cases. With the exception of triosephosphate isomerase and lactate dehydrogenase, enzyme activity is also reduced in bronchopneumonia. The effects of dementia and bronchopneumonia on the activities of glycolytic enzymes in human autoptic brain tissue are often difficult to distinguish.
Stereologic parameters of the capillaries and nerve cells of the brain cortex and putamen were investigated. Thirty-eight brains from subjects aged between 19 and 94 years were examined. All cases were free of metabolic, neurologic and psychiatric diseases. It is demonstrated that the capillary diameter remains unchanged during aging in both brain cortex and putamen. However, in the putamen the total capillary length per unit volume and the capillary volume fractions increase (approximately 60%) progressively with age. Consequently the mean inter-capillary distances in the putamen decrease (approximately 15%). These age-induced changes in the putamen indicate shrinking of subcortical brain structures. In contrast to those of the putamen, the morphometric data of the capillaries in the cortex remain unchanged during the aging process. Stereologic investigations of nerve cells in the brain cortex and putamen revealed that only in brains over 85 years of age can a significant decrease in nerve cell size be demonstrated. A correlation of all the data by a correspondence analytical procedure showed that only the surface/volume ratio of the capillaries correlates with the nerve cell size. This observation suggests a functional interaction between the nerve cells and the capillaries. From the data presented it becomes apparent that the shrinkage of the gyri in the aging brain is not a change in the volume of the cortex, but a decrease in the volume of subcortical structures.
Changes in the pericapillary microenvironment of adult (18-month-old) and senescent (27 1/2-month-old) Fischer-344 rats treated for 6 weeks with daily IP injections of brovincamine or apovincamine (0, 2.5, 5, 10 mg/kg) were correlated with spontaneous locomotor activity and [14C]-2-deoxyglucose uptake of the brain. The animals were tested for spontaneous locomotor activity in a tunnel maze. Twenty-four hr after behavioral testing and subsequently after a [14C]-2-deoxyglucose injection, brains were removed and capillaries stained with alkaline phosphatase reaction, being later measured with an optical-electronic image analysis technique. Results revealed an increase in intercapillary distance, as a sensitive parameter for capillary density, in the hippocampus (CA1) and in the parietal cortex (area 39) in association with aging. Capillary diameter in the parietal cortex was found to be increased age dependently. A similar age-related increase was also observed in the CA1 field but this age trend was not significant. Chronic treatment with the vincamines produced a dose-dependent reduction in intercapillary distance in senescent animals which approached the level of untreated adult control rats. Significant negative correlations were found between maze locomotion and intercapillary distance among senescent rats. Furthermore, intercapillary distance and local relative 2-deoxyglucose uptake tended to be negatively correlated in both age groups. These findings provide evidence for the working hypothesis that mean intercapillary distance can be considered as an indicator of neuronal activity in the pericapillary microenvironment.
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It is known, that plasmin is capable of specifically activating the complement factors C1 q and C3. In addition plasmin can activate procollagenase to collagenase. Since both mechanisms could possibly play a decisive role in the pathogenesis of rheumatoid arthritis, we have carried out animal experiments to investigate the primary role of plasmin in the development of arthritis. Twenty-two rabbits were subjected to intraarticular injection with an equal dose of plasmin on days 1, 4, and 8. An aspirate was taken on day 9 for a white cell count and a histological investigation of the synovial tissue. Already after a single dose of 0.25 CU plasmin an inflammatory reaction was clearly observed. Increasing amounts of plasmin (2.5 and 12.5 CU) caused an increased inflammatory response. On the basis of these results, it is discussed whether the observed arthritic reaction after plasmin injection is caused by complement activation. Possible analogies with rheumatoid arthritis are discussed.
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