Brain ischemia, obscenity, and the elusive cerebral perfusion pressure*
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Brain ischemia
Energy deficiency and oxidative stress are stages of the biochemical cascade in brain damage of ischemic origin. There is information in the literature about their changes in certain types of ischemia, but there are no data on the features and comparative characteristics in cerebral ischemia of varying severity. It was found that the most pronounced disturbances in the prooxidant-oxidant balance and energy metabolism were observed in total cerebral ischemia. Similar, however, less pronounced disorders were found in daily subtotal ischemia and in the subgroup of stepped subtotal ischemia with an interval between ligation of the common carotid arteries of 1 day. The least pronounced disorders were in the subgroup with an interval between ligation of the common carotid arteries 7 days The aim of the work is to assess the state of the energy and oxidative processes of the brain during its ischemia of varying severity.
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Cerebrovascular disease is the third leading cause of death in the industrialized world and is also a major cause of long-lasting disability. The development of gene deficient and transgenic mice has recently aided in research into and development of specific surgical procedures for brain ischemia in mice. The models of brain ischemia are divided into global ischemia and focal ischemia. Global ischemia is divided into two sub-models, forebrain ischemia and total ischemia. Forebrain ischemia is widely used to analyze delayed neuronal cell death including apoptosis, while total ischemia is used to clarify the neuronal cell death by the systemic ischemia such as cardiac arrest. On the other hand, focal ischemia is used to analyze pathological stroke. Pathophysiology of brain ischemia has been clarified by the use of these models. This review outlines the pathways that lead to cell death following ischemia. Moreover, we have reviewed these currently-used mouse experimental models of global and focal ischemia.
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The general failure of neuroprotectants in clinical trials of ischemic stroke points to the possibility of a fundamental blind spot in the current conception of ischemic brain injury, the "ischemic cascade". This is the first in a series of four papers whose purpose is to work towards a revision of the concept of brain ischemia by applying network concepts to develop a bistable model of brain ischemia. This first paper sets the stage for developing the bistable model of brain ischemia. Necessary background in network theory is introduced using examples from developmental biology which, perhaps surprisingly, can be adapted to brain ischemia with only minor modification. Then, to move towards a network model, we extract two core generalizations about brain ischemia from the mass of empirical data. First, we conclude that all changes induced in the brain by ischemia can be classified as either damage mechanisms that contribute to cell death, or stress responses that contribute to cell survival. Second, we move towards formalizing the idea of the "amount of ischemia", I, as a continuous, nonnegative, monotonically increasing quantity. These two generalizations are necessary precursors to reformulating brain ischemia as a bistable network.
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AIM:Platelet-activating factor(PAF) bas been reported to be an active mediator of neuronal damage in regional cerebral ischemia on the basis of indirect pharmacological data from PAF antagonists. The direct measurement of PAF has not been reported previously in regional cerebral ischemia. It prompted us to investigate the change of PAF in unilateral ischemia in gerbils and regional ischemia in rats.METHODS:Thin layer chromatography was combined with biological methods for the determination of PAF in brain after cerebral ischemia.RESULTS:(1) The PAF content of ischemic brain was increaesd significantly in gerbils subjected to 3 h unilateral cerebral ischemia followed by 2h reperfusion respectively(4.40±0.90) and (1.30±0.40) pg/g, P 0.05. (2)The PAF content of ischemic brain was increased significantly also in rats subjected to 48 h regional ischemia respectively(5.74±0.75) and (0.76±0.05)pg/g, P 0.05. CONCLUSION:PAF could contribute to secondary neuronal damage after regional cerebral ischemia.
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The general failure of neuroprotectants in clinical trials of ischemic stroke points to the possibility of a fundamen-tal blind spot in the current conception of ischemic brain injury, the “ischemic cascade”. This is the first in a se-ries of four papers whose purpose is to work towards a revision of the concept of brain ischemia by applying network concepts to develop a bistable model of brain ischemia. This first paper sets the stage for developing the bistable model of brain ischemia. Necessary background in network theory is introduced using examples from developmental biology which, perhaps surprisingly, can be adapted to brain ischemia with only minor mod-ification. Then, to move towards a network model, we extract two core generalizations about brain ischemia from the mass of empirical data. First, we conclude that all changes induced in the brain by ischemia can be classified as either damage mechanisms that contribute to cell death, or stress responses that contribute to cell survival. Second, we move towards formalizing the idea of the “amount of ischemia”, I, as a continuous, non-negative, monotonically increasing quantity. These two generalizations are necessary precursors to reformulat-ing brain ischemia as a bistable network.
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Microdialysis
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Objective To study the effect of β aescinate on NO metabolism in acute ischemia and ischemia reperfusion model of rat brain. Methods The acute ischemia and ischemia reperfusion model of rat brain was induced by blocking of four vessels. The rats were divided into seven groups: control group; 30 minute global ischemia group; 30 minute global ischemia+drug group; 30 minute global ischemia and 30 minute reperfusion group; 30 minute global ischemia and 30 minute reperfusion +drug group; 30 minute global ischemia and 5 day reperfusion group; 30 minute global ischemia and 5 day reperfusion group. β aescinate (10 mg/kg, iv) was injected before operation. The changes of the contents of NO, MDA and SOD in the cortex and serum were observed. Results Compared with the rats in the drug group, those in the ischemia group and ischemia reperfusion group showed a significant increase in concentrations of NO and MDA in the cortex and serum ( F=18.51-123.66, q=5.41- 29.59 , P 0.01), but a significant decrease in the level of SOD ( F=5.87, q=4.81-26.02, P 0.05). Conclusion β aescinate may influence NO metabolism and protect the neuron cells by means of anti free radicals.
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