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- Schürer, L, et al.
(författare)
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Effects of neutrophil depletion and superoxide dismutase on postischemic hypoperfusion of rat brain.
- 1990
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Ingår i: Advances in Neurology. - 0091-3952. ; 52, s. 57-62
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Tidskriftsartikel (refereegranskat)abstract
- In the present investigation, the involvement of PMNLs and oxygen free radicals was explored in rats with postischemic perfusion disturbances of the brain. Reversible forebrain ischemia was induced by bilateral clamping of both carotid arteries in combination with hemorrhagic hypotension. This procedure resulted in a reproducible DPH 1 hr after start of recirculation. Neutropenia was induced by sheep ANS. One group received ANS before and a second group immediately after termination of ischemia. Two additional groups received SOD before or immediately after ischemia. Regional postischemic CBF was determined by [14C]iodoantipyrine autoradiography. It was found that CBF significantly improved in cortical structures of animals treated with ANS before ischemia. Treatment with ANS at the end of ischemia had no effect on the postischemic CBF depression. Neither was injection of SOD effective to influence DPH, irrespective whether given before or after ischemia. It is concluded that PMNLs play a role in the development of DPH of the brain, whereas free radical mechanisms seem to be less relevant.
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- Schürer, L, et al.
(författare)
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Is postischemic hypoperfusion related to brain edema?
- 1990
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Ingår i: Advances in Neurology. - 0091-3952. ; 52, s. 155-64
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Tidskriftsartikel (refereegranskat)abstract
- The effect of reversible cerebral ischemia on brain edema development was studied with a gravimetric method. CBF changes after ischemia were correlated with alterations in brain SG. Forebrain ischemia (15 min) was induced in rats by reversible bilateral ligation of both carotid arteries plus induction of controlled hypotension to 50 mm Hg. The SG of different brain structures was determined in a Percoll column up to 24 hr after ischemia. In addition, rCBF was measured by [14C]iodoantipyrine autoradiography. Cerebral ischemia resulted in reduction of CBF to less than 1% of normal in cortical structures and the caudatoputamen. One hour after the end of ischemia, blood flows were still reduced to 30% to 50% of the control level indicative of DPH. SG in cortex and hypothalamus reached a maximal decrease 10 min after the end of the ischemia and was still significantly reduced at 1 hr, although it was normal again 6 hr later. Regression analysis revealed a significant correlation between CBF obtained during ischemia and the corresponding SG found at 10-min recirculation, which could also be established at 1-hr recirculation. Therefore, a causal relation between the development of the DPH and the formation of ischemia might be considered.
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- Siesjö, B. K., et al.
(författare)
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Epileptic brain damage : pathophysiology and neurochemical pathology.
- 1986
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Ingår i: Advances in neurology. - 0091-3952. ; 44, s. 813-847
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Forskningsöversikt (refereegranskat)abstract
- In this chapter, the pathophysiology and neurochemical pathology of epileptic brain damage is discussed on the basis of an integrative approach in which a comparison is made to cell necrosis resulting from ischemia and hypoglycemia. Two main questions are asked. First, is the brain damage resulting from these three disorders of cerebral energy metabolism similar in distribution and structural characteristics, as previously proposed? Second, is it possible to identify one or several neurochemical events, at the cellular and subcellular level, that qualify as the final common pathways leading to neuronal necrosis? A related question is, will seizures cause structural damage even if they do not critically curtail cellular oxygen supply? A review of the literature and of recent results obtained in animals with long-term recovery following status epilepticus of known duration suggests that although brain damage caused by epilepsy shows some similarities to that incurred due to ischemic and hypoglycemic insults, it is far from identical. In well oxygenated animals with an adequate cardiovascular function, 2 hr of status epilepticus causes moderate neuronal necrosis in the cerebral cortex (layers 3-4), the hippocampus (CA4 and CA1 pyramidal cells), and the thalamus (ventromedial nuclei). In rats, status epilepticus of 30 min duration or longer invariably causes infarction of the substantia nigra (pars reticularis), with some affectation of globus pallidus as well. Notably, CA3 pyramids and dentate neurons are spared, as is the pars compacta of the substantia nigra. Neurochemical events in ischemia, hypoglycemia, and status epilepticus show some striking dissimilarities, yet all three conditions lead to neuronal necrosis. In complete or near-complete ischemia, in which metabolic rate virtually ceases; deterioration of tissue energy state is rapid and extensive, with dramatic loss of ion homeostasis; cellular redox systems are reduced; and acidosis is marked to excessive. In hypoglycemic coma, oxygen consumption continues, albeit at a reduced rate; loss of high energy phosphates is extensive but less than complete, as is loss of ion homeostasis; cellular redox system become oxidized; and acidosis is absent. In epileptic seizures, finally, metabolic rate is markedly enhanced; perturbation of tissue energy state and of ion homeostasis is minimal to small; and acidosis is moderate. Results obtained in experimental animals suggest that neuronal necrosis, when incurred, is unrelated to energy failure and occurs in spite of adequate cellular oxygenation. Four neurochemical events are common to all three conditions discussed.(ABSTRACT TRUNCATED AT 400 WORDS)
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- Widner, H
(författare)
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The case for neural tissue transplantation as a treatment for Parkinson's disease
- 1999
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Ingår i: Advances in neurology. - 0091-3952. ; 80, s. 9-641
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Forskningsöversikt (refereegranskat)abstract
- Neural tissue grafting can be highly effective and constitutes a potentially curative approach for progressive neurodegenerative disorders such as PD. Virtually all signs and symptoms of PD have been shown to improve after grafting but not necessarily simultaneously in one patient. Several technical aspects require improvement before widespread use of neural tissue implants can be recommended. These include better definition of donor tissue in terms of infectious risks, the need and duration of immunosuppressive treatment, and the minimal amount of tissue needed for definite benefit. Somatotropism within the basal ganglia system (with specific targeted grafts) aimed at relieving certain symptoms need to be elucidated experimentally. Interaction with the underlying disease process is also important to consider, and the role of intracerebral grafts in differing patterns of parkinsonism needs to be addressed. Grafting is potentially a very powerful therapeutic approach that may evolve to be the ideal treatment for patients with young-onset disease who, when starting to experience fluctuations, may have a life expectancy of 25 years with the disease. For these patients, grafting is likely to be both effective and long-lasting. For these patients, it is likely to become an efficient and also economically sound treatment for the patients and society. Provided that the transplantation procedure is performed judiciously and with strict adherence to basic principles defined from animal and human experimentation, more patients are likely to benefit from the procedure.
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