Journal ArticleDOI
Models for studying long-term recovery following forebrain ischemia in the rat. 2. A 2-vessel occlusion model
TLDR
By the use of intubation, muscle paralysis with suxamethonium chloride, and insertion of tail arterial and venous catheters, it was possible to induce reversible ischemia for long‐term recovery studies.Abstract:
A model is described in which transient ischemia is induced in rats anaesthetized with N2O:O2 (70:30) by bilateral carotid artery clamping combined with a lowering of mean arterial blood pressure to 50 mm Hg, the latter being achieved by bleeding, or by bleeding supplemented with administration of trimetaphan or phentolamine. By the use of intubation, muscle paralysis with suxamethonium chloride, and insertion of tail arterial and venous catheters, it was possible to induce reversible ischemia for long-term recovery studies. Autoradiographic measurements of local CBF showed that the procedure reduced CBF in neocortical areas, hippocampus, and caudoputamen to near-zero values, flow rates in a number of subcortical areas being variable. Administration of trimethaphane or phentolamine did not affect ischemic and postischemic flow rates, nor did they alter recovery of EEG and sensory-evoked responses, but trimetaphan blunted the changes in plasma concentrations of adrenaline and noradrenaline. Recovery experiments showed that 10 min of ischemia gave rise to clear signs of permanent brain damage, with a small number of animals developing postischemic seizures that led to the death of the animals in status epilepticus. After 15 min of ischemia, such alterations were more pronounced, and the majority of animals died. It is concluded that the short revival times noted are explained by the fact that the model induces near-complete ischemia, and that recovery following forebrain ischemia is critically dependent on residual flow rates during the period of ischemia.read more
Citations
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Journal ArticleDOI
Ischemic Cell Death in Brain Neurons
TL;DR: A major unifying thread of the review is a consideration of how the changes occurring during and after ischemia conspire to produce damaging levels of free radicals and peroxynitrite to activate calpain and other Ca(2+)-driven processes that are damaging, and to initiate the apoptotic process.
Journal ArticleDOI
The density and distribution of ischemic brain injury in the rat following 2–10 min of forebrain ischemia
TL;DR: Mild brain damage was observed in some animals already after 2 min, and more consistently after 4 min of ischemia, and selective neuronal necrosis of the cerebral cortex worsened into infarction after higher doses of insult.
Journal ArticleDOI
Selective vulnerability of the hippocampus in brain ischemia.
TL;DR: *Department of Neurophysiology, Institute of Physiology, Medical Faculty, Ruhr-Universitlt Bochum, and MRC Anatomical Neuropharmacology Unit, _ Department of Pha-rmacology, University of Oxford, Oxford, U.K.R.G.
Journal ArticleDOI
Rodent models of cerebral ischemia.
Myron D. Ginsberg,Raul Busto +1 more
TL;DR: This work critically examine and summarize several rodent models of transient global ischemia, resulting in selective neuronal injury within vulnerable brain regions, and focal ischemIA, typically giving rise to localized brain infarction.
Journal ArticleDOI
Differential regulation of mRNAs for nerve growth factor, brain-derived neurotrophic factor, and neurotrophin 3 in the adult rat brain following cerebral ischemia and hypoglycemic coma.
Olle Lindvall,Patrik Ernfors,Johan Bengzon,Zaal Kokaia,Maj-Lis Smith,Bo K. Siesjö,Håkan Persson +6 more
TL;DR: In situ hybridization was used to study expression of mRNAs for members of the nerve growth factor (NGF) family in the rat brain after 2 and 10 min of forebrain ischemia and 1 and 30 min of insulin-induced hypoglycemic coma to influence functional outcome and neuronal necrosis following ischemic and hypogly diabetic insults.
References
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Journal ArticleDOI
A new model of bilateral hemispheric ischemia in the unanesthetized rat.
W A Pulsinelli,J B Brierley +1 more
TL;DR: A new model of transient, bilateral hemispheric ischemia in the unanesthetized rat is described, with the ease of preparation of large numbers of animals, a high rate of predictable ischemic neuronal damage, a low incidence of seizures and the absence of anesthesia.
Journal ArticleDOI
Simultaneous radioenzymatic determination of plasma and tissue adrenaline, noradrenaline and dopamine within the femtomole range.
Mosé Da Prada,Gerhard Zürcher +1 more
TL;DR: A radiometric-enzymatic assay for measuring simultaneously femtomole quantities of adrenaline, noradrenaline and dopamine has been developed and promises to be a valid alternative to the gas chromatography-mass spectrometry technique.
Journal ArticleDOI
Colorimetric determination of free fatty acids in biological fluids.
Koichi Itaya,Michio Ui +1 more
TL;DR: The optimum conditions for chloroform extraction of FFA from blood or other biological fluids were studied and a degree and rate of extraction similar to those with Dole’s extraction mixture were obtained.
Journal ArticleDOI
Experimental cerebral ischemia in mongolian gerbils. I. Light microscopic observations.
TL;DR: Light microscopic observations were carried out on Mongolian gerbils subjected to a partial cerebral ischemia by occlusion of the left common carotid artery at the neck and a “reactive change” observed in the H3 neurons of the hippocampus suggested a feature of selective vulnerability.
Journal ArticleDOI
Brain lactic acidosis and ischemic cell damage: 1. Biochemistry and neurophysiology.
TL;DR: It is concluded that a high degree of tissue lactic acidosis during brain ischemia impairs postischemic recovery and that different degrees of tissue nacreous acidosis may explain why severe incomplete ischemIA, in certain experimental models, is more deleterious than complete brain is chemia.
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Temporal profile of neuronal damage in a model of transient forebrain ischemia.
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