Neuroprotective Agents and Cerebral Ischaemia

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Ischemic Stroke and Neuroprotection

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Advanced Search. View Full Size. Materials and Methods Results Discussion References. Chiara Adembri, M.

De Gaudio, M. Pellegrini-Giampietro, M. Article Information. Anesthesiology 1 , Vol. You will receive an email whenever this article is corrected, updated, or cited in the literature. You can manage this and all other alerts in My Account. You must be logged in to access this feature.

PROPOFOL 2,6-diisopropylphenol is an intravenous sedative—hypnotic agent commonly used in anesthesia and intensive care that has been tested as a neuroprotective agent in models of cerebral ischemia. Mitochondria are involved in the energetic supply and are implicated in ischemic dysfunction in all living cells, especially in neurons. Finally, we examined the effects of propofol on the extent of the infarct and the neurobehavioral outcome in rats subjected to permanent middle cerebral artery occlusion MCAO , a severe model of focal ischemia in vivo. Propofol 2,6-diisopropylphenol in an intralipid emulsion Diprivan was supplied by Astra-Zeneca Basiglio, Milano, Italy.

Organotypic hippocampal slice cultures were prepared as previously reported. These were placed in six-well tissue culture plates containing 1. Experiments were conducted after 14 days in vitro. Oxygen-glucose deprivation was induced as previously described. Cell injury was assessed using PI, a polar dye that enters the cells only if the membrane is damaged and becomes fluorescent after binding to DNA. PI fluorescence was viewed using an Intracellular Imaging Inc.

To quantify cell death, the CA1 hippocampal subfield was identified and encompassed by a frame using the drawing function in the image software, and the intensity of PI fluorescence i. Background PI fluorescence was determined in control cultures not exposed to OGD and was subtracted from all experimental values. There was a linear correlation between PI fluorescence and the number of injured CA1 pyramidal cells as detected by morphological criteria see Pellegrini-Giampietro et al. Swelling of isolated mitochondria is a recognized index of increased mitochondrial membrane permeability.

Controls were preincubated with an equal concentration of dimethylsulfoxide 0. The effects of propofol on the mitochondrial ultrastructural changes of CA1 pyramidal cells evoked by OGD were analyzed in organotypic hippocampal slices by transmission electron microscopy. Hippocampal slices were then dehydrated in graded acetone, passed through propylene oxide, and embedded in Epon Ultrathin sections were stained with uralyl acetate and alkaline bismuth and viewed under a Jeol Tokyo, Japan electron microscope at 80 kV.

Adult male Sprague-Dawley rats weighing — g were used. All animals were fasted overnight before the experiment but had free access to water. Efficacy of ventilation and oxygenation was assessed by measuring carbon dioxide and oxygen tension in tail artery blood samples. Blood pressure was monitored noninvasively. Permanent MCAO was induced using a relatively noninvasive technique with an intraluminal filament according to Zea Longa et al. The external and internal right carotid arteries were dissected under an operating microscope, and a silk suture was tied loosely around the external carotid stump.

The silicone-coated nylon filament was then inserted through the external into the internal carotid artery up to the circle of Willis to occlude the right middle cerebral artery. The silk suture was finally tightened around the intraluminal filament to prevent bleeding and dislodgment. Recovery of the righting reflex occurred approximately 5 min after isoflurane administration was terminated, and the animals were returned to their cages.

Brains were quickly removed and inspected to confirm the position of the intraluminal filament and the absence of subarachnoid hemorrhage. After MCAO, the occurrence of a turning behavior ipsilateral to the ischemic side upon tail stimulation was searched as an index of ischemia in the territory of the middle cerebral artery. To assess the neuroprotective effects of propofol, a neurobehavioral examination according to Garcia et al.

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  4. This testing assesses the following: spontaneous activity—no movement 0 points to normal behavior 3 points ; motor symmetry in all limbs—no movement at the left side 0 points to normal behavior 3 points ; symmetry in the outstretching of forelimbs—no movement 0 points to normal motor symmetry 3 points ; climbing—falls trying to climb 1 point to normal climbing 3 points ; body proprioception—no response at the left side 1 point to symmetrical response 3 points ; and response to vibrissae touch—no response on the left side 1 point to symmetrical response 3 points.

    Neurobehavioral testing was performed by a single observer blinded to group assignment. To avoid the influence of daily fluctuations in neurologic performance, the evaluation was conducted at the same time of day. Exposure of slices to propofol alone for 24 h did not induce any increase in PI fluorescence not shown. Propofol attenuates CA1 injury induced by 30 min of oxygen-glucose deprivation OGD in rat organotypic hippocampal slices. Background fluorescence was determined in control sister slices not exposed to OGD and was subtracted from all experimental values.

    Data are expressed as percentage of maximal propidium iodide fluorescence observed in untreated slices 24 h after OGD. To investigate the possible mechanism of action of propofol, we then examined its effects on brain mitochondria. Mitochondria were isolated from adult rat brain by conventional sequential centrifugation. CaCl 2 was added to a suspension containing a constant aliquot of mitochondria, and mitochondrial swelling was quantified by measuring the reduction in light transmission at nm.

    To determine whether these findings on isolated brain mitochondria are relevant to ischemia, we used transmission electron microscopy to examine the effects of propofol on the OGD-induced mitochondrial damage of CA1 pyramidal cells in hippocampal slices. Observation of control hippocampal slices under the electron microscope fig. Mitochondria were elongated or round and had numerous transversae cristae with a regular pattern and an electron-dense intramitochondrial matrix. After OGD, CA1 pyramidal cell mitochondria showed substantial ultrastructural alterations, such as swelling i.

    In particular, the treatment substantially decreased the ischemia-induced mitochondrial swelling. Ultrastructural evidence that propofol reduces CA1 pyramidal cell mitochondrial swelling after oxygen-glucose deprivation in organotypic hippocampal slices.

    Rats not displaying a clear-cut turning behavior after MCAO and rats with subarachnoid hemorrhage at postmortem examination were excluded from the study.

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    Written by world experts on the mechanisms involved in neurodegeneration, Neuroprotective Agents and Cerebral Ischaemia presents an up-to-date review of current research and developing therapies. This book is essential reading for all clinicians and researchers searching for neuroprotective drugs. Researchers, clinicians, and graduate students in neuroscience, cell genetics, pharmacology, biology, and physiology.

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