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Correlation Between Myeloperoxidase‐Quantified Neutrophil Accumulation and Ischemic Brain Injury in the Rat: Effects of Neutrophil Depletion
TLDR
Depletion of neutrophils by RP3 treatment completely inhibited the increase in MPO activity in the ischemic brain after 24 hours of reperfusion and significantly attenuated the postischemic increase in brain water content at 24 hours after reperfusions. Expand
Peri-infarct depolarizations lead to loss of perfusion in ischaemic gyrencephalic cerebral cortex.
TLDR
In this model of occlusive stroke, reductions in perfusion linked to peri-infarct depolarization events contribute to secondary deterioration in penumbral areas and are suggested to play a central rather than a subsidiary role in cerebral infarction in the gyrencephalic brain. Expand
Protective Effect of Endothelin Type A Receptor Antagonist on Brain Edema and Injury After Transient Middle Cerebral Artery Occlusion in Rats
TLDR
The data demonstrate that infusion with S-0139, an ETA antagonist, results in significant reduction of brain injury and plasma extravasation after transient MCAO, suggesting ETs may contribute to cerebral ischemia/reperfusion injury at least partly by increasing the BBB permeability via ETAs. Expand
Role of cell adhesion molecules in brain injury after transient middle cerebral artery occlusion in the rat
TLDR
Results strongly implicate the invasion of neutrophils in the development of post-ischemic brain injury, and suggest that interactions between CD11a/CD18 and ICAM-1 contribute to neutrophil infiltration into the ischemic brain. Expand
P/Q-type Ca2+ channel blocker ω-agatoxin IVA protects against brain injury after focal ischemia in rats
TLDR
The results suggest that P/Q-type Ca2+ channels may be involved in the development of focal ischemic brain injury and that blockers of these channels might be therapeutically useful against isChemic injury. Expand
Synergistic Effect of an Endothelin Type A Receptor Antagonist, S-0139, With rtPA on the Neuroprotection After Embolic Stroke
TLDR
The data suggest that S-0139 provides the neuroprotection by suppressing ischemia- and rtPA-triggered molecules that evoke thrombosis and BBB disruption and synergistically reduced loss of laminin, ZO1, and occludin in cerebral vessels. Expand
Role of Neutrophils in Radical Production during Ischemia and Reperfusion of the Rat Brain: Effect of Neutrophil Depletion on Extracellular Ascorbyl Radical Formation
TLDR
Neutrophils are a major source of oxygen radicals during reperfusion after focal cerebral ischemia–reperfusion and require no spin-trapping agents, according to the endogenous ascorbyl radical concentration. Expand
Glutamate efflux via the reversal of the sodium-dependent glutamate transporter caused by glycolytic inhibition in rat cultured astrocytes
TLDR
iodoacetic acid-induced intracellular acidosis was more rapid and severe in the presence of 5-[N-ethyl-N-isopropyl]amiloride, and the results suggest that the reversal of the Na+-dependent glutamate transporter may be caused by not only intrACEllular Na+ overload but also intrace cellular acidosis. Expand
Role of platelet-activating factor and thromboxane A2 in radical production during ischemia and reperfusion of the rat brain
TLDR
PAF and TXA2 might contribute to cerebral ischemia-reperfusion injury by increasing the generation of oxygen radicals. Expand
The nonpeptide α-eudesmol from Juniperus virginiana Linn. (Cupressaceae) inhibits ω-agatoxin IVA-sensitive Ca2+ currents and synaptosomal 45 Ca 2+ uptake
TLDR
The present data indicated that alpha-eudesmol is a potent nonpeptidergic compound which blocks the presynaptic omega-Aga-IVA-sensitive Ca2+ channel with relative selectivity. Expand
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