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Title: Malignant infarction in cats after prolonged middle cerebral artery occlusion : glutamate elevation related to decrease of cerebral perfusion pressure
Authors: Toyota, Shingo
Graf, Rudolf
Valentino, Mario
Yoshimine, Toshiki
Heiss, Wolf-Dieter
Keywords: Cerebral infarction -- Diagnosis
Cerebral ischemia -- Diagnosis
Intracranial pressure
Perfusion (Physiology)
Glutamic acid
Issue Date: 2002
Publisher: Lippincott Williams & Wilkins
Citation: Toyota, S., Graf, R., Valentino, M., Yoshimine, T., & Heiss, W. D. (2002). Malignant infarction in cats after prolonged middle cerebral artery occlusion: glutamate elevation related to decrease of cerebral perfusion pressure. Stroke, 33(5), 1383-1391.
Abstract: Background and Purpose—To study the putative role and predictive significance of glutamate elevation in space- occupying ischemic stroke, we investigated the correlation between perfusional disturbances and glutamate alterations in a transient ischemia model in cats that is susceptible to secondary deterioration after reperfusion. Methods—In 10 halothane-anesthetized cats, the left middle cerebral artery was occluded for 3 hours, followed by 6 hours of reperfusion. Laser-Doppler flowmetry (LDF) probes, microdialysis/high-performance liquid chromatography, and pressure sensors measured simultaneously regional cerebral blood flow (CBF), extracellular amino acids, mean arterial blood pressure, and intracranial pressure, respectively. Cerebral perfusion pressure (CPP) was calculated. In complementary experiments (n2), regional CBF was assessed by sequential positron emission tomography. Results—Middle cerebral artery occlusion reduced LDF-measured CBF in all animals to 25% of control. In 5 of 10 cats, glutamate rose approximately 30-fold during ischemia. LDF-measured CBF and glutamate primarily recovered after reperfusion. Glutamate rose again in the late reperfusion phase, when CPP decreased to 60 mm Hg, and symptoms of transtentorial herniation were recognized. Positron emission tomography revealed ischemic thresholds of 15 to 20 mL/100 g per minute for secondary deterioration. In the other 5 cats, ischemic elevation of glutamate was significantly smaller, and signs of secondary deterioration were not recognized. Conclusions—Glutamate determinations during ischemia predict fatal outcome, as do intracranial pressure and CPP measurements during early reperfusion. Secondary amino acid elevation during reperfusion is presumably caused by a drastic decrease of CPP to 50 mm Hg in the final stage of space-occupying, malignant focal ischemia. At this stage, a further progression of injury due to increased glutamate may be irrelevant with respect to fatal outcome.
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