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Ischemic Neurons in Rat Brains After 6, 8, or 10 Minutes of Transient Hypoxic Ischemia
Ann Radovsky
Safar Center for Resuscitation Research, University of Pittsburgh, Pittsburgh, Pennsylvania
Laurence Katz
Safar Center for Resuscitation Research, University of Pittsburgh, Pittsburgh, Pennsylvania
Uwe Ebmeyer
Safar Center for Resuscitation Research, University of Pittsburgh, Pittsburgh, Pennsylvania
Peter Safar
Safar Center for Resuscitation Research, University of Pittsburgh, Pittsburgh, Pennsylvania
The incidence and distribution of ischemic (necrotic) neurons in the brains of rats 72 hr after hypoxic ischemia induced via asphyxiation is described and scored. Anesthetized Sprague-Dawley rats (10/group) were endotracheally intubated and had their airways occluded for 6, 8, or 10 min, which resulted, respectively, in approximately 3, 5, or 7 min of pulselessness (MABP < 10 mm Hg). Survival was 10/10, 9/10, and 6/10 in the 6-, 8-, and 10-min groups: deaths occurred within 1 hr after resuscitation. At 72 hr, rats were reanesthetized and their brains were perfusion-fixed with 3% buffered paraformaldehyde. Paraffin-embedded, 5-µm-thick, H&E-stained sections at 5 coronal levels of the brain had shrunken, hypereosinophilic ischemic neurons in 12 anatomic regions. Ischemic neurons were most consistently found in the lateral reticular thalamic nucleus; lateral caudoputamen; CA1 region of the hippocampus; subiculum; and, with longer asphyxia times, among cerebellar Purkinje neurons. Categorical histologic damage scores were assigned to affected regions on the basis of manual counts of ischemic neurons and summed for the whole brain. Brain histologic damage scores were significantly (p < 0.01) different for the 6-, 8-, and 10-min groups (means of 8 ± 2; 14 ± 4; and 22 ± 4). Brain regions where both the number of rats affected and ranked categorical scores for ischemic neurons increased with asphyxia time were the lateral caudoputamen and cerebellar Purkinje neurons.
Key Words: Neuropathology • animal model • asphyxiation • clinical deficit • cardiac arrest
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Toxicologic Pathology, Vol. 25, No. 5,
500-505 (1997)
DOI: 10.1177/019262339702500512
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