A new model of bilateral hemispheric ischemia in the unanesthetized rat.

TLDR

The study introduces a new model of transient, bilateral hemispheric ischemia in unanesthetized rats. The model involves electrocauterizing the vertebral arteries under ether anesthesia, placing reversible carotid clamps, and after 24 h tightening the clamps in awake rats to induce 4‑vessel occlusion for 10–30 min before perfusion fixation 72 h later, with convulsing animals excluded. Rats subjected to 20–30 min of 4‑vessel occlusion consistently showed ischemic neuronal damage, especially in the H1 and paramedian hippocampus, striatum, and layers 3, 5, 6 of the posterior neocortex, and the model offers easy preparation, high predictability, low seizure incidence, and no anesthesia.

Abstract

A new model of transient, bilateral hemispheric ischemia in the unanesthetized rat is described. During ether anesthesia the rat's vertebral arteries were electrocauterized through the alar foramina of the first cervical vertebra and reversible clasps placed loosely around the common carotid arteries. Twenty-four hr later, the awake rats were restrained and the carotid clasps tightened to produce 4-vessel occlusion. The carotid clasps were removed after 10, 20 or 30 min of 4-vessel occlusion and the animals killed by perfusion fixation 72 hr later. Rats which convulsed during the ischemic or post-ischemic period were excluded from further study. All rats subjected to 20 or 30 min of 4-vessel occlusion demonstrated ischemic neuronal damage. The H1 and paramedian hippocampus, striatum and layers 3, 5 and 6 of the posterior neocortex were the regions most frequently damaged. The advantages of this model are 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.