Models for studying long-term recovery following forebrain ischemia in the rat. 2. A 2-vessel occlusion model

Abstract

A model is described in which transient ischemia is induced in rats anaesthetized with N2O:O2 (70:30) by bilateral carotid artery clamping combined with a lowering of mean arterial blood pressure to 50 mm Hg, the latter being achieved by bleeding, or by bleeding supplemented with administration of trimetaphan or phentolamine. By the use of intubation, muscle paralysis with suxamethonium chloride, and insertion of tail arterial and venous catheters, it was possible to induce reversible ischemia for long-term recovery studies. Autoradiographic measurements of local CBF showed that the procedure reduced CBF in neocortical areas, hippocampus, and caudoputamen to near-zero values, flow rates in a number of subcortical areas being variable. Administration of trimethaphane or phentolamine did not affect ischemic and postischemic flow rates, nor did they alter recovery of EEG and sensory-evoked responses, but trimetaphan blunted the changes in plasma concentrations of adrenaline and noradrenaline. Recovery experiments showed that 10 min of ischemia gave rise to clear signs of permanent brain damage, with a small number of animals developing postischemic seizures that led to the death of the animals in status epilepticus. After 15 min of ischemia, such alterations were more pronounced, and the majority of animals died. It is concluded that the short revival times noted are explained by the fact that the model induces near-complete ischemia, and that recovery following forebrain ischemia is critically dependent on residual flow rates during the period of ischemia.

Changes in Insulin-like Growth Factor 1 Receptor Density after Transient Cerebral Ischemia in the Rat. Lack of Protection against Ischemic Brain Damage following Injection of Insulin-Like Growth Factor 1

“…The model of ce-rebral ischemia used in these studies has been described in detail by Smith et al (1984b). Male Wi star rats were anesthetized wit 3.5% halothane in N 2 0/0 2 (2:1).…”

The effect of granulocyte-colony stimulating factor in global cerebral ischemia in rats

“…We used the 2-vessel occlusion (2VO) model of global ischemia first described by Smith et al (1984) with modifications. After induction of general anesthesia with ketamine (100 mg/kg IP) and xylazine (20 mg/kg IP) rats (Sprague-Dawley, male, 280-320g, Harlan, Indianapolis, IN) were intubated and ventilated with a small animal ventilator (Kent Scientific, Torrington, CT).…”

“…In the present study we tested G-CSF in the 2-vessel occlusion (2VO) model of global cerebral ischemia in rats (Smith et al, 1984). G-CSF was administered in a combined pre-and postischemic treatment protocol (described below) in an effort to maximize potential protective effects from the drug, and animals were euthanized for further study on postoperative Day 2, 3 and 14.…”

Eicosanoid Production in the Caudate Nucleus and Dorsal Hippocampus after Forebrain Ischemia: A Microdialysis Study

“…The control group animals were left undisturbed for the duration of the ex periment. The three experimental groups were SUbjected to incomplete forebrain ischemia according to the tech nique of Smith et al (1984) for intervals of 8 (Group 1), 14 (Group 2), or 20 (Group 3) min. Thirty units of heparin was injected through the right external jugular vein cath eter.…”

“…However, the technique has not previously been applied to investigations of cere bral ischemia. In the present study, temporary fore brain ischemia was induced by bilateral carotid ar tery occlusion (BCAO) with simultaneous hypoten sion (Smith et al, 1984). This approach permitted a comparison of the patterns of TxB2 and 6-keto PGF 1a elaboration over time in two distinct brain regions.…”