Global Cerebral Ischemia in Primates

Oxidative neuronal damage also contributes to delayed neuronal death after global cerebral ischemia as demonstrated by studies in humans (Love et al. 1998, 1999). 

All experimental and surgical procedures were approved by the Animal Care and Ethics Committee of Kanazawa University. The subjects of our investigations were female Japanese macaque monkeys (Macaca fuscata). These were kept in air-conditioned cages sized approximately 1 m on a side. The monkeys were allowed free access to water and were daily fed with artificial animal food, and fruits or vegetables. In total, tissues from 29 monkeys were included in the present study one monkey was neonatal (14 days old, sacrificed on postnatal day 14 P14), while the rest of the monkeys were sexually mature (age of 5-13 years). 

BrdU (5-bromo-2 -deoxyuridine) was purchased from Sigma-Aldrich Japan (Tokyo, Japan), and was dissolved in saline with 0.007 N NaOH at a concentration of up to 10 mg/ml. BrdU was intravenously injected in the saphenous vein as each injection was at a dose of 100 mg/kg. The neonatal monkey received two injections one on the day of birth, and one on PI4. Of the 28 adult monkeys, 22 received 5 injections on five consecutive days, and were sacrificed on various periods after the last BrdU injection. Based on these periods, two monkey groups emerged a group with short-term survival after BrdU, the monkeys within which 

At respective intervals as described above the monkeys were euthanized by lethal doses of sodium pentobarbital, the chest was opened, and intracardial perfusion of 0.51 ice-cold saline with heparin was performed, immediately followed by 2.51 of ice-cold solution of 4% paraformaldehyde in phosphate-buffered saline (PBS), pH = 7. The cranium was opened, and the brain was removed. 

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