Effect of experimental ischemia on cerebral water and electrolytes

Abstract

✓ In dogs, while the middle cerebral artery (MCA) was clipped, an apparent ischemia was demonstrated with fluorescein angiography when the dye was injected through the lingual artery. Injection of fluorescein into the femoral artery or perfusion of carbon black particles through the heart demonstrated considerable collateral blood supply to the affected area. Water, sodium, and potassium content of cerebral tissues normally supplied by the occluded artery remained unchanged. At 48 hours after clipping, focal areas of infarction developed in 70% of the animals; edema could then be demonstrated in tissue surrounding the infarction. The collateral blood supply was compromised by subjecting the dogs with clipped MCA to hemorrhagic hypotension for 1 hour. Following restoration of the systemic blood pressure by infusion of the shed blood, an area of ischemia in the territory normally supplied by the clipped artery could be easily demarcated by fluorescein angiography through the femoral and lingual arteries and by carbon perfusion. The involved cerebral cortex tissue showed marked changes that started immediately after restoration of the blood pressure, and which consisted of a fall in percentage dry weight and potassium content and an increase in sodium content. These findings were clearly correlated with gross and histological evidence of massive necrosis and were interpreted as indicating cell death rather than tissue swelling. In the underlying white matter, moderate delayed changes in water and electrolyte content were compatible with the development of vasogenic edema.