Brain edema during ischemia and after restoration of blood flow. Measurement of water, sodium, potassium content and plasma protein permeability.

TLDR

The study used the left cerebral hemisphere of Mongolian gerbils to investigate the mechanisms of brain edema that arise during cerebral ischemia and after reperfusion. Edema was quantified by measuring water content via tissue drying, sodium and potassium concentrations by flame photometry, and plasma protein permeability using 131I‑albumin passage assessed with a gamma scintillation counter. Pure cytotoxic edema occurs during ischemia and shortly after reperfusion, while vasogenic edema—driven by plasma leakage—develops after reperfusion; reperfusion reduces edema after less than 1 hr of ischemia but exacerbates it when ischemia exceeds 3 hrs.

Abstract

The left cerebral hemisphere of Mongolian gerbils was used to elucidate the mechanisms of brain edema which develop during cerebral ischemia and after restoration of cerebral blood flow following temporary ischemia. Water content was measured by the tissue-drying method. Sodium and potssium ion concentration was measured by flame photometry. Passage of 131I-albumin (RISA) from blood to the cerebral parenchyma was measured on a gamma scintillation counter. Our findings indicate that pure cytotoxic edema develops during ischemia and during a short period after restoration of cerebral blood flow. Vasogenic edema, which is accelerated by the leakage of plasma constitutents from blood due to blood-brain barrier damage, developed after restoration of the cerebral blood flow. After less than 1 hr of ischemia, restoration of the cerebral blood flow drastically reduced the degree of brain edema. However, restoration of the cerebral blood flow greatly worsened the brain edema following more than 3 hr of ischemia.