局所性脳虚血病巣の辺縁部に始まる脳浮腫の発生

BRAIN EDEMA INITIALLY DEVELOPS IN THE PERIPHERY OF FOCAL CEREBRAL ISCHEMIA

　抄録　局所性脳虚血病巣においては血流と接する虚血辺縁部においてまず脳浮腫が発生する。この作業仮説の検定のため，Mongolian gerbil片側大脳半球虚血モデルおよびrat脳塞栓モデルを用い，水分，電解質含有昂測定と組織化学的手法により，K^＋，Ca^2＋などを画像化して検討した。gerbil片側虚血後2時間の虚血中心部，虚血辺縁部，非虚血部の水分含有量はそれぞれ，80.7±0.9,82.0±1.0,79.0±0.9でその差は互いに有意であった。また，gerbilおよびratのモデルにおいて，K^＋の減少と外因性Ca^2＋の蓄積は虚血辺縁部からおこる事が組織化学的に認められた。以上より，これらのモデルでは局所性脳虚血病巣に伴う脳浮腫は病巣辺縁部より発生し，同部の水，電解質バランスの異常が最も大きい事が示された。

Ischemia causes disturbances of the ionic equili-brium, i.e., Na⁺ and water influx and K⁺ efflux. When the ischemic tissue keeps contact with cerebral blood flow, brain tissue equilibrates with systemic circulation and consequently shifts of electrolytes and water are induced. Therefore, brain edema should initiate in the peripheral area of focal cerebral ischemia. To test this hypothesis, we performed the following experiments.

Focal ischemia was induced by occlusion of the right common carotid artery in gerbils and by em-bolization with microspheres in rats. Water and electrolyte content was determined using punched out samples and regional K⁺ and Ca²⁺ distribution was visualized by histochemical K⁺ staining and ⁴⁵Ca-autoradiography, respectively. Cerebral blood flow and glucose metabolism were evaluated by ¹⁴C-iodoantipyrine or ¹⁸F-fluoroantipyrine and ¹⁴C-deoxyglucose autoradiographies, respectively.

Two hours of ischemia in gerbils with definite hemiparesis caused K⁺ depletion in the ischemic area, often most pronounced in the periphery of the lesion. Water content of cerebral cortex was 79.0±0.9, 82.0±1.0, 80.7±0.9 (%; means±SD) for nonischemic, periphery and center of ischemia, respectively (significantly different with each other). Na⁺ content was increased and K⁺ content was decreased most prominently in the periphery of ischemia. Exogenous Ca²⁺ was also accumulated in the periphery.

In the embolized stroke in rats, K⁺ depletion and Ca²⁺ accumulation obviously rimmed the is-chemic focus. Furthermore the infarcted area was only part of the disturbed area of acute-phase glu-cose metabolism.

Thus water and ionic disturbances were different between in the periphery and in the center of focal cerebral ischemia. Therefore, brain edema initially develops in the periphery of focal cerebral ische-mia.