CEREBRAL PHOSPHOLIPID CONTENT AND NA+,K+-ATPASE ACTIVITY DURING ISCHEMIA AND POSTISCHEMIC REPERFUSION IN THE MONGOLIAN GERBIL

Using bilateral carotid artery occlusion in adult gerbils the effects of ischemia and ischemia/reperfusion on cerebral phospholipid content and Na+,K+-ATPase (EC 3.6.1.3) activity was examined. In contrast to the large changes in phospholipid content and membrane-bound enzyme activity that were observed in liver and heart tissues, relatively small changes in the cerebral content of total phospholipid, phosphatidylcholine (PC) phosphatidylserine (PS) and phosphatidylethanolamine (PE) following ischemic intervals of up to 240 min were observed. Following 15 min of ischemia the cerebral content of sphingomyelin (SM) was decreased to < 50% of control values but returned to near-normal levels with longer ischemic periods. Significant decreases in the cerebral content of phosphatidylinositol (PI) and phosphatidic acid (PA) were observed following shorter intervals of ischemia (15-45 min). Na+,K+-ATPase activity of cerebral homogenates prepared from the brains of gerbils subjected to 30-240 min of ischemia was decreased but significantly different from control activity only after 30 min of ischemia (-29%, P .ltoreq. 0.05). With the exception of PS, reperfusion for 60 min following 60 min of ischemia resulted in marked increases in cerebral phospholipid content with PC, SM, PI and PA levels exceeding and PE levels equal to preischemic values. Longer periods of reperfusion (180 min) resulted in decreases in cerebral phospholpid content toward (PC, SM, PI and PA) or below (PE) preischemic levels. In contrast, the cerebral content of PS significantly decreased during reperfusion (-51% at 60 min, P .ltoreq. 0.05) and remained below preischemic values even after 180 min of reperfusion. The activity of cerebral Na+,K+-ATPase increased to values slightly above preischemic values following reperfusion for either 60 or 180 min after 60 min of ischemia. Major differences exist in the responses of neural and nonneural tissues to ischemia and raise important questions concerning the role of changes in membrane structure and function in irreversible ischemic injury.