Cerebral Phospholipid Content and Na⁺, K⁺‐ATPase Activity During Ischemia and Postischemic Reperfusion in the Mongolian Gerbil

Abstract

Using bilateral carotid artery occlusion in adult gerbils we examined the effects of ischemia and ischemia/reperfusion on cerebral phospholipid content and Na+,K+-ATPase (EC 3.6.1.3) activity. In contrast to the large changes in phospholipid content and membrane-bound enzyme activity that have been observed in liver and heart tissues, we observed 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. Following 15 min of ischemia the cerebral content of sphingomyelin (SM) was decreased to less than 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 less than or equal to 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 phospholipid 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 less than or equal to 0.05) and remained below preischemic values even after 180 min of reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of minaprine on changes in monoamine contents in Mongolian gerbils with 5-min occlusion of common carotid arteries.

“…According to mechanisms related to de layed neuronal death, intracellular calcium overload (24), the release of excitotoxin (25), accumulation of free fatty acid (26), alter nations of protein synthesis (27) and so on may be involved. The delayed neuronal death inhibition seen with minaprine remains the subject of ongoing studies.…”

Degradation of phospholipid molecular species during experimental cerebral ischemia in rats.

“…Yoshida et al 10 observed a 4% decrease in PC (not significant) and a 16% decrease in PE content of gerbil brain after 30 minutes of ischemia. Enseleit et al 5 reported small changes in the total cerebral phospholipid, PC, phosphatidylserine (PS), and PE content, which might depend on the different rates of lipid metabolism of gerbil brains subjected to various periods of ischemia. These discrepancies are probably due to a combination of factors such as differences in sampling procedures, analytic methodology, animal model, and duration of the ischemic insult.…”

Gangliosides (GM1 and AGF2) reduce mortality due to ischemia: protection of membrane function.

“…26 " 28 Ganglioside protection from loss of Na, K-ATPase activity may indicate protection of membrane structure and function since there is considerable evidence that ischemia causes significant reductions in this enzyme's activity. 31 By stabilizing membrane function and therefore "normal" ionic gradients, membrane failure and subsequent deterioration may well be minimized. The protection of this enzyme from the loss of activity probably reflects effects on one or a series of biochemical changes (e.g., lipid hydrolysis, phospholipase activation, production and membrane action of arachidonic acid, ionic imbalance) that occur as a result of injury and lead to membrane failure.…”