Acidic phospholipids, diacylglycerols, and free fatty acids in gerbil brain: A comparison of ischemic changes resulting from carotid ligation and decapitation

Abstract

The levels of brain acidic phospholipids (poly-PI, PI, PA, and PS), DG, and FFA and their acyl group profiles were determined after induction of ischemia in gerbils by ligation of the common carotid arteries and decapitation. Ischemia induced by both procedures resulted in a significant decrease in poly-PI (20% for 1-min decapitation and 1-min ligation). Except for a 16% increase in PI in the 5-min decapitation group, no apparent change was found in other phospholipids after either ischemic condition. The level of DG was increased one- and three-fold after 1 and 5 min, respectively, of decapitative ischemic treatment. Ligation of the carotid arteries for 1 min resulted also in a one-fold increase in the DG level. The decapitative model resulted in a one- and five-fold increase in FFA level (with respect to 1 and 5 min, respectively), whereas ligation for 1 min resulted in an increase of 42% of the FFA. The acyl groups of poly-PI and PI in the control gerbil brain are enriched in 18:0 and 20:4, but those of DG, FFA, and PA have a higher proportion of 16:0 besides 18:0 and 20:4. However, a preferential increase in the proportion of 18:0 and 20:4 was shown for the DG and FFA in both types of ischemic treatments. It is concluded from the results that both models of ischemic treatment elicit a similar decrease in poly-PI and increase in DG, but differ in the amount of FFA release. The higher level of FFA release in the decapitative model suggests that other biochemical mechanisms may be activated to cause the additional release.

Platelet‐Activating Factor Antagonist BN52021 Decreases Accumulation of Free Polyunsaturated Fatty Acid in Mouse Brain During Ischemia and Electroconvulsive Shock

“…The loss of 150 nmol of PIP2 during ischemia is not accounted for by a gain in free 20:4 acid, free 18:O acid, and DG. This observation is in agreement with a recent report of changes in gerbil brain lipids following decapitation (Huang and Sun, 1987). This pool of PIP,, which represents -50% of the total loss, may be degraded to phosphatidylinositol-4-phosphate and phosphatidylinositol via phosphatases.…”

“…This source may be phosphatidylinositol or phosphatidylinositol-4-phosphate via phospholipase C, or triacylglycerol or phosphatidic acid via triacylglycerol lipase or phosphatidic acid phosphohydrolase. In fact, in rat brain, the triacylglycerol and phosphatidic acid pools are enriched in saturated fatty acids and have been suggested as a source for saturated DG accumulation during ischemia (Aveldaiio and Bazan, 1975a,b;Ikeda et al, 1986;Huang and Sun, 1987). A likely candidate for "X' fatty acid is 18: 1 acid, the level of which increases by 89 nmol in the DG pool after ECS.…”

“…One of the most rapid biochemical alterations in brain following seizures or other trauma is an accumulation of free fatty acids (FFAs) (Bazan, 1970) and diacylglycerols (DGs) (Aveldaiio and Bazan,197%) and a degradation of phosphatidylinositol-4,5-bisphosphate (PIP,) (Ikeda et al, 1986;Huang and Sun, 1987;Reddy and Bazan, 1987;Vadnal and Bazan, 1987). These effects are mediated largely by the activation of phospholipase A2, which removes the fatty acid acylated at the 2-position of phospholipids, and phospholipase C, which removes the polar head group of phospholipids, resulting in the degradation of PIP2 and the accumulation of DG and inositol phosphates.…”

Changes in Cerebral Acyl‐CoA Concentrations Following Ischemia‐Reperfusion in Awake Gerbils

“…We conclude that connections between the posterior and anterior circulations are variable and must be accounted for if a bimodal distribution in results is evident. Other investigators have reported increased fatty acid concentrations in the gerbil ischemiareperfusion model (De Medio et al, 1980;Yoshida et al, 1983Yoshida et al, , 1984 and in rat brain 3 and 15 mm after decapitation (Deutsch et al, 1997), as well as increased lysophospholipids and diglycerides and decreased diphosphophosphatidylinositol (Abe and Kogure, 1986;Huang and Sun, 1987). Our pattern of fatty acid changes agrees with previous reports (De Medio et al, 1980;Yoshida et al,, 1983Yoshida et al,, , 1984Huang and Sun, 1987) and FIG.…”

“…The increase in arachidonic acid concentration is relatively higher than for other fatty acids and can contribute to edema (Chan et al, 1985). Fatty acids also are released by combined activation of phospholipase C and diglyceride lipase (De Medio et a!., 1980;Yoshida et al, 1983Yoshida et al, , 1984Rordorf et al, 1991) and by lysophospholipase (Abe and Kogure, 1986;Huang and Sun, 1987) acting on lysophospholipids produced by the activation of phospholipase A 2 (Bonventre and Koroshetz, 1993). Lysolecithin formed by the action of phospholipase A2 on phospholipids can form micelles (Purdon et al, 1975) and destabilize cell membrane bilayers.…”