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.