Premium
Acute Uteroplacental Ischemic Embryo: Lactic Acid Accumulation and Prostaglandin Production in the Fetal Rat Brain
Author(s) -
Magal Ella,
Goldin Ehud,
Harel Shaul,
Yavin Ephraim
Publication year - 1988
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1988.tb04837.x
Subject(s) - fetus , medicine , lactic acid , endocrinology , ischemia , prostaglandin e , prostaglandin , chemistry , biology , andrology , pregnancy , genetics , bacteria
A new experimental model for studying the effects of acute ischemia on brain development in the near‐term fetal rat has been devised. Ischemic conditions are achieved by complete clamping of blood vessels branching from the uterine vasculature into each individual fetus for designated times followed by removal of the clamps to permit reperfusion. Accumulation of lactic acid in the fetal orain depends on the length of the restriction period, reaching a plateau level of 29 μmol/g tissue at about 30 min. It also depends on the reperfusion time. Thus after a period of 15 min of restriction lactate levels show an increase over the next 30‐min reperfusion to a value of 25.5 μmol/g followed by a rapid decrease to normal values by 3 h of reperfusion. Restriction of 15 min followed by reperfusion of 45 min causes an elevation of prostaglandin E 2 (PGE 2 ) level from 12.4 ± 0.86 ng/g to 21.1 ± 0.6 ng/g (p < 0.001). This elevation in PGE 2 level is less apparent after 20 min of restriction. No effects are seen on the level of PGF 2α . Both PGE 2 and PGF 2α accumulate in vitro in a time‐dependent manner by brain paniculate fraction. In vitro synthesis of both PGE 2 and PGF 2α is inhibited by indomethacin (100% and 68%, respectively) and AA861 (94% and 76%, respectively). BW755c and nordihydro‐guaiaretic acid do not affect PGE 2 formation but enhance PGF 2a production by 112% and 152%, respectively. Paniculate fractions from restricted brain produce less PGF 2α than control brains (6.38 ± 1.62 versus 11.43 ± 2.2, p < 0.01). The new experimental model should be adequate for studying the consequences of perinatal ischemia on the developing brain.