LTC4, which enhances vascular permeability and promotes tissue
edema, and
LTB4, which is a potent chemotactic and activating factor for leukocytes, were measured in rat brain after
ischemia and several time periods of reperfusion. Forebrain
ischemia was induced by 4-vessel occlusion.
LTC4/
LTB4 in the brain were measured by RIA. We also studied the effects of a
5-lipoxygenase inhibitor,
AA-861 and a PAF antagonist,
CV-3988 on
LTC4/
LTB4 concentrations.
LTC4 in brain tissue increased during 30 min forebrain
ischemia (p < 0.001). After reperfusion,
LTC4 increased further, but at 15 min reperfusion
LTC4 returned to the control level. Tissue levels of
LTB4 in the brain increased during 30 min
ischemia and remained high until 5 min after reperfusion (p < 0.01) returning at 15 min reperfusion to the control level.
AA-861 inhibited elevation of
LTC4/
LTB4 in the reperfusion phase, but was not effective during
ischemia.
CV-3988 had a similar effect.
LTC4 and
LTB4 may be involved in the pathogenesis of
ischemia brain edema and leukocyte infiltration. Further, PAF and LTs have many similarities of their pathophysiological properties, and may interact therefore in pathologic process.