Complete cerebral ischemia, prostacyclin deficiency, and therapeutic possibilities.
This report summarizes the results of our studies on the effects of prostacyclin (PGI2) on the outcome of global cerebral ischemia (GCI). GCI was produced for 15 and 20 min. In vivo dialysis of the hippocampus was used to determine the changes in extracellular concentrations of calcium (Ca/2e) and blood-brain barrier (BBB) permeability. Moreover, EEG and general physiological parameters were recorded. This was combined with morphological observations. PGI2 was infused continuously i.v. at a rate of 2 micrograms/kg/min. Rabbits with untreated GCI served as reference. Treatment with PGI2 significantly enhanced EEG recovery and normalization during recirculation, and reduced both the decrease in Ca+2e, and the BBB leakage. The number of ischemic neurons in the PGI2-treated rabbits was significantly lower than in the non-treated ones. PGI2 reduced brain edema. These data suggest that PGI2 may protect against postischemic brain damage, in part by inhibiting excessive calcium influx to neurons and in part by tightening of BBB.
Pluta
R
R
Department of Neuropathology, Medical Research Centre, Polish Academy of Sciences, Warsaw.
D000818:Animals; D001812:Blood-Brain Barrier / Q000187:drug effects / Q000502:physiology; D001925:Brain Damage, Chronic / Q000473:pathology / Q000503:physiopathology; D001929:Brain Edema / Q000473:pathology / Q000503:physiopathology*; D002545:Brain Ischemia / Q000473:pathology / Q000503:physiopathology*; D002118:Calcium / Q000378:metabolism; D004569:Electroencephalography; D011464:Epoprostenol / Q000172:deficiency* / Q000494:pharmacology; D006624:Hippocampus / Q000098:blood supply / Q000187:drug effects / Q000473:pathology; D011817:Rabbits; D015427:Reperfusion Injury / Q000473:pathology / Q000503:physiopathology
D011464:Epoprostenol; D002118:Calcium