Electron microscopic investigation of rat brain after brief cardiac arrest

Rats were submitted to 10-min cardiac arrest, followed by resuscitation and survival for 1 day, 3 days or 1 week. Five regions of interest (CAL and CA 3 sector of hippocampus, dentate gyrus, reticular nucleus of thalamus and p arietal cortex) where studied by light and electron microscopy at each of t he survival times, and compared with non-ischemic control rats. Cell counts revealed delayed neuronal loss of about 30% after 3 days in both CA1 and C A3 sectors. Ischemic cell changes consisting of cy toplasmic condensation a nd nuclear pyknosis appeared in these regions on day 7 and - to a lesser de gree - also affected dentate gyrus, the reticular nucleus of thalamus and c erebral cortex. Ultrastructural alterations were evaluated using an ultrast ructural injury catalogue. In all brain regions similar, although quantitat ively differently expressed, changes occurred except ribosomal disaggregati on, which was restricted to neurons of hippocampal CA1 sector on the first day after cardiac arrest. Progressive alterations included swelling of mito chondria and endoplasmic reticulum, which was most pronounced in CA1 and CA 3 sectors of hippocampus, as well as chromatin aggregation and alterations of neuronal volume, which affected mainly the granule cells of dentate gyru s. Other alterations, such as osmiophilic inclusions or the formation of nu clear pore complexes, were transient with a maximum on the first day after cardiac arrest. Treatment with the free-radical scavenger alpha -phenyl-N-t ert-butyl nitrone (PBN) suppressed the formation of nuclear pores but other wise did not markedly change the morphological outcome. In comparison to pr evious studies of global brain ischemia induced by arterial inflow occlusio n of the same duration, the present data demonstrate remarkable preservatio n of tissue integrity in CA1 sector but also distinct changes in brain regi ons considered to be resistant to ischemic injury.