Effects of one-day reperfusion after transient forebrain ischemia on circulatory system in the rat.

Although ischemia/reperfusion injury remains incompletely understood, it appears that reactive oxygen species produced mainly during postischemic recirculation play a critical role. The present study examined the impact of forebrain ischemia and subsequent one-day reperfusion on several blood parameters. We determined glutamate concentration in whole blood, measured Cu/Zn- and Mn-SOD (superoxide dismutase) activity in blood cells as well as plasma, and investigated the prevalence of single and double strand breaks of lymphocyte DNA.

Chemokines as possible targets in modulation of the secondary damage after acute spinal cord injury: a review.

In spite of many promising experimental studies, an effective treatment dramatically eliminating the secondary damage after spinal cord injury (SCI) is still missing. Since clinical data on the therapeutical effect after methylprednisolone treatment are not conclusive, new therapeutical modalities targeting specific components of secondary spinal cord damage needs to be developed. It is known that immune cells are recruited to injury sites by chemokines, which are small, structurally similar proteins released locally at the site of inflammation.

Postconditioning and anticonditioning: possibilities to interfere to evoked apoptosis.

The aim of this study was to validate the ability of postconditioning, used 2 days after kainate intoxication, to protect selectively vulnerable hippocampal CA1 neurons against delayed neuronal death. Kainic acid (8 mg/kg, i.p.

Bradykinin postconditioning protects pyramidal CA1 neurons against delayed neuronal death in rat hippocampus.

Aims: The present study was undertaken to evaluate possible neuroprotective effect of bradykinin against delayed neuronal death in hippocampal CA1 neurons if applied two days after transient forebrain ischemia in the rat.

Methods: Transient forebrain ischemia was induced in male Wistar rats by four-vessel occlusion for 8 min. To assess efficacy of bradykinin as a new stressor for delayed postconditioning we used two experimental groups of animals: ischemia 8 min and 3 days of survival, and ischemia 8 min and 3 days of survival with i.

Transient forebrain ischemia impact on lymphocyte DNA damage, glutamic acid level, and SOD activity in blood.

Aims: Brain ischemia-reperfusion injury remains incompletely understood but appears to involve a complex series of interrelated biochemical pathways caused mainly by a burst of reactive oxygen species (ROS). In the present work we studied the impact of postischemic condition in the early phase of reperfusion on plasma and blood cells.

Methods: Transient forebrain ischemia was induced in Wistar rats by four-vessel occlusion model.