Abstract
ObjectiveRemote Ischemic Postconditioning (RIPC) is a promising therapeutic intervention wherein a sub-lethal ischemic insult induced in one organ (limb) improves ischemia in an organ distant to it (brain). The main objective of this study was to investigate the long-term functional effects of delayed RIPC in a neonatal hypoxia-ischemia (HI) rat model.Method10 day old rat pups were subjected to delayed RIPC treatment and randomized into four groups: 1) Sham, 2) HI induced, 3) HI +24 hr delayed RIPC, and 4) HI +24 hr delayed RIPC with three consecutive daily treatments. Neurobehavioral tests, brain weights, gross and microscopic brain tissue morphologies, and systemic organ weights were evaluated at five weeks post surgery.ResultsHI induced rats performed significantly worse than sham but both groups of delayed RIPC treatment showed improvement of sensory motor functions. Furthermore, compared to the HI induced group, the delayed RIPC treatment groups showed no further detrimental changes on brain tissue, both grossly and morphologically, and no changes on the systemic organ weights.ConclusionDelayed RIPC significantly improves long term sensory motor deficits in a neonatal HI rat model. A 24 hr delayed treatment does not significantly attenuate morphological brain injury but does attenuate sensory motor deficits. Sensory motor deficits improve with both a single treatment and with three consecutive daily treatments, and the consecutive treatments are possibly being more beneficial.
Highlights
Hypoxic Ischemic (HI) brain injury begins with an initial insult and may continue into the recovery period after reperfusion [1,2]
HI induced rats performed significantly worse than sham but both groups of delayed Remote Ischemic Postconditioning (RIPC) treatment showed improvement of sensory motor functions
Known as Hypoxic Ischemic Encephalopathy (HIE), it is more likely to occur in an immature brain rather than in the brain of a full-term neonate [4]
Summary
Hypoxic Ischemic (HI) brain injury begins with an initial insult and may continue into the recovery period after reperfusion [1,2]. Reperfusion injury causes damage that with current medical treatment is largely irreversible. It may occur in the prenatal, perinatal or postnatal periods. Damage resulting from hypoxic ischemia may lead to chronic conditions such as cerebral palsy, mental retardation, learning disabilities, and epilepsy [2,5]. These conditions confer significant challenges to the affected individual, their family, and society. The remaining 75% of cases that consist of mild and moderate HIE may be diagnosed weeks or even months after the initial insult
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