TY - JOUR
T1 - Delayed remote ischemic postconditioning improves long term sensory motor deficits in a neonatal hypoxic ischemic rat model
AU - Perera, Pradilka N.Drunalini
AU - Hu, Qin
AU - Tang, Junjia
AU - Li, Li
AU - Barnhart, Margaret
AU - Doycheva, Desislava M.
AU - Zhang, John H.
AU - Tang, Jiping
N1 - Objective Remote 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.
PY - 2014/2/28
Y1 - 2014/2/28
N2 - Objective: Remote 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. Method: 10 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. Results: HI 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. Conclusion: Delayed 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. © 2014 Drunalini Perera et al.
AB - Objective: Remote 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. Method: 10 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. Results: HI 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. Conclusion: Delayed 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. © 2014 Drunalini Perera et al.
KW - Animals, Newborn
KW - Hindlimb/blood supply
KW - Organ Size
KW - Rats
KW - Motor Activity
KW - Rats, Sprague-Dawley
KW - Brain/blood supply
KW - Recovery of Function
KW - Animals
KW - Hypoxia-Ischemia, Brain/physiopathology
KW - Maze Learning
KW - Ischemic Postconditioning
KW - Disease Models, Animal
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UR - http://www.scopus.com/inward/citedby.url?scp=84896517851&partnerID=8YFLogxK
UR - https://www.mendeley.com/catalogue/0f7eabbd-61c9-37b4-94a1-d600da8f8bf1/
U2 - 10.1371/journal.pone.0090258
DO - 10.1371/journal.pone.0090258
M3 - Article
C2 - 24587303
SN - 1932-6203
VL - 9
JO - PLoS ONE
JF - PLoS ONE
IS - 2
M1 - e90258
ER -