Faculty Opinions recommendation of Remote ischemic preconditioning protects the brain against injury after hypothermic circulatory arrest.

Aim: The aim of the present study is to explore the neuroprotective effects of remote ischemic preconditioning in long term cognitive impairment after global cerebral ischemia induced-vascular dementia in mice. Material and methods: The mice were subjected to global cerebral ischemia by occluding the bilateral common carotid arteries for 12 minutes followed by the 24 hours of the reperfusion. The remote ischemic preconditioning stimulus was delivered in the form of 4 cycles of ischemia/reperfusion for 5 minutes each. The cerebral ischemic injury induced-long term cognitive impairment-related learning and memory alterations was assessed using morris water maze, the motor performances of the animals were evaluated using rota-rod test and neurological severity score. The cerebral infract size of the brain were quantified using triphenyltetrazolium chloride staining. Results: Global cerebral ischemia causes long term memory impairment, decreases motor performances and increases the brain infract size in animals. The delivery of remote ischemic preconditioning stimulus significantly abolished the long-term cognitive impairment and ameliorates the motor performances as well as cerebral infract size in brain. Conclusion: The remote ischemic preconditioning mediates neuro protection against global cerebral ischemic injury induced long-term cognitive impairment.

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Inhibition of microRNA-29c protects the brain in a rat model of prolonged hypothermic circulatory arrest

Journal of Thoracic and Cardiovascular Surgery ◽

10.1016/j.jtcvs.2015.04.062 ◽

2015 ◽

Vol 150 (3) ◽

pp. 675-684.e1 ◽

Cited By ~ 12

Author(s):

Yongchao Wang ◽

Tianxiang Gu ◽

Enyi Shi ◽

Lei Yu ◽

Chun Wang ◽

...

Keyword(s):

Rat Model ◽

Circulatory Arrest ◽

Hypothermic Circulatory Arrest ◽

The Brain

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Abstract 2594: Remote Ischemic Preconditioning Protects the Brain Against Injury Following Hypothermic Circulatory Arrest

Circulation ◽

10.1161/circ.118.suppl_18.s_749-b ◽

2008 ◽

Vol 118 (suppl_18) ◽

Author(s):

Hanna Kaakinen ◽

Stavros P Loukogeorgakis ◽

Viktor Tsang ◽

Eija Niemelä ◽

Hannu Tuominen ◽

...

Keyword(s):

Intracranial Pressure ◽

Ischemic Preconditioning ◽

Circulatory Arrest ◽

Lactate Concentration ◽

T Test ◽

Histopathological Analysis ◽

Eeg Activity ◽

Behavioral Score ◽

The Brain ◽

Brain Lactate

Ischemic preconditioning (IPC) is an innate mechanism that protects tissues from injury during ischemia and reperfusion. IPC has systemic effects that protect tissues remote from those undergoing preconditioning (remote IPC; RIPC). RIPC can be elicited by applying brief periods of ischemia to tissues with ischemic tolerance (skeletal muscle) yet protect vital organs that are more susceptible to ischemic damage. Using a porcine model, we determined if RIPC of the limb is protective against brain injury caused by hypothermic circulatory arrest (HCA). 12 piglets were randomized to control and RIPC groups before undergoing cardiopulmonary bypass (CPB) and 60 minutes HCA at 18oC. RIPC was induced by 4 cycles of 5-minute ischemia alternating with reperfusion of the hind limb (inflation of pneumatic cuff to 200mmHg) prior to CPB. Intracranial pressure and temperature, brain lactate concentration and electroencephalographic (EEG) activity were monitored for 8 hours after HCA. Assessment of neurological status was performed daily for 7 days post-operatively, using a species-specific quantitative behavioral score. All animals were sacrificed and brain tissue was harvested for histopathological analysis. Data were analyzed using 2-way ANOVA or student’s t-test. Study groups were balanced for baseline and intra-operative parameters; no differences were observed in intracranial pressure and temperature. Brain lactate concentration was significantly lower (p<0.0001, ANOVA) and recovery of EEG activity faster (p<0.05, ANOVA) in the RIPC group compared to control. RIPC had a beneficial effect on neurological function during the 7-day follow-up period (behavioral score; p<0.0001 vs. control, ANOVA). Histopathological analysis demonstrated a significant reduction in total cerebral injury in RIPC animals compared to controls [injury score; median (interquartile range): control 6.4 (5.0 – 8.0) vs. RIPC 1.6 (0.5–2.5), p<0.001, t-test]. These data demonstrate, for the first time, that RIPC protects the brain against HCA-induced injury, resulting in accelerated recovery of neurological function. RIPC might be neuroprotective in patients undergoing surgery with HCA and improve long-term outcomes. Clinical trials to test this hypothesis are warranted.

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