Mild Hypothermia Has No Long-Term Impact on Postischemic Neurogenesis in Rats

Lasarzik, Irina; Winkelheide, Uta; Thal, Serge C.; Benz, Natascha; Lörscher, Matthias; Jahn‐Eimermacher, Antje; Werner, Christian; Engelhard, Kristin

doi:10.1213/ane.0b013e3181bab451

Cited by 27 publications

(18 citation statements)

References 35 publications

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“…Thus, we measured by the number of Ki67/DCX colabeled cells and found that hypothermia treatment did not affect neurogenesis. Overall, these findings are in line with previous results showing that neuroprotective treatments such as systemic hypothermia (Lasarzik et al, 2009;Silasi and Colbourne, 2011a) or ischemic preconditioning (Liu et al, 1998) do not alter postischemic neurogenesis. Notably, it remains possible that focal brain cooling may enhance the long-term survival of newly generated neurons in the DG, which we found to occur after systemic hypothermia, but this could not be examined with our current survival times.…”

Section: Discussionsupporting

confidence: 92%

Prolonged Therapeutic Hypothermia does not Adversely Impact Neuroplasticity after Global Ischemia in Rats

Silasi

Klahr

Hackett

et al. 2012

J Cereb Blood Flow Metab

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Hypothermia improves clinical outcome after cardiac arrest in adults. Animal data show that a day or more of cooling optimally reduces edema and tissue injury after cerebral ischemia, especially after longer intervention delays. Lengthy treatments, however, may inhibit repair processes (e.g., synaptogenesis). Thus, we evaluated whether unilateral brain hypothermia (∼33°C) affects neuroplasticity in the rat 2-vessel occlusion model. In the first experiment, we cooled starting 1 hour after ischemia for 2, 4, or 7 days. Another group was cooled for 2 days starting 48 hours after ischemia. One group remained normothermic throughout. All hypothermia treatments started 1 hour after ischemia equally reduced hippocampal CA1 injury in the cooled hemisphere compared with the normothermic side and the normothermic group. Cooling only on days 3 and 4 was not beneficial. Importantly, no treatment influenced neurogenesis (Ki67/Doublecortin (DCX) staining), synapse formation (synaptophysin), or brain-derived neurotropic factor (BDNF) immunohistochemistry. A second experiment confirmed that BDNF levels (ELISA) were equivalent in normothermic and 7-day cooled rats. Last, we measured zinc (Zn), which is important in plasticity, with X-ray fluorescence imaging in normothermic and 7-day cooled rats. Hypothermia did not alter the postischemic distribution of Zn within the hippocampus. In summary, cooling significantly mitigates injury without compromising neuroplasticity.

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Section: Discussionsupporting

confidence: 92%

Prolonged Therapeutic Hypothermia does not Adversely Impact Neuroplasticity after Global Ischemia in Rats

Silasi

Klahr

Hackett

et al. 2012

J Cereb Blood Flow Metab

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show abstract

“…Also, hypothermia for 2–4 h alone did not decrease the pathological score in the HI rat brain as compared to the normothermia and vehicle-treated group either. Other researchers also found that post-insult hypothermia offers neuroprotection only when the duration is as long as 24–72 h (Ohmura et al, 2005; Tomimatsu et al, 2001), while short-term hypothermia during brain recovery appears not to be neuroprotective (Guan et al, 2000; Jatana et al, 2006; Lasarzik et al, 2009). …”

Section: Discussionmentioning

confidence: 99%

Whole body hypothermia broadens the therapeutic window of intranasally administered IGF-1 in a neonatal rat model of cerebral hypoxia–ischemia

2011

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To investigate whether whole body hypothermia after neonatal cerebral hypoxia-ischemia (HI) could broaden the therapeutic window of intranasal treatment of IGF-1 (iN-IGF-1), postnatal day 7 rat pups were subjected to right common carotid artery ligation, followed by 8% oxygen inhalation for 2 h. After HI, one group of pups were returned to their dams and kept at room temperature (24.5±0.2°C). A second group of pups were subjected to whole body hypothermia in a cool environment (21.5±0.3°C) for 2 or 4 h before being returned to their dams. Two doses of 50 μg recombinant human IGF-1 were administered intranasally at a 1 h interval starting at 0, 2 or 4 h after hypothermia. Hypothermia decreased the rectal temperature of pups by 4.5°C as compared to those kept at room temperature. While hypothermia or iN-IGF-1 administered 2 h after HI alone did not provide neuroprotection, the combined treatment of hypothermia with iN-IGF-1 significantly protected the neonatal rat brain from HI injury. Hypothermia treatment extended the therapeutic window of IGF-1 to 6 h after HI. The extended IGF-1 therapeutic window by hypothermia was associated with decreases in infiltration of polymorphonuclear leukocytes and activation of microglia/macrophages and with attenuation of NF-κB activation in the ipsilateral hemisphere following HI.

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“…Sin embargo, en otro ensayo realizado en ratas adultas, se ha demostrado que la hipotermia no tiene ningún efecto en la neurogénesis [88]. Hay que señalar que el modelo experimental empleado fue diferente y que el protocolo de hipotermia utilizado fue tan solo de 45 min a 33 º C, frente a las 24 h a 32-33ºC del estudio de Xiong et al [82].…”

Section: Hipotermia Y Neurogénesisunclassified

Hipoxia-isquemia neonatal: bases celulares y moleculares del daño cerebral y modulación terapéutica de la neurogénesis

et al. 2019

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Mild Hypothermia Has No Long-Term Impact on Postischemic Neurogenesis in Rats

Cited by 27 publications

References 35 publications

Prolonged Therapeutic Hypothermia does not Adversely Impact Neuroplasticity after Global Ischemia in Rats

Prolonged Therapeutic Hypothermia does not Adversely Impact Neuroplasticity after Global Ischemia in Rats

Whole body hypothermia broadens the therapeutic window of intranasally administered IGF-1 in a neonatal rat model of cerebral hypoxia–ischemia

Hipoxia-isquemia neonatal: bases celulares y moleculares del daño cerebral y modulación terapéutica de la neurogénesis

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