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Resuscitative hypothermia protects the neonatal rat brain from hypoxic-ischemic injury.


Nedelcu, J; Klein, M A; Aguzzi, A; Martin, E (2000). Resuscitative hypothermia protects the neonatal rat brain from hypoxic-ischemic injury. Brain Pathology, 10(1):61-71.

Abstract

The effect of 24 h of hypothermic recovery on moderate hypoxic-ischemic brain damage in P7-rats was investigated for 42 d after the insult, using magnetic resonance and histopathology. Occlusion of right common carotid artery and 90 min exposure to 8% O2 at 37 degrees C body temperature produced cytotoxic edema of 51(+/-11)% brain volume (BV) and depression of brain energy metabolism (PCr/Pi) from 1.43(+/-0.21) to 0.14(+/-0.11). During recovery, the body temperature was reduced to 30 degrees C for 24 h in 36 animals, but was kept at 37 degrees C in 34 animals. The edema waned upon reoxygenation leaving only the core lesion at 2 h, but reappeared reaching a maximal extent of 11+/-8% BV under hypothermia compared to 45(+/-10)% under normothermia at around 24 h. PCr/Pi recovered transiently within 13 h and declined again to 1.07(+/-0.19) under hypothermia and to 0.48(+/-0.22) under normothermia at around 24 h. Hypothermia led to significant long term brain protection, leaving permanent tissue damage of 12(+/-6)% BV compared to 35(+/-12)% BV under normothermia. However, animals with severe initial injury developed large infarctions, despite hypothermic treatment. Even then, the time to develop infarction was significantly prolonged, leaving the opportunity for additional therapeutic intervention.

The effect of 24 h of hypothermic recovery on moderate hypoxic-ischemic brain damage in P7-rats was investigated for 42 d after the insult, using magnetic resonance and histopathology. Occlusion of right common carotid artery and 90 min exposure to 8% O2 at 37 degrees C body temperature produced cytotoxic edema of 51(+/-11)% brain volume (BV) and depression of brain energy metabolism (PCr/Pi) from 1.43(+/-0.21) to 0.14(+/-0.11). During recovery, the body temperature was reduced to 30 degrees C for 24 h in 36 animals, but was kept at 37 degrees C in 34 animals. The edema waned upon reoxygenation leaving only the core lesion at 2 h, but reappeared reaching a maximal extent of 11+/-8% BV under hypothermia compared to 45(+/-10)% under normothermia at around 24 h. PCr/Pi recovered transiently within 13 h and declined again to 1.07(+/-0.19) under hypothermia and to 0.48(+/-0.22) under normothermia at around 24 h. Hypothermia led to significant long term brain protection, leaving permanent tissue damage of 12(+/-6)% BV compared to 35(+/-12)% BV under normothermia. However, animals with severe initial injury developed large infarctions, despite hypothermic treatment. Even then, the time to develop infarction was significantly prolonged, leaving the opportunity for additional therapeutic intervention.

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Additional indexing

Item Type:Journal Article, refereed
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Institute of Neuropathology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:1 January 2000
Deposited On:11 Feb 2008 12:26
Last Modified:05 Apr 2016 12:21
Publisher:Wiley-Blackwell
ISSN:1015-6305
Publisher DOI:10.1111/j.1750-3639.2000.tb00243.x
Related URLs:http://www.blackwell-synergy.com/doi/abs/10.1111/j.1750-3639.2000.tb00243.x
PubMed ID:10668896

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