Twenty-four hours hypothermia has temporary efficacy in reducing brain infarction and inflammation in aged rats

TY - JOUR

T1 - Twenty-four hours hypothermia has temporary efficacy in reducing brain infarction and inflammation in aged rats

AU - Sandu, Raluca Elena

AU - Buga, Ana Maria

AU - Balseanu, Adrian Tudor

AU - Moldovan, Mihai

AU - Popa-Wagner, Aurel

PY - 2016

Y1 - 2016

N2 - Stroke is a major cause of disability for which no neuroprotective measures are available. Age is the principal nonmodifiable risk factor for this disease. Previously, we reported that exposure to hydrogen sulfide for 48 hours after stroke lowers whole body temperature and confers neuroprotection in aged animals. Because the duration of hypothermia in most clinical trials is between 24 and 48 hours, we questioned whether 24 hours exposure to gaseous hypothermia confers the same neuroprotective efficacy as 48 hours exposure. We found that a shorter exposure to hypothermia transiently reduced both inflammation and infarct size. However, after 1 week, the infarct size became even larger than in controls and after 2 weeks there was no beneficial effect on regenerative processes such as neurogenesis. Behaviorally, hypothermia also had a limited beneficial effect. Finally, after hydrogen sulfide-induced hypothermia, the poststroke aged rats experienced a persistent sleep impairment during their active nocturnal period. Our data suggest that cellular events that are delayed by hypothermia in aged rats may, in the long term, rebound, and diminish the beneficial effects.

AB - Stroke is a major cause of disability for which no neuroprotective measures are available. Age is the principal nonmodifiable risk factor for this disease. Previously, we reported that exposure to hydrogen sulfide for 48 hours after stroke lowers whole body temperature and confers neuroprotection in aged animals. Because the duration of hypothermia in most clinical trials is between 24 and 48 hours, we questioned whether 24 hours exposure to gaseous hypothermia confers the same neuroprotective efficacy as 48 hours exposure. We found that a shorter exposure to hypothermia transiently reduced both inflammation and infarct size. However, after 1 week, the infarct size became even larger than in controls and after 2 weeks there was no beneficial effect on regenerative processes such as neurogenesis. Behaviorally, hypothermia also had a limited beneficial effect. Finally, after hydrogen sulfide-induced hypothermia, the poststroke aged rats experienced a persistent sleep impairment during their active nocturnal period. Our data suggest that cellular events that are delayed by hypothermia in aged rats may, in the long term, rebound, and diminish the beneficial effects.

KW - Aging

KW - EEG

KW - HS

KW - Hypothermia

KW - Inflammation

KW - Neurogenesis

KW - Neuroprotection

KW - Phagocytosis

KW - Sleep

KW - Stroke

U2 - 10.1016/j.neurobiolaging.2015.11.006

DO - 10.1016/j.neurobiolaging.2015.11.006

M3 - Journal article

C2 - 26827651

AN - SCOPUS:84962279458

SN - 0197-4580

VL - 38

SP - 127

EP - 140

JO - Neurobiology of Aging

JF - Neurobiology of Aging

ER -