Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
Shum-Tim, D; Nagashima, M; Shinoka, T; Bucerius, J; Nollert, G; Lidov, HGW; du-Plessis, A; Laussen, PC; Jonas, RA.
Postischemic hyperthermia exacerbates neurologic injury after deep hypothermic circulatory arrest
J THORAC CARDIOV SUR. 1998; 116(5): 780-791.
Doi: 10.1016/S0022-5223(98)00449-8
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- Co-Autor*innen der Med Uni Graz
- Bucerius Jan Alexander
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- Abstract:
- Background: Aggressive surface warming is a common practice in the pediatric intensive care unit, However, recent rodent data emphasize the protective effect of mild (2 degrees-3 degrees C) hypothermia after cerebral ischemia, This study evaluates different temperature regulation strategies after deep hypothermic circulatory arrest with a survival piglet model. Methods: Fifteen piglets were randomly assigned to 3 groups. All groups underwent 100 minutes of deep hypothermic circulatory arrest at 15 degrees C, Brain temperature was maintained at 34 degrees C for 24 hours after cardiopulmonary bypass in group I, 37 degrees C in group II, and 40 degrees C in group III. Neurobehavioral recovery was evaluated daily for 3 days after extubation by neurologic deficit score (0, normal; 500, brain death) and overall performance category (1, normal; 5, brain death). Histologic examination was assessed for hypoxic-ischemic injury (0, normal; 5, necrosis) in a blinded fashion. Results: All results are expressed as mean +/- standard deviation. Recovery of neurologic deficit score (12.0 +/- 17.8, 47.0 +/- 49.95, 191.0 +/- 179.83; P = .05 for group I vs III), overall performance category (1.0 +/- 0,0, 1.4 +/- 0.6, 2.8 +/- 1.3; P < .05 for group I vs IU), and histologic scores (0.0 +/- 0,0, 1.0 +/- 1.2, 2.8 +/- 1.8; P < .05 for group I vs III cortex) were significantly worse in hyperthermic group III. These findings were associated with a significantly lower cytochrome aa, recovery determined by near-infrared spectroscopy in group III animals (P = .0041 for group I vs III). No animal recovered to baseline electroencephalographic value by 48 hours after deep hypothermic circulatory arrest. Recovery was significantly delayed in the hyperthermic group III animals, with a lower amplitude 14 hours after the operation, which gradually increased with time (P < .05 for group III vs groups I and II). Conclusions: Mild postischemic hyperthermia significantly exacerbates functional and structural neurologic injury after deep hypothermic circulatory arrest and should therefore be avoided.