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Cortical hypoperfusion precedes hyperperfusion following controlled cortical impact injury


Thomale, U W; Schaser, K; Kroppenstedt, S N; Unterberg, A W; Stover, J F (2002). Cortical hypoperfusion precedes hyperperfusion following controlled cortical impact injury. In: Acta neurochirurgica Supplement. Springer, 229-231.

Abstract

Impaired cerebral perfusion contributes to tissue damage following traumatic brain injury. In this longitudinal study persistence of reduced cortical perfusion employing laser doppler flowmetry was investigated following controlled cortical impact injury (CCII). Before, 30 minutes, 6, 24, and 48 hours after CCII, perfusion in pericontusional cortex was determined by moving a laser doppler probe in 50 x 0.2 mm steps over the traumatized hemisphere in 5 rats. Arterial blood gases and mean arterial blood pressure were monitored. Mean arterial blood pressure and arterial blood gases remained stable during the entire experiments. At 30 minutes and 6 hours following CCII, cortical perfusion was significantly diminished by 24% and 43% (p < 0.05), respectively compared to pre-trauma levels. At 24 and 48 hours after CCII, pericontusional blood flow was significantly increased by 64% and 123%. Cortical hypoperfusion found within the early phase following trauma is reversible and precedes a long lasting phase of hyperperfusion. Changes in tissue mediators (endothelin, acidosis, NO) could account for these findings.

Abstract

Impaired cerebral perfusion contributes to tissue damage following traumatic brain injury. In this longitudinal study persistence of reduced cortical perfusion employing laser doppler flowmetry was investigated following controlled cortical impact injury (CCII). Before, 30 minutes, 6, 24, and 48 hours after CCII, perfusion in pericontusional cortex was determined by moving a laser doppler probe in 50 x 0.2 mm steps over the traumatized hemisphere in 5 rats. Arterial blood gases and mean arterial blood pressure were monitored. Mean arterial blood pressure and arterial blood gases remained stable during the entire experiments. At 30 minutes and 6 hours following CCII, cortical perfusion was significantly diminished by 24% and 43% (p < 0.05), respectively compared to pre-trauma levels. At 24 and 48 hours after CCII, pericontusional blood flow was significantly increased by 64% and 123%. Cortical hypoperfusion found within the early phase following trauma is reversible and precedes a long lasting phase of hyperperfusion. Changes in tissue mediators (endothelin, acidosis, NO) could account for these findings.

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Additional indexing

Item Type:Book Section, not refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Division of Surgical Intensive Care Medicine
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:2002
Deposited On:02 Oct 2009 05:26
Last Modified:05 Apr 2016 12:51
Publisher:Springer
PubMed ID:12168311

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