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  • Title: Reversal of attenuation of cerebrovascular reactivity to hypercapnia by a nitric oxide donor after controlled cortical impact in a rat model of traumatic brain injury.
    Author: Zhang F, Sprague SM, Farrokhi F, Henry MN, Son MG, Vollmer DG.
    Journal: J Neurosurg; 2002 Oct; 97(4):963-9. PubMed ID: 12405388.
    Abstract:
    OBJECT: Traumatic brain injury (TBI) attenuates the cerebral vasodilation to hypercapnia. Cortical spreading depression (CSD) also transiently reduces hypercapnic vasodilation. The authors sought to determine whether the CSD elicited by a controlled cortical impact (CCI) injury masks the true effect of TBI on hypercapnic vasodilation, and whether a nitric oxide (NO) donor can reverse the attenuation of hypercapnic vasodilation following CCI. METHODS: Anesthetized rats underwent moderate CCI. Cerebral blood flow was monitored with laser Doppler flowmetry and the response to hypercapnia was determined for injured and sham-injured animals. The effect of the NO donor, S-nitroso-N-acetylpenicillamine (SNAP), on this response was also assessed. At an uninjured cortical site ipsilateral to the CCI, a single wave of CSD was recorded and the CO2 response at this location was significantly attenuated for up to 30 minutes (seven rats, p < 0.05). At the injured cortex, hypercapnic vasodilation continued to be attenuated for 7 hours. The cerebral vasodilation to CO2 was 37 +/- 5% in injured rats (six) compared with 84 +/- 10% in the sham-injured group (five rats, p < 0.05). After 30 minutes of topical superfusion with SNAP, hypercapnic vasodilation was restored to 74 +/- 7% (nine rats, p > 0.1 compared with that in the sham-injured group). In contrast, papaverine, an NO-independent vasodilator, failed to reverse the attenuation of the CO2 response to CCI. CONCLUSIONS: The authors conclude that CSD elicited by CCI can mask the true effect of TBI on hypercapnic vasodilation for at least 30 minutes. Exogenous NO, but not papaverine, can reverse the attenuation of cerebrovascular reactivity to CO2 caused by TBI. This result supports the hypothesis that NO production is reduced after TBI and that the NO donor has a potential beneficial role in the clinical management of head injury.
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