4.7 Article

Sevoflurane and Desflurane Exposures Following Aneurysmal Subarachnoid Hemorrhage Confer Multifaceted Protection against Delayed Cerebral Ischemia

Journal

BIOMEDICINES
Volume 9, Issue 7, Pages -

Publisher

MDPI
DOI: 10.3390/biomedicines9070820

Keywords

inhalational anesthesia; sevoflurane; desflurane; conditioning; delayed cerebral ischemia; aneurysmal subarachnoid hemorrhage

Funding

  1. Brain Aneurysm Foundation
  2. McDonnell Center for Cellular and Molecular Neurobiology
  3. NIH T32 Anesthesiology training grant-U.A.
  4. NIH [NS091603]

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Studies have shown that pre-treatment with sevoflurane or desflurane can alleviate large artery vasospasm and neurologic deficits caused by SAH. Further research is needed to confirm and understand the mechanisms of these protective effects in both preclinical and clinical settings, considering the frequent clinical use and safety profile of these anesthetics.
Numerous studies have demonstrated the ability of isoflurane conditioning to provide multifaceted protection against aneurysmal subarachnoid hemorrhage (SAH)-associated delayed cerebral ischemia (DCI); however, preclinical studies have not yet examined whether other commonly used inhalational anesthetics in neurological patients such as sevoflurane or desflurane are also protective against SAH-induced neurovascular deficits. We therefore sought to identify the potential for sevoflurane and desflurane conditioning to protect against DCI in an endovascular perforation mouse model of SAH. Neurological function was assessed daily via neuroscore. Large artery vasospasm and microvessel thrombosis were assessed three days after SAH or sham surgery. Four groups were examined: Sham, SAH + room air, SAH + 2% Sevoflurane, and SAH + 6% Desflurane. For the SAH groups, one hour after surgery, mice received 2% sevoflurane, 6% desflurane, or room air for one hour. We found that conditioning with sevoflurane or desflurane attenuated large artery vasospasm, reduced microvessel thrombosis, and improved neurologic function. Given their frequent clinical use and strong safety profile in patients (including those with SAH), these data strongly support further studies to validate these findings in preclinical and clinical studies and to elucidate the mechanisms by which these agents might be acting.

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