Anesthetics and cerebral ischemia — should we continue to dream the impossible dream?

Endothelin-1 induced MCAO: Dose dependency of cerebral blood flow

“…The low CBF required to induce neuronal death observed by TTC staining may be due to the anesthetic used during the occlusion. Anesthesia has been shown to have a neuroprotective effect in stroke and the presence of isoflurane does influence blood flow and reduces infarct size relative to the awake state (Gelb et al, 2001(Gelb et al, , 2002. Isoflurane has been shown to act as a vasodilator (Warner et al, 1991) resulting in higher CBF during ischemia.…”

Refinement of a model of repeated cerebrospinal fluid collection in conscious rats

“…A typical example is ketamine -a dissociative N-methyl-D-aspartate (NMDA) agonist anesthetic, although this is becoming controversialat least when used at low doses. Still the use of high-dose ketamine increases cerebral blood flow, 21,22 resulting in increased ICP. [22][23][24][25] For the model in this study, this would be an undesired side-effect, therefore MMF is advantageous compared with KX because of the minimal interference with the cerebral autoregulation mechanisms.…”

And the winner is…

“…The mere fact that anesthesia providers yearn to identify areas in which our ministrations are therapeutic rather than merely facilitatory 3 does not ipso facto make them exist. Could it be that no amount of pharmacological jiggery-pokery is any match for the gross distortions of structure and function that ensue when the skull is opened, and that provided we keep the patient still and avoid the most egregious errors, our choice of anesthetic agent is immaterial?…”