English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Following 5 minutes of global ischemia, local cerebral blood flow (LCBF) was shown to have an initial reactive hyperemia that was followed, within the first hour, by persistent hypoperfusion (Part I). Intracranial pressure (ICP) was never elevated during the period of poor reperfusion. These experiments attempted to reverse the state of subnormal LCBF by inducing hypercarbia or hyocarbia or maintaining normocarbia. Although hypocarbia did increase LCBF at several electrode sites, neither the intracerebral steal syndrome nor the "squeeze" syndrome are a dominant consequence of hypercarbia in this model of global ischemia. Hypercarbia was consistently more effective in elevating LCBFs and in recovery of the electrocorticogram. It appears that, in the absence of raised ICP, hypercarbia may be preferred to normal or low PACO2,. Even though hypercarbia was superior to normocarbia or hypocarbia, hypercarbia was not a completely satisfactory regimen for reversing the state of poor reperfusion.

Local cerebral blood flow following transient cerebral ischemia. II. Effect of arterial PCO2 on reperfusion following global ischemia.