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

Sudden death may follow subarachnoid hemorrhage which indicates involvement of neural mechanisms connected with the cardiovascular system. Since various regions of the brain mediate blood pressure and heart rate changes, these parameters and heart rhythm could be affected due to a subarachnoid hemorrhage near the circle of Willis which surrounds the hypothalamus, the highest center for autonomic control. To investigate this in the control group, intracranial pressure, blood pressure, and electrocardiogram were measured before and after a simulated subarachnoid hemorrhage; blood pressure and electrocardiogram were measured following midcollicular lesions in the decerebrate group both before and after a subarachnoid hemorrhage. The results demonstrate that an increase in systemic arterial blood pressure and premature ventricular contractions (with respect to unlesioned group, p less than 0.04) are mediated by forebrain areas and require the integrity of neuroanatomical connections with structures that are caudal to the midbrain. Since bradycardia and other electrocardiographic abnormalities could still be produced after midcollicular lesioning it is suggested that they can be mediated via the brainstem only without involvement of more rostral areas and may occur due to increased intracranial pressure.

Central neural control of blood pressure and cardiac arrhythmias during subarachnoid hemorrhage in rats.