Related Experiment Video
Updated: Aug 6, 2026
09:29
2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia
Published on: June 22, 2013
Brain tissue PO(2), PCO(2), and pH during cerebral vasospasm
F T Charbel1, X Du, W E Hoffman
1Department of Neurosurgery, University of Illinois at Chicago, Chicago, Illinois 60612, USA.
Surgical Neurology
|March 10, 2001
Summary
Brain tissue monitoring detected ischemia in subarachnoid hemorrhage (SAH) patients with vasospasm. Lower pH and higher carbon dioxide pressure (PCO2) indicated issues, while oxygen levels remained stable.
Area of Science:
- Neurology
- Neurosurgery
- Critical Care Medicine
Background:
- Aneurysmal subarachnoid hemorrhage (SAH) poses risks of cerebral vasospasm and ischemia.
- Early detection of ischemia is crucial for managing SAH patients.
Observation:
- Brain tissue monitoring using a Neurotrend 7 probe was performed in 10 SAH patients.
- Monitoring assessed brain tissue gases (PO2, PCO2) and pH over 7-10 days.
- Vasospasm onset was confirmed by angiography and Xe/CT.
Findings:
- Patients developing vasospasm showed significantly decreased brain tissue pH (to 6.7) and increased PCO2 (to 60 mmHg) compared to controls.
- Brain tissue oxygen pressure (PO2) did not significantly change in patients with vasospasm.
- These changes were statistically significant (p < 0.001).
Implications:
- Brain tissue monitoring can indicate ischemia during vasospasm in SAH patients.
- Monitoring provides valuable data for timely intervention and improved patient outcomes.
- This technique aids in understanding the physiological changes associated with vasospasm post-SAH.
Related Concept Videos
01:16Vascular Spasm
The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last for...
01:15Ischemic Stroke ll: Pathophysiology
An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
01:29Hemorrhagic Stroke ll: Pathophysiology
A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
01:29Increased Intracranial Pressure ll: Pathophysiology
Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...
01:19Cerebral Edema l: Introduction
Cerebral edema is a pathological increase in brain water content that disrupts intracranial pressure regulation and impairs neurological function. Because the cranial vault is rigid, even modest increases in tissue volume can compromise cerebral perfusion, distort neural structures, and initiate secondary injury. Cerebral edema develops through four principal mechanisms: vasogenic, cytotoxic, interstitial, and ionic.Vasogenic EdemaVasogenic edema arises from disruption of the blood–brain...
01:22Cerebral Edema ll: Pathophysiology
Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...