Cytotoxic brain edema induced by water intoxication and vasogenic brain edema induced by osmotic BBB disruption lead to distinct pattern of ICP elevation during telemetric monitoring in freely moving rats
Language English Country Sweden Media print
Document type Journal Article
PubMed
32200583
PII: NEL400619A03
Knihovny.cz E-resources
- MeSH
- Brain Edema diagnosis etiology physiopathology MeSH
- Blood-Brain Barrier physiopathology MeSH
- Water Intoxication complications diagnosis physiopathology MeSH
- Intracranial Hypertension complications diagnosis physiopathology MeSH
- Intracranial Pressure physiology MeSH
- Rats MeSH
- Monitoring, Physiologic methods MeSH
- Brain physiopathology MeSH
- Cerebrovascular Circulation physiology MeSH
- Rats, Wistar MeSH
- Telemetry MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
OBJECTIVES: A novel method of long-term telemetric monitoring of mean arterial pressure (MAP) and intracranial pressure (ICP) for the determination of current cerebral perfusion pressure (CPP) and the time course of ICP in freely moving rats under physiological conditions and with increased ICP due to the induced cerebral edema were studied. METHODS: The brain edema, that caused volume enlargement and ICP elevation was achieved in entirely experimental conditions without any parallel pathological process. Vasogenic/extracellular edema was induced by osmotic blood-brain barrier disruption (BBBd) and for induction of cytotoxic/intracellular edema the water intoxication model (WI) was used. RESULTS: The results showed significantly elevated values of ICP both in conditions of osmotic blood-brain barrier disruption (BBBd model) and cytotoxic/intracellular edema (WI model) compared to intact rats. The average values of ICP were significantly higher in WI model compared to osmotic BBBd model. Distinct pattern of elevated ICP, related to the selected way of experimental brain edema induction, was found. In the experimental model of osmotic BBB disruption, the elevation of ICP started earlier but was of very short duration. In WI model the elevation of ICP was present during the whole period of monitoring. CONCLUSION: Our results indicate that purely experimental models of brain edema (WI, BBBd) without any parallel pathological process can compromise the basic brain homeostatic activity.
Cerebral perfusion pressure and behavior monitoring in freely moving rats