Journal
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
Volume 37, Issue 2, Pages 694-705Publisher
SAGE PUBLICATIONS INC
DOI: 10.1177/0271678X16639060
Keywords
Intracranial hypertension; cerebral haemodynamics; pressure reactivity; vascular function; cerebral blood flow; intracranial pressure
Categories
Funding
- Woolf Fisher scholarship
- A.G. Leventis Foundation Scholarship
- Charter Studentship from St Edmund's College, Cambridge
- Bill Gates Scholarship
- Cambridge Commonwealth, European & International Trust Scholarship (University of Cambridge)
- National Institute of Health Research, Cambridge Biomedical Research Center (Neuroscience Theme)
- MRC [G0600986] Funding Source: UKRI
- Medical Research Council [G0600986] Funding Source: researchfish
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Intracranial hypertension is a common final pathway in many acute neurological conditions. However, the cerebral haemodynamic response to acute intracranial hypertension is poorly understood. We assessed cerebral haemodynamics (arterial blood pressure, intracranial pressure, laser Doppler flowmetry, basilar artery Doppler flow velocity, and vascular wall tension) in 27 basilar artery-dependent rabbits during experimental (artificial CSF infusion) intracranial hypertension. From baseline (similar to 9 mmHg; SE 1.5) to moderate intracranial pressure (similar to 41 mmHg; SE 2.2), mean flow velocity remained unchanged (47 to 45 cm/s; p = 0.38), arterial blood pressure increased (88.8 to 94.2 mmHg; p < 0.01), whereas laser Doppler flowmetry and wall tension decreased (laser Doppler flowmetry 100 to 39.1% p < 0.001; wall tension 19.3 to 9.8 mmHg, p < 0.001). From moderate to high intracranial pressure (similar to 75 mmHg; SE 3.7), both mean flow velocity and laser Doppler flowmetry decreased (45 to 31.3 cm/s p < 0.001, laser Doppler flowmetry 39.1 to 13.3%, p < 0.001), arterial blood pressure increased still further (94.2 to 114.5 mmHg; p < 0.001), while wall tension was unchanged (9.7 to 9.6 mmHg; p = 0.35). This animal model of acute intracranial hypertension demonstrated two intracranial pressure-dependent cerebroprotective mechanisms: with moderate increases in intracranial pressure, wall tension decreased, and arterial blood pressure increased, while with severe increases in intracranial pressure, an arterial blood pressure increase predominated. Clinical monitoring of such phenomena could help individualise the management of neurocritical patients.
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