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Physiological changes in intracranial pressure affect arterial pressure
Author(s) -
Guild SarahJane,
Saxena Utkarsh Anand,
Malpas Simon,
McBryde Fiona,
Ramchandra Rohit
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.1012.4
Subject(s) - intracranial pressure , medicine , cerebral perfusion pressure , blood pressure , hexamethonium , anesthesia , reflex , mean arterial pressure , cardiology , perfusion , heart rate , atropine
A number of cardiovascular diseases are characterised by increased levels of sympathetic nerve activity. However, the driving force behind this increase remains unclear. Studies have suggested that, in some of these diseases, reduced cerebral perfusion may cause a sympathetically mediated increase in arterial pressure in an effort to rectify the reduced cerebral perfusion e.g. Selfish Brain Hypothesis (Paton et al 2009). The objective of this research was to determine a) if physiological increases in intracranial pressure (ICP) will cause a reflex increase in arterial blood pressure to maintain cerebral perfusion pressure and b) if the response is driven by increased sympathetic nerve activity. Using an instrumented conscious sheep model, we measured intracranial pressure (subdural) and arterial pressure (carotid) using solid‐state Millar catheters. Saline was infused into the lateral ventricle through an intracerebroventricular catheter to increase intracranial pressure in a ramp‐like fashion. The ICP ramp was repeated after 2 hours of ganglionic blocker hexamethonium. The ramp increase in ICP led to a reflex linear increase in arterial pressure even when ICP remained within normal physiological levels (0–20 mmHg) (n=6, p<0.01). For example: a 10 mmHg increase in ICP lead to a 6.5 ± 1.4mmHg (n=6) increase in arterial pressure. Ganglionic blockade significantly reduced or abolished this increase in arterial pressure, suggesting mediation by increased sympathetic nerve activity. This is supported by preliminary direct renal sympathetic nerve recordings. We believe that this increase in arterial pressure is via an active control mechanism to try to correct reduced cerebral perfusion caused by the increased intracranial pressure. We speculate that alterations in this response may lead to increased sympathetic nerve activity and worsen prognosis in cardiovascular disease. Our preliminary data indicate that this response is active at physiological levels of intracranial pressure and not just at extreme levels where other reflexes such as the Cushing's response would be active. We propose that this response is an important novel addition to other known mechanisms protecting the brain from under‐perfusion. Support or Funding Information Supported by the Health Research Council of New Zealand