Abstract
There is a transient increase in intracranial pressure (ICP) 18–24 h after ischaemic stroke in rats, which is prevented by short-duration hypothermia using rapid cooling methods. Clinical trials of long-duration hypothermia have been limited by feasibility and associated complications, which may be avoided by short-duration cooling. Animal studies have cooled faster than is achievable in patients. We aimed to determine whether gradual cooling at a rate of 2°C/h to 33°C or 1°C/h to 34.5°C, with a 30 min duration at target temperatures, prevented ICP elevation and reduced infarct volume in rats. Transient middle cerebral artery occlusion was performed, followed by gradual cooling to target temperature. Hypothermia to 33°C prevented significant ICP elevation (hypothermia ΔICP = 1.56 ± 2.26 mmHg vs normothermia ΔICP = 8.93 ± 4.82 mmHg; p = 0.02) and reduced infarct volume (hypothermia = 46.4 ± 12.3 mm3 vs normothermia = 85.0 ± 17.5 mm3; p = 0.01). Hypothermia to 34.5°C did not significantly prevent ICP elevation or reduce infarct volume. We showed that gradual cooling to 33°C, at cooling rates achievable in patients, had the same ICP preventative effect as traditional rapid cooling methods. This suggests that this paradigm could be translated to prevent delayed ICP rise in stroke patients.
Highlights
Stroke is the second leading cause of death worldwide and the number one cause of permanent disability in adults [1, 2]
We have shown that clinically achievable gradual cooling to 33◦C, with only 30 min at target temperature, prevented significant elevation of intracranial pressure (ICP) and reduced infarct volume 24 h post-stroke
We have previously shown that 2.5 h hypothermia to 32.5◦C prevented ICP rise at 24 h in both young adult and aged rats, and in different strains [6, 7]
Summary
Stroke is the second leading cause of death worldwide and the number one cause of permanent disability in adults [1, 2]. A good collateral flow network is associated with better neurological outcome after stroke [3, 4]. Dramatic elevations in intracranial pressure (ICP) occur after experimental ischaemic stroke in animals - in young and aged rats, as well as rats of different strains [5,6,7]. Our preliminary data indicates a significant ICP rise occurs in stroke patients at 24 h [8]. This ICP rise is a potential mechanism for collateral failure associated with delayed infarct expansion, worsening
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