Article
The impact of hypo- and hyperthermia on Spreading Depolarization and delayed infarct progression after focal ischemia in C57BL/6 mice
Search Medline for
Authors
Published: | June 18, 2018 |
---|
Outline
Text
Objective: Spreading depolarization (SD) occurs in high frequency in patients with malignant hemispheric stroke (MHS) and is coupled to different hyperaemic or hypoaemic blood flow responses. Body temperature is a major trigger for SDs and influences the accompanied flow coupling. Here, we investigated neurovascular coupling and occurrence of SD during systemic hypo- and hyperthermia in a later phase of experimental cerebral ischemia.
Methods: Permanent focal ischemia was performed by distal occlusion of the left middle cerebral artery (MCA) in adult, male C57BL/6 mice. Twenty-four hours after MCA occlusion, SD was generated with the potassium-chloride method. During SD, systemic hypothermia (34±1°C) or hyperthermia (38±1°C) was induced and the neurovascular response was measured by continuous laser speckle perfusion imaging. Infarction progression was evaluated by sequential MRI. Four study groups were analysed: control group without SD, SD with potassium chloride, SD with hypothermia and SD with hyperthermia.
Results: 24 hours after stroke onset we observed 0.2±0.3 SD/hour with a mean duration of 1.7±0.6 minutes. An increase of SD duration was observed in hypothermia (3.3±1.3 min; *p<0.05), as well as in hyperthermia (3.1±0.9 min; *p<0.05). Neurovascular coupling during hyperthermia was associated with a reduced cerebral blood flow increase and a shorter hyperperfusion phase (*p<0.05). Repetitive induction of SD significantly increased the stroke volume (11.6±28.4mm3; *p<0,05). In contrast, infarct progression was prevented by systemic hypothermia (1.0±2.8 mm3).
Conclusion: Systemic temperature changes have a relevant impact on late SD occurrence, the associated CBF response and secondary infarct progression.