Preserved contractility without side bias in endovascular filament models for subarachnoid hemorrhage.
It is currently unknown whether endovascular filament (EF) models of acute subarachnoid hemorrhage (SAH) introduce any 'side bias' upon cerebrovascular reactivity by virtue of unilateral carotid manipulation, unilateral EF insertion, or potentially ipsilateral site of intracranial rupture. In this study, three experimental groups of adult male wistar rats were used: non-operated controls (n=20), sham operated controls (n=8), and SAH groups (n=26). All were anaesthetized with intraperitoneal 25% urethane (1 g/kg) except n=2 anaesthetized with intraperitoneal hypnorm/hypnovel. SAH was created by advancing an intraluminal thread through the intracranial internal carotid artery from an extracranial source in the neck. Using in vitro wire myography in all three groups, middle cerebral artery (MCA) responses ipsilateral and contralateral to EF insertion were compared using a range of vasoconstrictors and vasodilators within 3 h of SAH. No significant side differences in MCA reactivity were found with any agent in any group or sub-group analysed. In conclusion, EF-SAH models do not appear to introduce any significant 'side bias' upon ipsilateral MCA reactivity by virtue of the potentially confounding combination: (1) unilateral carotid manipulation, (2) unilateral EF insertion or (3) potentially ipsilateral intracranial rupture. They may thus be more confidentally used for post-SAH ex vivo cerebral vessel study--acute or delayed.
Marshman
Laurence A G
LA
Department of Neurosurgery, King's College Hospital, SE5 9RS, London, UK. l.a.g.marshman@btinternet.com
D000208:Acute Disease; D000818:Animals; D001794:Blood Pressure; D002560:Cerebrovascular Circulation / Q000502:physiology; D004195:Disease Models, Animal; D008297:Male; D020768:Middle Cerebral Artery / Q000503:physiopathology; D009213:Myography; D051381:Rats; D017208:Rats, Wistar; D013345:Subarachnoid Hemorrhage / Q000503:physiopathology*; D014661:Vasoconstriction / Q000502:physiology; D014664:Vasodilation / Q000502:physiology