Complement depletion does not reduce brain injury in a rabbit model of thromboembolic stroke. Brain Res Bull 1999 Feb;48(3):325-31
Date
05/06/1999Pubmed ID
10229342DOI
10.1016/s0361-9230(99)00004-0Scopus ID
2-s2.0-0032948941 (requires institutional sign-in at Scopus site) 33 CitationsAbstract
The contribution of the complement system to cerebral ischemic and ischemia/reperfusion injury was examined in a rabbit model of thromboembolic stroke by delivery of an autologous clot embolus to the intracranial circulation via the internal carotid artery. A two-by-two factorial design was employed to study the impact of complement depletion via pretreatment with cobra venom factor (CVF, 100 U/kg i.v.) in the setting of permanent (without tissue plasminogen activator; t-PA) and transient (with t-PA) cerebral ischemia. Thirty-two New Zealand white rabbits were assigned to one of four groups (n=8, each group): control without t-PA, control with t-PA, CVF without t-PA and CVF with t-PA. In the complement intact animals, t-PA administration resulted in an approximate 30% reduction in infarct size when compared to the group not receiving t-PA (20.4+/-6.6% of hemisphere area vs. 30.1+/-7.2%; mean+/-SEM). However, infarct sizes in the complement depleted rabbits, with (30.7+/-8.2%) or without (30.2+/-7.9%) t-PA, were no different from the control group receiving no therapy. Similarly, no difference in regional cerebral blood flow or final intracranial pressure values was noted between any of the four groups. Complement activation does not appear to be a primary contributor to brain injury in acute thromboembolic stroke.
Author List
Lew SM, Gross CE, Bednar MM, Russell SJ, Fuller SP, Ellenberger CL, Howard DAuthor
Sean Lew MD Chief, Professor in the Neurosurgery department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsBrain
Brain Ischemia
Cerebrovascular Circulation
Cerebrovascular Disorders
Complement C3-C5 Convertases
Complement Inactivator Proteins
Complement System Proteins
Disease Models, Animal
Elapid Venoms
Female
Fibrinolytic Agents
Intracranial Embolism and Thrombosis
Male
Neutrophils
Rabbits
Reperfusion Injury
Tissue Plasminogen Activator
