title: Vasospasm in monkeys resolves because of loss of and encasement of subarachnoid blood clot.
abstract: OBJECTIVE
  We studied in monkeys why vasospasm resolves after subarachnoid hemorrhage (SAH).
  
  
  METHODS
  Monkeys underwent angiography and right (n=17) or bilateral (n=8) SAH. Animals with bilateral SAH underwent angiography 1, 3, 5, and 7 days later. Animals with right SAH underwent angiography 7 days later. The clot was then not removed (n=5), removed and replaced with fresh clot (n=7), or removed and not replaced (n=5). At the same time on day 7, the removed clot (n=12) or fresh clot (n=5) was placed on the left side. Angiography was repeated every 2 days until day 14.
  
  
  RESULTS
  SAH caused significant vasospasm on day 7 that resolved by day 14. Removal of clot on day 7 resulted in more rapid resolution of vasospasm. Placement of fresh clot onto arteries that had already been exposed to clot for 7 days produced vasospasm that persisted without resolving for an additional 7 days. Placement of 7-day-old clot from the right onto previously unexposed left arteries or of clot from blood removed from an animal 7 days after SAH caused significantly more rapid onset of vasospasm compared with de novo vasospasm. Microscopic examination of the clots showed they were surrounded by macrophages 7 days after SAH. Arterial compliance and contractility were reduced in relation to duration of the exposure of arteries to clot.
  
  
  CONCLUSIONS
  Vasospasm resolves because of loss of subarachnoid blood clot. We hypothesize that reduced spasmogen release from the clot contributes to resolution of vasospasm. There was no response in the cerebral arteries that rendered them less responsive to the subarachnoid clot.
authors.affiliation: Section of Neurosurgery, Department of Surgery, Pritzker School of Medicine, University of Chicago Medical Center, Chicago, Illinois, USA.
authors.forename: Z D
authors.initials: ZD
authors.lastname: Zhang
authors.forename: B
authors.initials: B
authors.lastname: Yamini
authors.forename: T
authors.initials: T
authors.lastname: Komuro
authors.forename: S
authors.initials: S
authors.lastname: Ono
authors.forename: L
authors.initials: L
authors.lastname: Johns
authors.forename: L S
authors.initials: LS
authors.lastname: Marton
authors.forename: B
authors.initials: B
authors.lastname: Weir
authors.forename: R L
authors.initials: RL
authors.lastname: Macdonald
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001488:Basilar Artery / Q000187:drug effects; D002533:Cerebral Angiography; D004195:Disease Models, Animal; D018450:Disease Progression; D006454:Hemoglobins / Q000032:analysis; D066298:In Vitro Techniques; D008252:Macaca fascicularis; D020768:Middle Cerebral Artery / Q000000981:diagnostic imaging / Q000187:drug effects / Q000503:physiopathology; D011189:Potassium Chloride / Q000494:pharmacology; D012075:Remission, Spontaneous; D013345:Subarachnoid Hemorrhage / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D013346:Subarachnoid Space / Q000473:pathology; D013927:Thrombosis / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D014654:Vascular Patency; D014661:Vasoconstriction / Q000187:drug effects; D020301:Vasospasm, Intracranial / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*
chemical_list: D006454:Hemoglobins; D011189:Potassium Chloride