title: Norepinephrine-induced hypertension dilates vasospastic basilar artery after subarachnoid haemorrhage in rabbits.
abstract: BACKGROUND
  Vasopressor-induced hypertension is routinely indicated for prevention and treatment of cerebral vasospasm (CVS) after subarachnoid haemorrhage (SAH). Mechanisms underlying patients' clinical improvement during vasopressor-induced hypertension remain incompletely understood. The aim of this study was to evaluate angiographic effects of normovolaemic Norepinephrine (NE)-induced hypertension therapy on the rabbit basilar artery (BA) after SAH.
  
  
  METHODS
  Cerebral vasospasm was induced using the one-haemorrhage rabbit model; sham-operated animals served as controls. Five days later the animals underwent follow-up angiography prior to and during NE-induced hypertension. Changes in diameter of the BA were digitally calculated in mean microm +/- SEM (standard error of mean).
  
  
  RESULTS
  Significant CVS of 14.2% was documented in the BA of the SAH animals on day 5 compared to the baseline angiogram on day 0 (n = 12, p < 0.01), whereas the BA of the control animals remained statistically unchanged (n = 12, p > 0.05). During systemic administration of NE, mean arterial pressure increased from 70.0 +/- 1.9 mmHg to 136.0 +/- 2.1 mmHg in the SAH group (n = 12, p < 0.001) and from 72.0 +/- 3.1 to 137.8 +/- 1.3 in the control group (n = 12, p < 0.001). On day 5 after SAH, a significant dilatation of the BA in response to norepinephrine could be demonstrated in both groups. The diameter of the BA in the SAH group increased from 640.5 +/- 17.5 microm to 722.5 +/- 23.7 microm (n = 12, p < 0.05; ). In the control group the diameter increased from 716.8 +/- 15.5 microm to 779.9 +/- 24.1 microm (n = 12, p < 0.05).
  
  
  CONCLUSIONS
  This study demonstrated that NE-induced hypertension causes angiographic dilatation of the BA in the SAH rabbit model. Based on these observations, it can be hypothesised that clinical improvement during vasopressor-induced hypertension therapy after SAH might be explained with cerebral vasodilatation mechanisms that lead to improvement of cerebral blood flow.
authors.affiliation: Department of Intensive Care Medicine, Bern University Hospital and University of Bern, Bern, Switzerland.
authors.forename: Volker
authors.initials: V
authors.lastname: Neuschmelting
authors.forename: Ali-Reza
authors.initials: AR
authors.lastname: Fathi
authors.forename: Eveline Teresa
authors.initials: ET
authors.lastname: Hidalgo Staub
authors.forename: Serge
authors.initials: S
authors.lastname: Marbacher
authors.forename: Gerhard
authors.initials: G
authors.lastname: Schroth
authors.forename: Jukka
authors.initials: J
authors.lastname: Takala
authors.forename: Stephan M
authors.initials: SM
authors.lastname: Jakob
authors.forename: Javier
authors.initials: J
authors.lastname: Fandino