title: Adrenaline increases blood-brain-barrier permeability after haemorrhagic cardiac arrest in immature pigs.
abstract: BACKGROUND
  Adrenaline (ADR) and vasopressin (VAS) are used as vasopressors during cardiopulmonary resuscitation. Data regarding their effects on blood-brain barrier (BBB) integrity and neuronal damage are lacking. We hypothesised that VAS given during cardiopulmonary resuscitation (CPR) after haemorrhagic circulatory arrest will preserve BBB integrity better than ADR.
  
  
  METHODS
  Twenty-one anaesthetised sexually immature male piglets (with a weight of 24.3 ± 1.3 kg) were bled 35% via femoral artery to a mean arterial blood pressure of 25 mmHg in the period of 15 min. Afterwards, the piglets were subjected to 8 min of untreated ventricular fibrillation followed by 15 min of open-chest CPR. At 9 min of circulatory arrest, piglets received amiodarone 1.0 mg/kg and hypertonic-hyperoncotic solution 4 ml/kg infusions for 20 min. At the same time, VAS 0.4 U/kg was given intravenously to the VAS group (n = 9) while the ADR group received ADR 20 μg/kg (n = 12). Internal defibrillation was attempted from 11 min of cardiac arrest to achieve restoration of spontaneous circulation. The experiment was terminated 3 h after resuscitation.
  
  
  RESULTS
  The intracranial pressure (ICP) in the post-resuscitation phase was significantly greater in ADR group than in VAS group. VAS group piglets exhibited a significantly smaller BBB disruption compared with ADR group. Cerebral pressure reactivity index showed that cerebral blood flow autoregulation was also better preserved in VAS group.
  
  
  CONCLUSIONS
  Resuscitation with ADR as compared with VAS after haemorrhagic circulatory arrest increased the ICP and impaired cerebrovascular autoregulation more profoundly, as well as exerted an increased BBB disruption though no significant difference in neuronal injury was observed.
authors.affiliation: Department of Surgical Sciences/Anaesthesiology and Intensive Care, Faculty of Medicine, Uppsala University, Uppsala, Sweden.
authors.forename: E
authors.initials: E
authors.lastname: Semenas
authors.forename: H S
authors.initials: HS
authors.lastname: Sharma
authors.forename: L
authors.initials: L
authors.lastname: Wiklund
mesh_terms: D000638:Amiodarone / Q000494:pharmacology / Q000627:therapeutic use; D000818:Animals; D001812:Blood-Brain Barrier / Q000187:drug effects*; D002199:Capillary Permeability / Q000187:drug effects*; D016887:Cardiopulmonary Resuscitation; D002560:Cerebrovascular Circulation / Q000187:drug effects; D004280:Dobutamine / Q000627:therapeutic use; D004554:Electric Countershock; D004789:Enzyme Activation / Q000187:drug effects; D004837:Epinephrine / Q000494:pharmacology / Q000627:therapeutic use / Q000633:toxicity*; D005440:Fluid Therapy; D006323:Heart Arrest / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy; D006439:Hemodynamics / Q000187:drug effects; D006470:Hemorrhage / Q000150:complications* / Q000503:physiopathology; D007427:Intracranial Pressure / Q000187:drug effects*; D008297:Male; D052248:Nitric Oxide Synthase Type I / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D034421:Sus scrofa / Q000254:growth & development; D013552:Swine; D014667:Vasopressins / Q000627:therapeutic use; D014693:Ventricular Fibrillation / Q000150:complications
chemical_list: D014667:Vasopressins; D004280:Dobutamine; D052248:Nitric Oxide Synthase Type I; D052247:Nitric Oxide Synthase Type II; D000638:Amiodarone; D004837:Epinephrine