title: Preoperative high dose methylprednisolone attenuates the cerebral response to deep hypothermic circulatory arrest.
abstract: OBJECTIVE
  The aim of this study was to assess the effects of preoperative high dose methylprednisolone on cerebral recovery following a period of deep hypothermic circulatory arrest (DHCA).
  
  
  METHODS
  Sixteen 1-week-old piglets were randomized to placebo (n=8), or 30 mg/kg intramuscular methylprednisolone sodium succinate (MPRED) given at 8 and 2 h before induction of anaesthesia. All piglets underwent cardiopulmonary bypass, cooling to 18 degrees C, 60 min of circulatory arrest followed by 60 min of reperfusion and rewarming. The radiolabelled microsphere method was used to determine the global and regional cerebral blood flow (CBF) and cerebral oxygen metabolism (CMRO(2)) at baseline before DHCA and after 60 min of reperfusion.
  
  
  RESULTS
  In controls, mean global CBF (+/-1 standard error) before DHCA was 53.7+/-2.4 ml/100 g per min and fell to 23.8+/-1.2 ml/100 g per min following DHCA (P<0.0001). This represents a post-DHCA recovery to 45.1+/-3.3% of the pre-DHCA value. In the MPRED group recovery of global CBF post-DHCA was significantly higher at 63.6+/-5.2% of the pre-DHCA value (P=0.009). The regional recovery of CBF in the cerebellum, brainstem and basal ganglia was 80, 75 and 69% of pre-DHCA values in the MPRED group respectively compared to 66, 60 and 55% in controls (P<0.05). Global CMRO(2) in controls fell from 3.9+/-0.2 ml/100 g per min before to 2. 3+/-0.2 ml/100 g per min after DHCA (P=0.0001). This represents a post-DHCA recovery to 58.6+/-4.4% of the pre-DHCA value. In the MPRED group, however, recovery of global CMRO(2) post-DHCA was significantly higher at 77.9+/-7.1% of the pre-DHCA value (P=0.04).
  
  
  CONCLUSIONS
  Treatment with high dose methylprednisolone at 8 and 2 h preoperatively attenuates the normal cerebral response to a period of deep hypothermic ischaemia. This technique may therefore offer a safe and inexpensive strategy for cerebral protection during repair of congenital heart defects with the use of DHCA.
authors.affiliation: Department of Pediatric Cardiac Surgery, Duke University Medical Center, Durham, NC, USA. stephenlangley@dial.pipex.com
authors.forename: S M
authors.initials: SM
authors.lastname: Langley
authors.forename: P J
authors.initials: PJ
authors.lastname: Chai
authors.forename: J J
authors.initials: JJ
authors.lastname: Jaggers
authors.forename: R M
authors.initials: RM
authors.lastname: Ungerleider
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism; D002545:Brain Ischemia / Q000517:prevention & control*; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D005938:Glucocorticoids / Q000008:administration & dosage / Q000494:pharmacology*; D006324:Heart Arrest, Induced; D006330:Heart Defects, Congenital / Q000601:surgery; D007036:Hypothermia, Induced; D008775:Methylprednisolone / Q000008:administration & dosage / Q000494:pharmacology*; D010100:Oxygen / Q000378:metabolism; D013552:Swine
chemical_list: D005938:Glucocorticoids; D010100:Oxygen; D008775:Methylprednisolone