title: Histamine-2-receptor blockade does not affect hyperemia after cerebral ischemia in young swine.
abstract: OBJECTIVE
  To determine whether histamine-2 (H2) receptor antagonists can blunt the increase in cerebral blood flow after cerebral ischemia.
  
  
  METHODS
  Prospective, randomized trial.
  
  
  METHODS
  Animal laboratory.
  
  
  METHODS
  Piglets aged 1 to 2 wks.
  
  
  METHODS
  Three groups of piglets were anesthetized with pentobarbital, mechanically ventilated, and hemodynamically monitored. Each animal was randomized to receive one of three treatments 20 mins before ischemia: famotidine (0.6 mg/kg i.v.), cimetidine (5 mg/kg i.v.), or an equivalent volume of saline (3 mL). Ischemia was maintained for 15 mins by tightening ligatures around the brachiocephalic trunk and left subclavian arteries plus the induction of hemorrhagic hypotension (50 mm Hg). Reperfusion was initiated by the reinfusion of shed blood and removal of the ligatures.
  
  
  RESULTS
  The three groups were not different with regard to baseline arterial blood gases, cerebral perfusion pressure, microsphere-determined cerebral blood flow, or oxygen consumption (VO2). Ischemia (cerebral blood flow < 5 mL/min/100 g of tissue) was demonstrated in all brain regions for all groups during arterial ligation with hemorrhage-induced hypotension. Blood flow rates were increased compared with preischemic values in all regions at 7 mins of reperfusion. For example, mean forebrain blood flow rates increased from 36 +/- 3 to 95 +/- 14 (SEM) mL/min/100 g of tissue in the group receiving saline, from 36 +/- 3 to 102 +/- 9 mL/min/100 g of tissue in the group receiving famotidine, and from 31 +/- 4 to 119 +/- 26 mL/min/100 g in the group receiving cimetidine. Overall, the three groups did not differ in regard to blood flow rates and cerebral VO2 values during ischemia and at 30 mins of reperfusion.
  
  
  CONCLUSIONS
  We demonstrated that famotidine or cimetidine as compared with saline did not affect the pattern or extent of hyperemia after ischemia. This finding does not support the hypothesis that a H2-receptor mechanism is necessary for postischemic hyperemia.
authors.affiliation: Department of Anesthesiology/Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, MD.
authors.forename: W S
authors.initials: WS
authors.lastname: Tung
authors.forename: M A
authors.initials: MA
authors.lastname: Helfaer
authors.forename: J R
authors.initials: JR
authors.lastname: Kirsch
authors.forename: R J
authors.initials: RJ
authors.lastname: Traystman
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000150:complications*; D002560:Cerebrovascular Circulation; D002927:Cimetidine / Q000627:therapeutic use*; D015738:Famotidine / Q000627:therapeutic use*; D006940:Hyperemia / Q000209:etiology / Q000517:prevention & control*; D007427:Intracranial Pressure; D008863:Microspheres; D010101:Oxygen Consumption; D011446:Prospective Studies; D011659:Pulmonary Gas Exchange; D011897:Random Allocation; D013552:Swine
chemical_list: D015738:Famotidine; D002927:Cimetidine