title: [Propranolol protects the myocardium and prevents arterial hypotension in an experimental organ donation model].
abstract: OBJECTIVE
  To analyze the role that sympathetic nervous system hyperactivity immediately following brain death plays in the cardiovascular dysfunction of an organ donor.
  
  
  METHODS
  Fifteen New Zealand white rabbits were placed in three groups: a control group, a brain-death group without propranolol and a brain-death group with propranolol. Brain death was caused by severe intracranial hypertension; in the third group propranolol was first perfused intravenously. We recorded hemodynamic (heart rate, number of extrasystoles, central venous pressure, systemic and pulmonary arterial pressure), biochemical (adrenaline, noradrenaline, dopamine and troponin T) and histologic data.
  
  
  RESULTS
  Catecholamine levels rose significantly in both experimental groups after brain death, which coincided with clinical signs of sympathetic hyperactivity in the group not receiving propranolol but not in the group receiving the beta-blocker. The myocardium of animals not receiving the beta-blocker showed myocytolysis, edema, subendocardial bleeding and leukocyte infiltration. Such changes were practically absent in the animals that received beta-blockers. In the beta-blocker group, serum troponin, and index of myocytolysis, rose significantly less than in the non-premedicated group. Blood pressure in all the brain-dead animals was significantly lower than in the control group, but was more severe in animals that had not received propranolol.
  
  
  CONCLUSIONS
  Sympathetic nervous system hyperactivity after brain death affects the histology and functioning of the myocardium in this experimental organ donor model. Pretreatment with propranolol prevents damage.
authors.affiliation: Servicio de Anestesiología y Reanimación, Hospital Universitario Virgen del Rocío, Sevilla.
authors.forename: R
authors.initials: R
authors.lastname: Ojeda Rivero
authors.forename: J
authors.initials: J
authors.lastname: Cerro Sánchez
authors.forename: A
authors.initials: A
authors.lastname: Ordóñez Fernández
authors.forename: J M
authors.initials: JM
authors.lastname: Domínguez Roldán
authors.forename: A
authors.initials: A
authors.lastname: Hernández Fernández
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology* / Q000627:therapeutic use; D000818:Animals; D015415:Biomarkers; D001926:Brain Death / Q000503:physiopathology*; D002395:Catecholamines / Q000097:blood; D002404:Catheterization; D003399:Craniotomy; D006439:Hemodynamics / Q000187:drug effects*; D007022:Hypotension / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D019586:Intracranial Hypertension / Q000150:complications / Q000503:physiopathology*; D017202:Myocardial Ischemia / Q000517:prevention & control*; D009206:Myocardium / Q000473:pathology*; D011180:Postmortem Changes; D011433:Propranolol / Q000494:pharmacology* / Q000627:therapeutic use; D011817:Rabbits; D012021:Reflex, Abnormal; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000503:physiopathology*; D013997:Time Factors; D009927:Tissue and Organ Procurement; D019210:Troponin I / Q000097:blood
chemical_list: D000319:Adrenergic beta-Antagonists; D015415:Biomarkers; D002395:Catecholamines; D019210:Troponin I; D011433:Propranolol