title: Effects of arterial hypoxia and beta-adrenoceptor blockade on cerebral blood flow and oxygen uptake following E. coli endotoxin in dogs.
abstract: Earlier studies in normoxia have shown that an endotoxin injection in dogs leads to an increase in cerebral metabolic rate of oxygen (CMRo2), a decrease in cerebral blood flow (CBF) and increased concentrations of monoamines in blood and cerebrospinal fluid (CSF). In animals pretreated with propranolol (PPL) the CMRo2 increase was abolished and thus beta-adrenoceptor mediated. Arterial hypoxia normally increases CBF without any influence on CMRo2. The aim of this study was to investigate the effects of moderate arterial hypoxia on CBF, CMRo2 and catecholamine concentrations in blood and CSF after endotoxin with and without pretreatment with PPL. Three groups of dogs were studied. Group 1: Six animals were subjected to arterial hypoxia without any other intervention. Group 2: Six animals were given an endotoxin injection (E. coli lipopolysaccharide O 111: B 4), before the induction of hypoxia. Group 3: Eight animals were pretreated with PPL per os, 12.5 mg.kg-1 twice a day for one week before the experiments, and the effects of arterial hypoxia were studied both before and after an intravenous injection of endotoxin. Two levels of hypoxia were studied; oxygen saturation in arterial blood aiming at 75 and 50%. Endotoxin was given intravenously in a dose of 1 mg.kg-1 bodyweight over a 5 minute period. After an endotoxin injection, the response to arterial hypoxia was an increase in CMRo2, in contrast to the unchanged CMRo2 without endotoxin. After pretreatment with PPL the increase in CMRo2 after endotoxin was prevented. The CBF reaction to hypoxia was uniformly an increase.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Anaesthesiology, Sahlgren's Hospital, University of Göteborg, Sweden.
authors.forename: A
authors.initials: A
authors.lastname: Westerlind
authors.forename: L E
authors.initials: LE
authors.lastname: Larsson
authors.forename: J
authors.initials: J
authors.lastname: Häggendal
authors.forename: B
authors.initials: B
authors.lastname: Ekstr om-Jodal
mesh_terms: D000818:Animals; D001812:Blood-Brain Barrier / Q000187:drug effects; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D004285:Dogs; D004731:Endotoxins / Q000009:adverse effects*; D004837:Epinephrine / Q000097:blood / Q000134:cerebrospinal fluid / Q000378:metabolism; D004926:Escherichia coli; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000097:blood / Q000503:physiopathology*; D008070:Lipopolysaccharides / Q000009:adverse effects*; D009638:Norepinephrine / Q000097:blood / Q000134:cerebrospinal fluid / Q000378:metabolism; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption / Q000187:drug effects*; D011433:Propranolol / Q000097:blood / Q000494:pharmacology*; D011943:Receptors, Adrenergic, beta / Q000187:drug effects
chemical_list: D004731:Endotoxins; D008070:Lipopolysaccharides; D011943:Receptors, Adrenergic, beta; C044101:endotoxin, Escherichia coli; D011433:Propranolol; D010100:Oxygen; D009638:Norepinephrine; D004837:Epinephrine