title: Interaction of metabolic and respiratory acidosis with α and β-adrenoceptor stimulation in rat myocardium.
abstract: BACKGROUND
  The effects of acute respiratory versus metabolic acidosis on the myocardium and their consequences on adrenoceptor stimulation remain poorly described. We compared the effects of metabolic and respiratory acidosis on inotropy and lusitropy in rat myocardium and their effects on the responses to α- and β-adrenoceptor stimulations.
  
  
  METHODS
  The effects of acute respiratory and metabolic acidosis (pH 7.10) and their interactions with α and β-adrenoceptor stimulations were studied in isolated rat left ventricular papillary muscle (n=8 per group). Intracellular pH was measured using confocal microscopy and a pH-sensitive fluorophore in isolated rat cardiomyocytes. Data are mean percentages of baseline±SD.
  
  
  RESULTS
  Respiratory acidosis induced more pronounced negative inotropic effects than metabolic acidosis did both in isotonic (45±3 versus 63±6%, P<0.001) and isometric (44±5 versus 64±3%, P<0.001) conditions concomitant with a greater decrease in intracellular pH (6.85±0.07 versus 7.12±0.07, P<0.001). The response to α-adrenergic stimulation was not modified by respiratory or metabolic acidosis. The inotropic response to β-adrenergic stimulation was impaired only in metabolic acidosis (137±12 versus 200±33%, P<0.001), but this effect was not observed with administration of forskolin or dibutiryl-cyclic adenosine monophosphate. This effect might be explained by a change in transmembrane pH gradient only observed with metabolic acidosis. The lusitropic response to β-adrenergic stimulation was not modified by respiratory or metabolic acidosis.
  
  
  CONCLUSIONS
  Acute metabolic and respiratory acidosis induce different myocardial effects related to different decreases in intracellular pH. Only metabolic acidosis impairs the positive inotropic effect of β-adrenergic stimulation.
authors.affiliation: Université Victor Segalen, Emergency Department, Hôpital Pellegrin, Bordeaux, France.
authors.forename: Matthieu
authors.initials: M
authors.lastname: Biais
authors.forename: Romain
authors.initials: R
authors.lastname: Jouffroy
authors.forename: Aude
authors.initials: A
authors.lastname: Carillion
authors.forename: Sarah
authors.initials: S
authors.lastname: Feldman
authors.forename: Aude
authors.initials: A
authors.lastname: Jobart-Malfait
authors.forename: Bruno
authors.initials: B
authors.lastname: Riou
authors.forename: Julien
authors.initials: J
authors.lastname: Amour
mesh_terms: D000138:Acidosis / Q000378:metabolism*; D000142:Acidosis, Respiratory / Q000378:metabolism; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D004305:Dose-Response Relationship, Drug; D007424:Intracellular Fluid / Q000378:metabolism; D008297:Male; D009206:Myocardium; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism*; D009924:Organ Culture Techniques; D010210:Papillary Muscles / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011942:Receptors, Adrenergic, alpha / Q000378:metabolism*; D011943:Receptors, Adrenergic, beta / Q000378:metabolism*
chemical_list: D000316:Adrenergic alpha-Agonists; D000318:Adrenergic beta-Agonists; D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta