title: In vivo diaphragm metabolism: comparison of paced and inspiratory resistive loaded breathing in piglets.
abstract: OBJECTIVE
  We hypothesized that spontaneous, loaded diaphragm contractions would lead to diaphragm fatigue, which would correlate with inadequate oxidative metabolism as measured by phosphorus-31 nuclear magnetic resonance spectroscopy.
  
  
  METHODS
  Prospective, randomized, crossover trial.
  
  
  METHODS
  University hospital research laboratory.
  
  
  METHODS
  Eight piglets, 4 to 6 wks of age.
  
  
  METHODS
  Each animal underwent, in random order, a 20-min period of diaphragm pacing and a 45-min period of loaded spontaneous breathing, separated by a 20-min recovery period. Mechanical ventilation was used during diaphragm pacing to maintain a PaCO2 of 35 to 45 torr (4.7 to 6.0 kPa) and a PaO2 of > 100 torr (> 13.3 kPa). During spontaneous breathing, inspiratory loading was achieved with a 2.0-mm inner diameter endotracheal tube in the breathing circuit.
  
  
  RESULTS
  During pacing, mean transdiaphragmatic pressure decreased by 35%, from 23 +/- 5 (SD) to 15 +/- 3 mm Hg (p < .05), and this decrease correlated with a 335% increase in the ratio of inorganic phosphate to phosphocreatine, from 0.23 +/- 0.1 to 1.0 +/- 0.7 (p < .05). During loaded spontaneous breathing, arterial pH decreased from 7.42 +/- 0.06 to 7.25 +/- 0.05 (p < .05), secondary to an increase in PaCO2 from 41 +/- 4 to 65 +/- 11 torr (5.3 +/- 0.5 to 8.7 +/- 1.5 kPa) (p < .05). Despite respiratory acidosis, there was no decrease in trandiaphragmatic pressure during the period of loaded breathing, nor was any change in the ratio of inorganic phosphate to phosphocreatine seen.
  
  
  CONCLUSIONS
  Diaphragm fatigue in a pacing model correlates with inadequate oxidative metabolism. In contrast, severe inspiratory resistive loaded breathing did not result in changes in oxidative metabolism or decreased diaphragm force output, despite hypercapnia and respiratory acidosis.
authors.affiliation: The Department of Anesthesia and Critical Care Medicine, The Johns Hopkins Medical Institutions, Baltimore, MD, USA.
authors.forename: P J
authors.initials: PJ
authors.lastname: Radell
authors.forename: S M
authors.initials: SM
authors.lastname: Eleff
authors.forename: R J
authors.initials: RJ
authors.lastname: Traystman
authors.forename: D G
authors.initials: DG
authors.lastname: Nichols
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003964:Diaphragm / Q000378:metabolism*; D006439:Hemodynamics; D009682:Magnetic Resonance Spectroscopy; D010710:Phosphates / Q000378:metabolism; D010725:Phosphocreatine / Q000378:metabolism; D011312:Pressure; D012119:Respiration; D013552:Swine
chemical_list: D010710:Phosphates; D010725:Phosphocreatine; D000255:Adenosine Triphosphate