title: Hypercapnic acidosis preserves gastric mucosal microvascular oxygen saturation in a canine model of hemorrhage.
abstract: The authors aimed to clarify the effects of hypercapnic acidosis and its timing on gastric mucosal oxygenation in a canine model of hemorrhage. This was designed as a prospective, controlled, randomized animal study set in a university research laboratory. Five chronically instrumented dogs were used. Dogs were repeatedly anesthetized (sevoflurane 1.5 MAC), mechanically ventilated, and randomized to each of the following protocols. In a control series (CON), animals underwent hemorrhage during normoventilation (etCO2, 35 mmHg). In a second series, hypercapnia (etCO2, 70 mmHg) was applied before onset of hemorrhage (prophylactic hypercapnia), whereas in the third series, hypercapnia was applied after hemorrhage (therapeutic hypercapnia, THE). Microvascular oxygenation (μHbO2) of the gastric mucosa was continuously assessed by tissue reflectance spectrophotometry. Cardiac output was continuously measured, and oxygen delivery (DO2) was intermittently calculated. In CON, hemorrhage decreased DO2 (from 11 ± 3 mL·kg⁻¹·min⁻¹ to 8 ± 2 mL·kg⁻¹·min⁻¹ and 8 ± 2 mL·kg⁻¹·min⁻¹ after 30 and 75 min, respectively) and μHbO2 (from 57% ± 4% to 43% ± 11% and 50% ± 11%). Prophylactic hypercapnia attenuated the effects of hemorrhage on DO2 (12 ± 2 mL·kg⁻¹·min⁻¹ to 10 ± 2 mL·kg⁻¹·min⁻¹ and 11 ± 2 mL·kg⁻¹·min⁻¹) and preserved μHbO2 (52% ± 3% to 47% ± 5% and 57% ± 3%). Initial effects of hemorrhage in THE were comparable to CON (DO2 from 11 ± 2 mL·kg⁻¹·min⁻¹ to 8 ± 1 mL·kg⁻¹·min⁻¹; μHbO2 from 56% ± 7% to 43% ± 9%), but after application of hypercapnic acidosis, baseline levels were restored (DO2 10 ± 3 mL·kg⁻¹·min⁻¹; μHbO2 52% ± 14%). Hypercapnic acidosis applied before or after hemorrhage (THE) preserves microvascular mucosal oxygenation. If these experimental findings may be transferred to the clinical setting, deliberate hypercapnic acidosis could serve to augment oxygenation of the splanchnic region in states of compromised circulation, e.g., hemorrhage.
authors.affiliation: Department of Anaesthesiology, University Hospital Duesseldorf, Duesseldorf, Germany. ingo.schwartges@med.uni-duesseldorf.de
authors.forename: Ingo
authors.initials: I
authors.lastname: Schwartges
authors.forename: Olaf
authors.initials: O
authors.lastname: Picker
authors.forename: Christopher
authors.initials: C
authors.lastname: Beck
authors.forename: Thomas W L
authors.initials: TW
authors.lastname: Scheeren
authors.forename: Lothar A
authors.initials: LA
authors.lastname: Schwarte
mesh_terms: D000142:Acidosis, Respiratory / Q000503:physiopathology*; D000818:Animals; D004285:Dogs; D005260:Female; D005753:Gastric Mucosa / Q000098:blood supply*; D006935:Hypercapnia / Q000503:physiopathology*; D008297:Male; D008833:Microcirculation / Q000502:physiology; D010100:Oxygen / Q000378:metabolism*; D011897:Random Allocation; D012771:Shock, Hemorrhagic / Q000503:physiopathology
chemical_list: D010100:Oxygen