title: Myocardial tissue oxygen during coronary artery constriction and hypotension in dogs.
abstract: BACKGROUND
  Sodium nitroprusside (SNP) may decrease myocardial tissue oxygenation in dogs with normal coronary arteries. We compared SNP- with desflurane-induced hypotension on myocardial tissue oxygen and pH in dogs with left anterior descending artery constriction.
  
  
  METHODS
  Twenty-four dogs were anesthetized with 8% desflurane for baseline anesthesia. Catheters were inserted into the femoral artery and vein and the coronary sinus. A flow probe and flow restriction device was placed on the left anterior descending (LAD) artery. A probe that measured myocardial oxygen pressure was inserted into the middle myocardium in the LAD region. Baseline measures were made of LAD artery flow, arterial and coronary sinus blood gases, and myocardial tissue gases. A 30% decrease in blood pressure was induced with SNP with unrestricted LAD flow (n=6) or when LAD artery flow was restricted by 30% from baseline (n=6). In separate dogs, a 30% decrease in blood pressure was produced with 14 +/- 1% desflurane with unrestricted LAD flow (n=6) or with baseline LAD artery flow restricted by 30% (n=6).
  
  
  RESULTS
  During SNP-induced hypotension with no LAD constriction, LAD artery flow and coronary sinus oxygen tension increased but myocardial tissue oxygen tension (PmO2) decreased by 40%. When baseline artery flow was decreased by 30% by LAD constriction, SNP-induced hypotension decreased tissue oxygen pressure by 80%, and ischemic acidosis was produced. During unrestricted LAD artery flow or with a 30% flow restriction, desflurane-induced hypotension produced no significant change from baseline myocardial tissue oxygen tension or pH.
  
  
  CONCLUSIONS
  During coronary artery constriction, desflurane-induced hypotension maintained myocardial tissue oxygenation and pH better than did SNP-induced hypotension. The divergence between tissue and coronary sinus oxygen tension during SNP suggests that arteriovenous shunting may occur.
authors.affiliation: Department of Anesthesiology, University of Illinois at Chicago and West Side Veterans Administration, Chicago, IL, USA. whoffman@uic.edu
authors.forename: William E
authors.initials: WE
authors.lastname: Hoffman
authors.forename: R F
authors.initials: RF
authors.lastname: Albrecht
authors.forename: Z S
authors.initials: ZS
authors.lastname: Jonjev
mesh_terms: D018685:Anesthetics, Inhalation / Q000494:pharmacology*; D000818:Animals; D001784:Blood Gas Analysis; D001794:Blood Pressure / Q000502:physiology; D023921:Coronary Stenosis; D000077335:Desflurane; D004285:Dogs; D006339:Heart Rate / Q000187:drug effects; D007022:Hypotension / Q000139:chemically induced* / Q000473:pathology*; D007530:Isoflurane / Q000031:analogs & derivatives / Q000494:pharmacology*; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D009599:Nitroprusside / Q000494:pharmacology*; D010100:Oxygen / Q000502:physiology*; D010101:Oxygen Consumption / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D018685:Anesthetics, Inhalation; D014665:Vasodilator Agents; D009599:Nitroprusside; D000077335:Desflurane; D007530:Isoflurane; D010100:Oxygen