title: Sodium nitroprusside-induced, but not desflurane-induced, hypotension decreases myocardial tissue oxygenation in dogs anesthetized with 8% desflurane.
abstract: OBJECTIVE
  To compare sodium nitroprusside (SNP)-induced hypotension with desflurane-induced hypotension for the effects on myocardial blood flow and tissue oxygenation in dogs.
  
  
  METHODS
  Prospective, randomized, crossover, nonblinded.
  
  
  METHODS
  University teaching hospital.
  
  
  METHODS
  Male nonpurpose-bred hounds (n = 8).
  
  
  METHODS
  Dogs were anesthetized with 8% desflurane. Catheters were inserted into the femoral artery and coronary sinus. A flow probe was placed in the left anterior descending (LAD) branch of the coronary artery. A sensor that measured myocardial oxygen pressure (PmO(2)) was inserted into the myocardium of the left ventricle. Myocardial oxygen consumption (MVO(2)) was calculated as LAD flow x arterial - coronary sinus oxygen content.
  
  
  RESULTS
  Measurements were made at baseline blood pressure levels of 99 mmHg (measure 1), during hypotension to 62 to 66 mmHg using intravenous SNP or 14% desflurane (measure 2), and during SNP or 14% desflurane with blood pressure support using phenylephrine (measure 3). Each dog randomly received both hypotensive treatments, separated by 1 hour. Baseline measures were PmO(2) = 46 +/- 9 mmHg, LAD flow = 43 +/- 11 mL/min, and MVO(2) = 2.47 +/- 0.73 mL O(2)/min. During hypotension induced with SNP, PmO(2) decreased 30% (p < 0.05), LAD flow increased 40% (p < 0.05), and MVO(2) did not change. During hypotension induced with 14% desflurane, PmO(2) did not change, and LAD flow and MVO(2) decreased 25% and 40% (p < 0.05). Blood pressure support with phenylephrine increased LAD flow and MVO(2) but did not change PmO(2) during SNP or 14% desflurane treatment.
  
  
  CONCLUSIONS
  SNP-induced hypotension produced myocardial vasodilation, but tissue oxygenation was impaired. PmO(2) was maintained during desflurane-induced hypotension.
authors.affiliation: Departments of Anesthesiology and Physiology, University of Illinois at Chicago, Chicago, IL60612, USA. whoffman@uic.edu
authors.forename: William E
authors.initials: WE
authors.lastname: Hoffman
authors.forename: Ronald F
authors.initials: RF
authors.lastname: Albrecht
authors.forename: Zivojin S
authors.initials: ZS
authors.lastname: Jonjev
mesh_terms: D000758:Anesthesia; D018685:Anesthetics, Inhalation / Q000494:pharmacology*; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects; D002245:Carbon Dioxide / Q000097:blood; D003326:Coronary Circulation / Q000187:drug effects; D000077335:Desflurane; D004285:Dogs; D006339:Heart Rate / Q000187:drug effects; D007022:Hypotension / Q000139:chemically induced / Q000378:metabolism*; D007530:Isoflurane / Q000031:analogs & derivatives* / Q000494:pharmacology*; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D009599:Nitroprusside / Q000494:pharmacology*; D010100:Oxygen / Q000097:blood / Q000378:metabolism*; D014664:Vasodilation / Q000187:drug effects
chemical_list: D018685:Anesthetics, Inhalation; D000959:Antihypertensive Agents; D002245:Carbon Dioxide; D009599:Nitroprusside; D000077335:Desflurane; D007530:Isoflurane; D010100:Oxygen