title: Nitrous oxide impairs functional recovery of stunned myocardium in barbiturate-anesthetized, acutely instrumented dogs.
abstract: The purpose of this investigation was to characterize the effects of nitrous oxide or nitrogen (70%) on systemic and regional hemodynamics and myocardial tissue perfusion after a brief coronary artery occlusion (15 min) and reperfusion (3 h). Two groups of experiments (14 experiments total) were completed with 24 open-chest, barbiturate-anesthetized dogs. Coronary collateral blood flow was diverted from the ischemic zone during coronary artery occlusion to eliminate a source of variability in degree of ischemia produced by differences in degrees of collateral blood flow among animals. Seven of 16 dogs treated with nitrous oxide and 7 of 8 dogs treated with nitrogen survived coronary occlusion and reperfusion (P less than 0.05). Coronary artery occlusion produced paradoxical systolic bulging in the ischemic zone in both groups of experiments. After reperfusion, segment shortening gradually returned toward control levels but remained depressed from the preocclusion state after 3 h in the nitrogen-treated control group. Similar results were observed after reperfusion in the nitrous oxide group; however, segment function in the ischemic region was significantly (P less than 0.05) depressed throughout the 3-h reperfusion period compared with the control group. Transmural coronary collateral blood flow during occlusion was not significantly different (P greater than 0.05) between groups, indicating that differences in recovery of contractile function observed between groups could not be attributed to differences in myocardial oxygen supply. In addition, the similarity in systemic hemodynamics between the nitrous oxide and control groups indirectly suggests that differences in recovery of function could not be attributed to differences in myocardial oxygen demand. The results indicate that 70% nitrous oxide produces greater mortality after coronary artery occlusion and reperfusion and reduces functional recovery of post-ischemic, reperfused myocardium compared with 70% nitrogen in open-chest, acutely instrumented dogs.
authors.affiliation: Department of Anesthesiology, Medical College of Wisconsin, Milwaukee.
authors.forename: D
authors.initials: D
authors.lastname: Siker
authors.forename: P S
authors.initials: PS
authors.lastname: Pagel
authors.forename: L R
authors.initials: LR
authors.lastname: Pelc
authors.forename: J P
authors.initials: JP
authors.lastname: Kampine
authors.forename: W T
authors.initials: WT
authors.lastname: Schmeling
authors.forename: D C
authors.initials: DC
authors.lastname: Warltier
mesh_terms: D000758:Anesthesia; D000818:Animals; D001463:Barbiturates; D004285:Dogs; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects* / Q000502:physiology; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D009609:Nitrous Oxide / Q000009:adverse effects*
chemical_list: D001463:Barbiturates; D009609:Nitrous Oxide