Anesth Analg 1992; 75:539-548
© 1992 International Anesthesia Research Society
Nitrous Oxide Impairs Functional Recovery of Stunned Myocardium in Barbiturate-Anesthetized, Acutely Instrumented Dogs
Daniel Siker, MD,
Paul S. Pagel, MD,
Lorie R. Pelc, PhD,
John P. Kampine, MD, PhD,
William T. Schmeling, MD, PhD, and
David C. Warltier, MD, PhD
Departments of Anesthesiology, Pharmacology, and Medicine, Medical College of Wisconsin; Zablocki Veterans Administration Medical Center; and Children's Hospital of Wisconsin, Milwaukee, Wisconsin
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 < 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 < 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 > 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 postishemic, reperfused myocardium compared with 70% nitrogen in open-chest, acutely instrumented dogs.
This article has been cited by other articles:

|
 |

|
 |
 
R. Schulz, M. Kelm, and G. Heusch
Nitric oxide in myocardial ischemia/reperfusion injury
Cardiovasc Res,
February 15, 2004;
61(3):
402 - 413.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
M. Zaugg, E. Lucchinetti, M. Uecker, T. Pasch, and M. C. Schaub
Anaesthetics and cardiac preconditioning. Part I. Signalling and cytoprotective mechanisms
Br. J. Anaesth.,
October 1, 2003;
91(4):
551 - 565.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
K. Y. Yoo, S. T. Jeong, I. H. Ha, and J. Lee
Nitrous Oxide Attenuates Pressor but Augments Norepinephrine Response to Laryngoscopy and Endotracheal Intubation
Anesth. Analg.,
May 1, 2003;
96(5):
1516 - 1521.
[Abstract]
[Full Text]
[PDF]
|
 |
|
|