Key result
In dogs with critical coronary stenosis, the addition of N2O to fentanyl or sufentanil rapidly produced myocardial dysfunction with significant postsystolic shortening in the stenotic territory.
Why the study?
Does the addition of nitrous oxide to narcotic anesthesia cause regional ventricular dysfunction in the presence of critical coronary stenosis in a canine model?
Population
16 dogs with left ventricular myocardium supplied by a critically narrowed and a normal coronary artery
Comparison
Addition of nitrous oxide to narcotic anesthesia… vs Narcotic anesthesia with O2:N2 during critical…
Design
Preclinical
Authors
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May warrant caution with N2O in narcotic-anesthetized coronary stenosis; leaves open translation from this canine model.
Does the addition of nitrous oxide to narcotic anesthesia cause regional ventricular dysfunction in the presence of critical coronary stenosis in a canine model?
In a canine model of critical coronary stenosis, adding nitrous oxide to narcotic anesthesia induces regional myocardial dysfunction without altering systemic hemodynamics or coronary flow.
Philbin et al. (1985) studied Critical coronary artery stenosis (animal model) (n=16). Nitrous oxide (N2O) added to fentanyl or sufentanil vs. Fentanyl or sufentanil without N2O (O2:N2) was evaluated on Regional ventricular function (postsystolic shortening). In dogs with critical coronary stenosis, the addition of N2O to fentanyl or sufentanil rapidly produced myocardial dysfunction with significant postsystolic shortening in the stenotic territory.
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