NITROUS OXIDE AND THE CORONARY CIRCULATION
Nitrous oxide does not produce direct effects on the coronary
vasculature in vitro.[239]
[500]
[501]
This anesthetic gas
alters coronary blood flow concomitant with changes in MVO2
in dogs.[502]
[503]
Nitrous oxide decreases myocardial segment shortening,[504]
[505]
increases post-systolic shortening,[506]
and redistributes transmural coronary blood flow preferentially to the subepicardium
(i.e., decreased endo/epi)[505]
in experimental
models of coronary artery disease. Nitrous oxide also decreases the recovery of
contractile function of stunned myocardium.[507]
Nitrous oxide-induced sympathetic nervous system activation and imbalances of myocardial
oxygen supply and MVO2
represent potential
mechanisms by which this anesthetic gas further delays contractile recovery of stunned
myocardium.[508]
In the presence of a volatile
anesthetic, nitrous oxide decreases MVO2
and myocardial oxygen extraction[195]
[486]
and may exacerbate myocardial ischemia during concomitant reductions in arterial
pressure in patients with coronary artery disease.[194]
However, later studies demonstrated that the addition of nitrous oxide to volatile
or opioid anesthetics did not increase the incidence of new regional wall motion
abnormalities as assessed by transesophageal echocardiography.[195]
[509]
