Myocardial Protection by Volatile Anesthetics in Humans
APC occurs in human myocardium, but evaluation of this process
in patients is complicated by simultaneous alterations in systemic and coronary hemodynamics;
the use of other anesthetics, analgesics, or vasoactive drugs; preexisting disease
states; and the influence of surgery on cardiovascular homeostasis. Isoflurane[335]
and desflurane[422]
enhanced the recovery of contractile
function of human atrial trabeculae by adenosine receptor stimulation and KATP
channel activation. A role for adenosine receptors, MAP kinases,[334]
and ROS[423]
has been previously demonstrated in
other forms of preconditioning in human atrial myocytes concomitant with mitochondrial
KATP
channel opening. Isoflurane decreased postoperative release of troponin
I and creatine kinase-MB in patients undergoing CABG surgery, suggesting a reduction
in the severity of myocardial necrosis.[424]
Administration
of enflurane before cardioplegic arrest also enhanced postischemic contractile functional
recovery in CABG patients.[425]
Sevoflurane, but
not the intravenous anesthetic propofol, was shown to preserve myocardial function
in patients undergoing CABG concomitant with a reduction in troponin I release.[426]
These compelling data emphasize that volatile anesthetics may exert beneficial effects
against ischemic injury in humans. Volatile anesthetics may represent an important
therapeutic modality to reduce the risk of perioperative myocardial ischemia and
infarction,[427]
although this conclusion has yet
to be confirmed in a large-scale, randomized, clinical trial.
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