XENON
The anesthetic properties of the noble gas xenon were first described
more than 50 years ago.[510]
Xenon has a blood
gas partition coefficient less than that of nitrous oxide,[511]
does not undergo biotransformation,[512]
provides
rapid induction and emergence from anesthesia,[513]
[514]
[515]
and
exerts
analgesic effects[516]
independent of α2
-adrenergic
and opioid receptors.[517]
Despite these advantageous
properties, xenon has not been routinely used for clinical anesthesia in the United
States because it is more expensive than nitrous oxide and volatile anesthetics.
More efficient manufacturing techniques and development of low-flow administration
and recycling systems have reduced the cost of xenon and rekindled interest in its
clinical use.[514]
[518]
[519]
Many of these issues are succinctly summarized
in an excellent review by Lynch and colleagues.[520]
Xenon causes minimal systemic and pulmonary hemodynamic effects
in vivo,[513]
[514]
[521]
[522]
[523]
preserves[513]
or very modestly reduces[524]
myocardial contractility, and attenuates alterations in hemodynamics and increases
in plasma epinephrine and cortisol concentrations associated with surgical stimulation.
[521]
[525]
[526]
Xenon did not alter cardiac function or major ion currents in isolated guinea pig
hearts and ventricular myocytes.[527]
Similar findings
were observed in isolated human atrial myocytes.[528]
Xenon exerted modest cardioprotective effects when administered during early reperfusion
after regional myocardial ischemia in rabbit hearts.[529]
However, the mechanisms responsible for this protective effect are unclear based
on data indicating that xenon does not affect the amplitudes of Na,+
L-type
Ca,2+
and inward-rectifier K+
channels in whole-cell patch-clamped
myocytes.[527]
The effects of xenon on systemic
hemodynamics, LV systolic and diastolic function, and the determinants of LV afterload
have also been examined in chronically instrumented dogs before and after the development
of rapid LV pacing-induced cardiomyopathy.[530]
Xenon was remarkably devoid of hemodynamic effects in normal and cardiomyopathic
dogs anesthetized with isoflurane. Xenon did not alter isoflurane-induced reductions
in the PRSW slope (Mw
) in the presence and absence of pacing-induced LV
dysfunction ( Fig. 7-25
).
Xenon caused greater increases in the time constant of isovolumic relaxation in
isoflurane-anesthetized, cardiomyopathic dogs compared with normal dogs, but indices
of early LV filling and chamber compliance remained unchanged, suggesting that xenon
does not appreciably influence LV diastolic function during isoflurane anesthesia.
Xenon also produced relatively minor alterations in the determinants of LV afterload
in dogs before and after pacing. Taken together, these data indicate that xenon
produces very subtle cardiovascular effects during isoflurane anesthesia in dogs
with and without experimental dilated cardiomyopathy.[530]
A level of 56% xenon (end-tidal concentration) depressed sympathetic and parasympathetic
nervous system transmission to a greater extent than 0.8 MAC of isoflurane in healthy
patients undergoing elective surgery.[531]
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