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London 2003 |
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In this talk I will
describe the development of a machine to facilitate xenon anaesthesia. It is an
attempt to make a system acceptable to the anaesthetist who wishes to use the
gas but wants to minimise the change to his practice.
Our solution has been
to create an automatic gas mixing system with a low-pressure outlet. The gas
mixture can be delivered at more than 5 l min-1 so that a high-flow
breathing system can be employed. However, the reserve volume of the mixing
system is very small and the mixture can only be produced de novo at
about 2 l min-1. In order to maintain high flows, waste gases from
the scavenging port of the patient breathing system must be returned to the gas
mixer for recycling, and the complete system of gas generator and patient
breathing system is then completely closed. This is not the first time that a
closed system has been formed from two physically distinct components so that
it appears that the patient is breathing from a high-flow system1.
In its present form the
system uses a cylinder of oxygen and a cylinder of balance gas, which may be
air or xenon. The addition of these gases to the gas mixture is controlled by
mass flow controllers, and the composition of the gas mixture within the
machine is measured by a fuel cell and a paramagnetic analyser for oxygen, an
ultrasonic xenon analyser and an infra-red analyser for carbon dioxide. The
automatic control algorithms are very simple: if the system gas has less than
the amount of oxygen set by the operator then oxygen is added; if the reservoir
volume reduces then balance gas is added. This control system has been used
successfully before2. Operation is simple if it is used as an
oxygen-air mixer but, for use with xenon, the machine – as well as the patient
– must be denitrogenated.
Initial use as an
oxygen-air mixer showed it to be an interesting monitor of oxygen consumption.
When used as a continuous-flow source for an oxygenator
during cardiopulmonary bypass, the effect of temperature changes on oxygen
consumption and respiratory quotient were apparent. At the time of writing it
has not yet been used as a xenon-oxygen gas source for patients.
1.
Jackson DE. A new method for the production of general
analgesia and anaesthesia with a description of the apparatus used. J Lab Clin Med 1915; 1: 1-12
2.
Humphrey SJE, White DC. A servo-controlled anaesthetic
machine. Br J Anaesth 1990; 66: 400P
Professor M Maze
Anesthesiology 2003; 98(3):690-698
Xenon Attenuates Cardiopulmonary Bypass-induced Neurologic and
Neurocognitive Dysfunction in the Rat
Daqing Ma, M.D., Ph.D. *; Hong Yang, M.D. †; John Lynch, M.D. ‡; Nicholas P. Franks, Ph.D. §; Mervyn Maze, M.B., Ch.B., F.R.C.P., F.R.C.A.
Hilary P. Grocott, M.D., F.R.C.P.C. #
Background:
With clinical data suggesting a role for excitatory amino acid neurotransmission in the pathogenesis of cardiopulmonary bypass (CPB)-associated brain injury,
the current study was designed to determine whether xenon, an N-methyl-D-aspartate receptor antagonist, would attenuate CPB-induced neurologic and
neurocognitive dysfunction in the rat.
Methods:
Following surgical preparation, rats were randomly divided into four groups: (1) sham rats were cannulated but did not undergo CPB; (2) CPB rats were
subjected to 60 min of CPB using a membrane oxygenator receiving a gas mixture of 30% O2, 65% N2, and 5% CO2; (3) CPB + MK801 rats received
MK801 (0.15 mg/kg intravenous) 15 min prior to 60 min of CPB with the same gas mixture; and (4) CPB + xenon rats underwent 60 min of CPB using an
oxygenator receiving 30% O2, 60% xenon, 5% N2, and 5% CO2. Following CPB, the rats recovered for 12 days, during which they underwent standardized
neurologic and neurocognitive testing (Morris water maze).
Results:
The sham and CPB + xenon groups had significantly better neurologic outcome compared to both the CPB and CPB + MK801 groups on postoperative days
1 and 3 (P < 0.05). Compared to the CPB group, the sham, CPB + MK801, and CPB + xenon groups had better neurocognitive outcome on postoperative
days 3 and 4 (P < 0.001). By the 12th day, the neurocognitive outcome remained significantly better in the CPB + xenon group compared to the CPB group
(P < 0.01).
Conclusion:
These data indicate that CPB-induced neurologic and neurocognitive dysfunction can be attenuated by the administration of xenon, potentially related to its
neuroprotective effect via N-methyl-D-aspartate receptor antagonism.