CENTRAL NEURONAL PATHWAYS AND THE PROCESS OF ANESTHESIA
CENTRAL NEURONAL PATHWAYS AND THE PROCESS OF ANESTHESIA
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DOI:
10.1093/bja/71.1.148
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发表时间:
1993-07-01
影响因子:
9.8
通讯作者:
ANGEL, A
中科院分区:
文献类型:
--
作者:
ANGEL, A
The effects of anaesthetic agents are complex. When administered to humans they produce:(a) loss of conscious experience and a decrease in the amount of information which reaches the cerebral mantle, as measured by evoked responses to sensory stimulation;(b) loss of memory;(c) changes in the spontaneous activity recorded from the scalp (electroencephalogram (EEG)) or directly from the cortical surface (electrocorticogram (ECoG));(d) loss of volitional control of the skeletal musculature;(e) an attenuation of protective reflexes (reflex withdrawal, cough and gag reflexes);(f) loss of postural reflexes; and (g) wide ranging changes in cardiovascular and respiratory performance. As an experimental tool, anaesthesia may be designed, by appropriate choice of anaesthetic, to either enhance, suppress or leave unchanged various physiological variables which one wishes to study. For example, presynaptic inhibition may be enhanced or suppressed using barbiturates and urethane, respectively [13] and complex polysensory heterosegmental reflexes may be retained in animals anaesthetized with chloralose. The usual structure-activity relationship seen with most bioactive chemicals is absent in anaesthetics. There is a wide range in molecular structures, ranging from simple chemicals, such as nitrous oxide, to the complex steroids, such as alphaxalone which may, under appropriate conditions, lead to a state of anaesthesia. Although in an interpretational and behavioural sense, anaesthetics may be antagonized by for example, convulsant chemicals, the only effective antagonist is very great ambient pressure. The antagonism of anaesthesia by pressure is not an antagonistic effect of competition with a receptor site by a specific blocking chemical, but a physicochemical barrier to an anaesthetic, interacting with a putative hydrophobic receptor site. Looked at simplistically, the interaction between an anaesthetic and its putative site of action causes an increase in volume; increasing the ambient pressure prevents this volume increase.