PubMed · 5047615
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D Gruhl. 1972. [Malignant hyperthermie--a case report].. https://pubmed.ncbi.nlm.nih.gov/5047615/
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Haemodynamic responses are routinely used for monitoring anaesthesia, but they can be elicited at spinal or brainstem levels and therefore do not provide information on cerebrocortical activity. To test the possibility that electroencephalography (EEG) might provide an objective assessment of unconsciousness and depth of anaesthesia the haemodynamic and EEG data from 17 ewes anaesthetised with halothane were analysed. Data were recorded at least every five minutes. An increase of 10 per cent or more in heart rate, systolic arterial pressure (SAP), or mean arterial pressure (MAP) was defined as a positive haemodynamic response to surgical stimulation. Simultaneously recorded EEG variables included delta-, theta-, and beta-frequency band power, power ratios (theta/delta, alpha/delta, beta/delta), 80 per cent spectral edge frequency (SEF 80), and median frequency. In 11 of the ewes, a positive haemodynamic response was accompanied by a significant decrease in delta activity and significant increases in alpha/delta ratio, beta/delta ratio, and SEF 80, and there were significant correlations between the changes in heart rate, and delta activity and beta/delta ratio. In the other six ewes, there were no significant EEG responses in association with haemodynamic changes of less than 10 per cent.
Many properties of nitric oxide, NO, (localization, diffusiveness, half-life, vasodilatory affects) have supported its potential role in mediating the link between local cerebral activity and blood flow. However, evidence that both supports and refutes a role for NO in functional hyperemia have been presented. The present study employed multiple nitric oxide synthase inhibitors, two anesthetic regimes and laser-Doppler flowmetry to test the hypothesis that NO is critically involved in mediating the functional hyperemic response within rodent whisker-barrel cortex (WBC). In urethane anesthetized animals, functional hyperemic responses were obtained both before and after 1 mg/kg atropine infusion, 30 mg/kg i.v. L-NAME (N-Nitro-L-arginine methylester) infusion, 30 mg/kg L-NA (N-Nitro-L-arginine) infusion or 25 mg/kg 7-NI (7-nitroindazole). L-NAME was also tested in a group of animals pretreated with halothane before urethane anesthesia. Neither the magnitude of the blood flow response nor its time course was altered by NO blockade or atropine administration when compared to pre-infusion controls in urethane anesthetized rats. In contrast, animals that were pretreated with halothane exhibited a 33% inhibition of functional hyperemia after L-NAME administration. Taken together, these data do not support a primary role for NO in rat WBC functional hyperemia and suggest that previous reports of inhibition may have been secondary to the anesthesia employed.
In a recent paper the authors developed a stochastic model for the response of the cerebral cortex to a general anesthetic agent. The model predicted that there would be an anesthetic-induced phase change at the point of transition into unconsciousness, manifested as a divergence in the electroencephalogram spectral power, and a change in spectral energy distribution from being relatively broadband in the conscious state to being strongly biased towards much lower frequencies in the unconscious state. Both predictions have been verified in recent clinical measurements. In the present paper we extend the model by calculating the equilibrium distribution function for the cortex, allowing us to establish a correspondence between the cortical phase transition and the more familiar thermodynamic phase transitions. This correspondence is achieved by first identifying a cortical free energy function, then by postulating that there exists an inverse relationship between an anesthetic effect and a quantity we define as cortical excitability, which plays a role analogous to temperature in thermodynamic phase transitions. We follow standard thermodynamic theory to compute a cortical entropy and a cortical "heat capacity," and we investigate how these will vary with anesthetic concentration. The significant result is the prediction that the entropy will decrease discontinuously at the moment of induction into unconsciousness, concomitant with a release of "latent heat" which should manifest as a divergence in the analogous heat capacity. There is clear clinical evidence of heat capacity divergence in historical anesthetic-effect measurements performed in 1977 by Stullken et al. [Anesthesiology 46, 28 (1977)]. The discontinuous step change in cortical entropy suggests that the cortical phase transition is analogous to a first-order thermodynamic transition in which the comatose-quiescent state is strongly ordered, while the active cortical state is relatively disordered.