PubMed · 8453441
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C F Fear, C S Littlejohns, E C Rouse. 1993. Propofol and ECT.. https://doi.org/10.1192/bjp.162.3.421b
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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.