Measurements of electrical impedance have been made in focal volumes of approximately 1.0 mm 3 of allocortical and subcortical tissue in the cat, with microvolt signals at 1000 cycle/sec. The technique allows simultaneous recording of the relative magnitude of resistive and reactive components. Measurements were made with chronically implanted electrodes, and also in acute preparations, either immobilized with gallamine triethiodide or with an upper cervical spinal transection. Qualitative differences were noted in amygdaloid impedance changes during behavioral responses characterized by similar cortical EEG records, as in paradoxical sleep and behavioral arousal. Brief alerting stimuli reduced resistance and increased capacitance in the amygdala, hippocampus and midbrain reticular formation. These responses lasted 60–120 sec, and differed in relative size of resistive and reactive shifts in the various structures. Inhalation of 7% carbon dioxide in air produced only resistive shifts in the amygdala, but caused substantial shifts in both resistance and reactance in the hippocampus and midbrain reticular formation, amounting to 2–4% of baseline values. However, equally large impedance responses to physiological stimuli occurred with just detectable increases in endogenous carbon dioxide production. The effects of hypothermia in the range 28-21 C on cerebral impedance, carbon dioxide excretion and blood pressure were studied in shivering and immobilized preparations. In shivering animals, resistance and reactance showed only minor perturbations in hippocampus and midbrain reticular formation until the core temperature fell to approximately 25 C. Both resistance and reactance rose sharply in the range 25-21 C, and lagged in return to baseline during temperature recovery. In immobilized animals, impedance shifts followed the general contour of falling temperature, and closely paralleled the carbon dioxide excretion, both in the phase of falling temperature, and in the recovery phase when carbon dioxide excretion continued to drop below control levels. The characteristic excursions of resistive and capacitive impedance induced by hypothermia had no primary relationship to systemic blood pressure, which remained unaltered during their development, and which could also vary substantially without modifying the course or direction of impedance shifts. Temporary cardiac arrest in hypothermia was associated with impedance shifts an order of magnitude larger than those in physiological manipulations. The evidence suggests that impedance responses reflect changes in intrinsic characteristics of cerebral tissue, rather than relating in a direct fashion to cerebral blood flow or blood pressure. In a system with intraneuronal, intraneuroglial and extracellular compartments, carbon dioxide may exert a regulatory function on the selective exchange of sodium and chloride ions between neuronal elements and vascular capillaries, perhaps within the neuroglial compartment. The relative contributions of extracellular and neuroglial compartments to the observed conductance, and their possible relationship to substantial differences between impedance phenomena in physiological responses and in terminal asphyxia, are discussed.
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