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1 Department of Pharmacology, Karolinska Institutet, Stockholm, Sweden
Effects of cyclopropane, halothane, enibomal sodium (a fast acting barbiturate) and morphine on circulatory regulating mechanisms were studied in dogs. The heart rate, arterial pressure, blood flow to the hind limb and their responses to stimulation of the hypothalamic or mesencephalic vasoactive areas and to common carotid occlusion were measured during the conscious state and during anesthesia or sedation with these drugs. During light cyclopropane anesthesia, the arterial pressure rose. Vascular resistance in the hind limb increased. As anesthesia was deepened, the heart rate decreased. Changes in the arterial pressure were inconsistent. With halothane anesthesia, there was bradycardia and progressive hypotension. After administration of enibomal, tachycardia and hypotension occurred. Sedation with morphine was accompanied by bradycardia but no significant change in the arterial pressure. Cyclopropane, halothaneand enibomal depressed the pressor response to central stimulation and carotid occlusion in proportion to the depth of anesthesia. The sympathetic cholinergic vasodilator response was unimpaired except during enibomal and deep cyclopropane anesthesia. Morphine did not appear to affect circulatory responses to central stimulation and carotid occlusion. These results suggest that the excitatory vasomotor mechanisms (adrenergic) are depressed during anesthesia. The basis for the hypertension and other evidences of sympathetic activation observed during cyclopropane anesthesia remains to be determined.
Submitted on October 6, 1965