Methoxamine (approximately 0.2 mg./kg. body weight; range of total dose, 4 to 30 mg.) was given by intravenous infusion to two groups of patients: (1) 5 normotensive, nonanesthetized; and (2) 7 hypotensive under spinal anesthesia. In the nonanesthetized group, the criterion for dosage of methoxamine was elevation and maintenance of arterial blood pressure 25 per cent (+/-10 per cent) above the resting level. In the hypertensive group, administration of vasopressor was guided by the elevation of arterial blood pressure to the pre-spinal control level. In the normotensive group, cardiac output and the heart rate were both significantly reduced, with variable changes in stroke volume. The vasopressor effect was associated with an elevated total peripheral resistance. In the hypotensive spinal group methoxamine caused variable changes in the cardiac output: increase or decrease in cardiac output depended on changes in stroke volume. The heart rate was generally reduced below the spinal level. The vasopressor effect was apparently due to the elevated total peripheral resistance and, in some instances, to an increased cardiac output. This increase in cardiac output depended mainly on increased stroke volume. These findings suggest that methoxamine in clinical dosage is not a myocardial depressant but a vasopressor capable of increasing the venous return to the heart which responds with increased stroke output.
(C) 1965 American Society of Anesthesiologists, Inc.