Tsung-Han Li

Decreased Adrenal Venous Catecholamine Concentrations during Methoxyflurane Anesthesia

Plasma catecholamine concentrations were determined in adrenal venous and arterial blood samples withdrawn simultaneously from dogs before, during and after methoxyflurane anesthesia. During light anesthesia and at deeper levels, the adrenal venous concentrations of both epinephrine and norepinephrine were reduced significantly. Decreases were directly proportional to depths of anesthesia. Adrenal venous catecholamine concentrations increased during the recovery period, with wide variance from dog to dog. The findings indicate that methoxyflurane has a depressive effect on the sympathoadrenal system.There was no significant change in arterial catecholamine concentration, nor a significant correlation between adrenal arterial and venous catecholamine concentrations before, during or after anesthesia. It is evident that the arterial concentration of catecholamines is not a valid indicator of the neurohormonal effects of anesthesia.

METHOXAMINE AND CARDIAC OUTPUT IN NONANESTHETIZED MAN AND DURING SPINAL ANESTHESIA.

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.

Hemodynamics of mephentermine in man.

THE clinical use of mephentermine¶ to elevate the arterial-blood pressure in man is presumably based upon the rationale that its pressor action is primarily due to an increase in myocardial contrac...

Stellate ganglionic transmission and myocardial contractile force during halothane anesthesia.

The effect of halothane anesthesia upon transsynaptic transmission in the left stellate ganglion of the dog was determined by simultaneous measurement of postganglionic potentials and the maximal rate of change of myocardial contractile force in response to progressively increasing intensities of preganglionic stimulation. Preganglionic stimulation produced either an increase or the same magnitude of postganglionic potentials and myocardial contractile force response (in percentage) during halothane anesthesia as compared with the control state. These findings are presented as evidence that one mode of stellate ganglionic transmission is unimpaired and even facilitated during halothane anesthesia.