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The technique of microneurography and the assessment of muscle sympathetic nerve activity (MSNA) are used in laboratories throughout the world. The variables used to describe MSNA, and the criteria by which these variables are quantified from the integrated neurogram, vary among studies and laboratories and, therefore, can become confusing to those starting to learn the technique. Therefore, the purpose of this educational review is to discuss guidelines and standards for the assessment of sympathetic nervous activity through the collection and analysis of MSNA. This review will reiterate common practices in the collection of MSNA, but will also introduce considerations for the evaluation and physiological inference using MSNA., (Copyright © 2015 Elsevier B.V. All rights reserved.)

The relative contribution of alpha adrenergic receptor subtypes in the transduction of sympathetic nerve activity (SNA) during carotid baroreflex (CBR) engagement is not well understood. Therefore, we compared the hemodynamic consequence of CBR-mediated sympatho-excitation via neck pressure (NP) before and after alpha-2 adrenergic blockade with intra-arterial yohimbine. Leg blood flow was measured using 2D and Doppler ultrasound, and arterial blood pressure was determined directly. NP caused the expected vasoconstriction, and this response was significantly reduced (by 50-60%) when NP was repeated after yohimbine. These data indicate that alpha-2 adrenergic receptors contribute significantly to CBR-induced vasoconstriction in the human leg under resting conditions.

In order to characterize the stimulus-response relationships of the arterial, aortic, and carotid baroreflexes in mediating cardiac chronotropic function, we measured heart rate (HR) responses elicited by acute changes in mean arterial pressure (MAP) and carotid sinus pressure (CSP) in 11 healthy individuals. Arterial (aortic + carotid) baroreflex control of HR was quantified using ramped changes in MAP induced by bolus injection of phenylephrine (PE) and sodium nitroprusside (SN). To assess aortic-cardiac responses, neck pressure (NP) and suction (NS) were applied during PE and SN administration, respectively, to counter alterations in CSP thereby isolating the aortic baroreflex. Graded levels of NP and NS were delivered to the carotid sinus using a customized neck collar device to assess the carotid-cardiac baroreflex, independent of drug infusion. The operating characteristics of each reflex were determined from the logistic function of the elicited HR response to the induced change in MAP. The arterial pressures at which the threshold was located on the stimulus-response curves determined for the arterial, aortic and carotid baroreflexes were not significantly different (72+/-4, 67+/-3, and 72+/-4 mm Hg, respectively, P > 0.05). Similarly, the MAP at which the saturation of the reflex responses were elicited did not differ among the baroreflex arcs examined (98+/-3, 99+/-2, and 102+/-3 mm Hg, respectively). These data suggest that the baroreceptor populations studied operate over the same range of arterial pressures. This finding indicates each baroreflex functions as both an important anti-hypotensive and anti-hypertensive mechanism. In addition, this investigation describes a model of aortic baroreflex function in normal healthy humans, which may prove useful in identifying the origin of baroreflex dysfunction in disease- and training-induced conditions.

The effects of acute alcohol ingestion on the left ventricular performance of nine normal subjects, mean age 25 years, were studied before and after incomplete autonomic blockade, produced by atropine, 0.04 mg/kg body weight, and propranolol, 0.2 mg/kg body weight. Left ventricular (LV) function curves (stroke volume vs. end-diastolic volume) were plotted from data generated before and after large variations in cardiac preload. Increase in preload was produced by five degrees of head-down tilt for 90 minutes; decrease in preload was produced by graduated lower body negative pressure to -40 mmHg. After incomplete autonomic blockade, the negative inotropic effects of acute alcohol ingestion were minimal but significant and manifest by the reduction in mean velocity of circumferential fiber shortening (p less than 0.05). Studies during wide variations in preload confirmed the importance of maintaining central blood volume after alcohol ingestion. Lower body negative pressure after both incomplete autonomic blockade and alcohol produced a further deterioration in mean velocity of circumferential fiber shortening (p less than 0.05).