Abstract
The technique of microneurography was first developed in Sweden in the late 1960s and subsequently used to document the first measurements of sympathetic neural activity in humans. Since these early recordings, microneurography has proven useful for measuring regional sympathetic activity under many different circumstances in healthy and pathological populations. However, the standard approach of rectification and integration of the sympathetic signal results in a loss of neural information. Recently, Macefield and colleagues (and others) have adapted the microneurographic technique to detect and quantify the firing patterns of single post-ganglionic sympathetic neurones not apparent in integrated multi-unit recordings (Macefield et al. 1994). Using high-impedance electrodes, large discharges from single neurones can be isolated against the background of multi-unit activity. With this approach these authors (and others) have expanded our understanding of sympathetic vasomotor regulation by demonstrating that, at rest, sympathetic vasomotor neurones fire predominately only once within a given burst of activity (∼70% of bursts) (Macefield et al. 1994; Macefield & Wallin, 1999) and that multiple firings of the same neurone, within a burst, increase with stress (Macefield & Wallin, 1999) and with certain pathologies (i.e. congestive heart failure (CHF) and obstructive sleep apnoea (OSA)) (Macefield et al. 1999; Elam et al. 2002). As a logical progression from these previous observations, a recent article by Ashley et al. in The Journal of Physiology sought to characterize the firing properties of single sympathetic vasomotor neurones in patients with chronic obstructive pulmonary disease (COPD) (Ashley et al. 2010). The authors hypothesized that similar to OSA patients, who experience repetitive bouts of hypoxic–hypercapnic stress, the concomitant hypoxaemia and hypercapnia with which COPD commonly present cause an elevated chemical drive and result in an increased firing probability of single sympathetic vasomotor neurones. To test their hypothesis, the authors compared unitary firing properties recorded from nine COPD patients to a group of four bronchiectasis (BE) patients. BE patients exhibit similar airflow limitation and airway inflammation as COPD patients but have normal blood gases. Data from COPD and BE patients were further contrasted with a group of seven normal healthy subjects exhibiting high levels of resting sympathetic activity and a group of eight OSA patients, both described previously (Macefield & Wallin, 1999; Elam et al. 2002).
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