Stroke volume and sympathetic responses to lower-body negative pressure reveal new insight into circulatory shock in humans

• Published in: Autonomic neuroscience Vol. 111; no. 2; pp. 127 - 134
• Main Authors: Convertino, Victor A, Ludwig, David A, Cooke, William H
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 30.04.2004; Elsevier
• Subjects: Adult; Autonomic regulation; Biological and medical sciences; Central hypovolemia; Fundamental and applied biological sciences. Psychology; Humans; Lower Body Negative Pressure; Male; Medical sciences; Microneurography; Muscle, Skeletal - innervation; Neurology; Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ; Shock - physiopathology; Stroke Volume - physiology; Sympathetic Nervous System - physiology; Vascular diseases and vascular malformations of the nervous system; Vertebrates: nervous system and sense organs; Central hypovolemia; Microneurography; Autonomic regulation; Shock; Human; Nervous system diseases; Stroke; Cardiovascular disease; Sympathetic nervous system; Cerebral disorder; Vascular disease; Autonomic nervous system; Central nervous system disease; Cerebrovascular disease
• ISSN: 1566-0702; 1872-7484
• DOI: 10.1016/j.autneu.2004.02.007

We measured various hemodynamic responses and muscle sympathetic nerve activity (MSNA) in human subjects during a graded lower-body negative pressure (LBNP) protocol to test the hypotheses that: (1) reduced stroke volume (SV) is linearly related to increased MSNA; and (2) the onset of symptoms of impending cardiovascular collapse is associated with hypoadrenergic responses to central hypovolemia. We measured heart rates, arterial blood pressures, sympathetic neural activity (MSNA; peroneal nerve microneurography), and relative changes (% Δ) in SV (thoracic electrical bioimpedance) in 13 men during exposure to graded levels of LBNP. After a 12-min baseline data collection period, LBNP was initiated at −15 mm Hg for 12 min followed by continuous stepwise increments to −30, −45, and −60 mm Hg for 12 min each. Eight subjects completed the LBNP protocol (finishers), while the protocol was terminated prematurely during −60 mm Hg in five subjects due to onset of symptoms of cardiovascular collapse (nonfinishers). Of these subjects, we were able to record MSNA successfully throughout the LBNP protocol in four finishers and two nonfinishers. The relationship between average change in stroke volume and average change in MSNA was linear (% ΔMSNA=464–3.6 [% ΔSV], r 2=0.98). On average, MSNA was greater in the nonfinishers at each level of LBNP compared to finishers, but peripheral resistance was lower. Our results support the hypothesis that MSNA activation is inversely related and linear to stroke volume reductions during central hypovolemia. Sympathetic withdrawal rather than hypoadrenergic function may represent a fundamental mechanism for the development of circulatory shock.