Kingsley‐Berg, Shirley

Dehydration in humans decreases orthostatic tolerance and alters sympathetic neural control of the circulation, but the mechanisms involved are unclear. Our goal was to evaluate the role of angiotensin II (AngII) in altering the sympathetic control mechanisms in dehydration. We hypothesized that dehydration would increase resting muscle sympathetic nerve activity (MSNA) and increase sensitivity of baroreflex control of MSNA and that these changes are mediated in part by AngII via AT1 receptors. We measured resting MSNA and baroreflex control of MSNA in healthy young adults under two conditions: euhydration and dehydration after 24 hr fluid restriction. We continuously measured heart rate (ECG), beat‐to‐beat blood pressure (Finometer), central venous pressure (peripherally inserted central catheter) and MSNA (peroneal microneurography) in both conditions. In each condition, measurements were taken before and after 50 mg losartan (AT1 antagonist). Dehydration was associated with a ~52 % increase in resting MSNA, but losartan did not consistently influence resting MSNA. Contrary to our hypothesis, baroreflex sensitivity increased ~39 % following losartan administration during dehydration. Our results confirm the sympathoexcitatory influence of dehydration, but the role of AngII in this process requires further evaluation. Supported by AHA 0750036Z and NIH CTSA UL1‐RR24150.

In humans, sympathetic nerves in the skin provide tonic vasoconstrictor innervation. Although neural changes in type 2 diabetes mellitus (T2DM) are well recognized, it is unclear to what extent the activity of these vasoconstrictor nerves is altered in individuals with relatively uncomplicated T2DM. We tested the hypothesis that skin sympathetic nerve activity (SSNA) is decreased at rest in individuals with T2DM compared to healthy controls (C), and that the increase in SSNA with whole body cooling is smaller in T2DM than in C. We measured SSNA using microneurography, skin blood flow using laser‐Doppler flowmetry (LDF), and arterial pressure using Finometer in T2DM and C subjects at baseline and during 3–5 minutes of whole body cooling. LDF was measured on the foot at the site of innervation of the measured SSNA signal. Whole body cooling was followed by 35 min of local warming of the skin to 42°C to determine maximum cutaneous vascular conductance. In preliminary studies (N=3 per group), SSNA at baseline (T2DM: 22 ± 8 vs. C: 30 ± 1 bursts/min) and during whole body cooling (T2DM: 28 ± 11 vs. C: 43 ± 2 bursts/min; deltas: T2DM: + 6 ± 3 vs. C: +13 ± 1 bursts/min) tended to be lower in T2DM compared to C. Our data suggest that changes in control of SSNA in T2DM contribute to altered thermoregulatory responses in these individuals. Supported by NIH R01 HL73884 and CTSA UL1‐RR24150.

AimThe aim of this study was to compare passive muscle stiffness in children with cerebral palsy (CP) and children with typical development using a novel ultrasound technique: ultrasound shear wave elastography (SWE).MethodWe conducted a prospective study of 13 children with CP (six females and seven males, median age 5y 1mo [interquartile range 4y 4mo–7y 8mo]) and 13 children with typical development (six females and seven males, median age 5y 3mo [interquartile range 4y 4mo–9y 4mo]). Demographic information and physical exam measurements were obtained in addition to shear modulus measurements (passive muscle stiffness) of the lateral gastrocnemius muscle at 20° plantar flexion, 10° plantar flexion, and 0° plantar flexion using SWE.ResultsChildren with CP had significantly greater shear modulus measurements at all three foot positions (p<0.050). When the shear modulus values were normalized to the baseline value for each child, there was no significant difference between the two groups.InterpretationPassive muscle stiffness, measured without the influence of spasticity, is greater in children with CP than in children with typical development when a muscle is at slack and at stretch. When shear modulus was normalized, the results indicate that muscle in children in both groups responds similarly to passive stretch. Further work includes evaluating effect of botulinum toxin on passive muscle properties.