Cutaneous neural activity and endothelial involvement in cold-induced vasodilatation

Abstract

Whether sympathetic withdrawal or endothelial dilators such as nitric oxide (NO) contributes to cold-induced vasodilation (CIVD) events is unclear. We measured blood flow and finger skin temperature (T) of the index finger in nine participants during hand immersion in a water bath at 35 °C for 30 min, then at 8 °C for 30 min. Data were binned into 10 s averages for the entire 60 min protocol for laser-Doppler flux (LDF) and T. At baseline, T was 35.3 ± 0.2 °C and LDF was 227 ± 28 PU. During hand cooling, minimum T was 10.9 ± 0.4 °C and LDF was 15 ± 4 PU. All participants exhibited at least one CIVD event (T increase ≥ 1 °C), with a mean peak T 13.2 ± 0.8 °C and a corresponding peak LDF of 116 ± 34 PU. A Morlet mother wavelet was then used to perform wavelet analysis on the LDF signal, with frequency ranges of 0.005-0.01 Hz (endothelial NO-independent), 0.01-0.02 Hz (endothelial NO-dependent), and 0.02-0.05 Hz (neurogenic). The synchronicity of wavelet fluctuations with rising LDF coincident with CIVD events was then quantified using Auto-regressive Integrated Moving Average time-series analysis. Fluctuations in neural activity were strongly synchronized in real time with increasing LDF (stationary-r = 0.73 and Ljung-box statistic > 0.05), while endothelial activities were only moderately synchronized (NO-independent r = 0.15, > 0.05; NO dependent r = 0.16, > 0.05). We conclude that there is a direct, real-time correlation of LDF responses with neural activity but not endothelial-mediated mechanisms. Importantly, it seems that neural activity is consistently reduced prior to CIVD, suggesting that sympathetic withdrawal directly contributes to CIVD onset.

Interactions of mild hypothermia and hypoxia on finger vasoreactivity to local cold stress

“…The origin of such cold-induced vasodilation (CIVD) is still a matter of debate (for review, see 14). It may be mediated either centrally, via sympathetic vasoconstrictor withdrawal (24,34), or locally, via direct cold-induced paralysis of the peripheral vessels (37); either way, the arteriovenous anastomoses appear to play a major role (3). Regardless of the underlying mechanisms, CIVD alleviates the cold-evoked pain and thermal discomfort (40,43) and presumably enhances manual dexterity and tactile sensitivity.…”

Acral skin vasoreactivity and thermosensitivity to hand cooling following 5 days of intermittent whole body cold exposure

“…Although the exact mechanisms underlying the CIVD response are still unsettled (see Ref. 5 ), recurrent evidence suggests that the incidence and magnitude of the response are mediated, to a degree, centrally, via withdrawal of sympathetic tone ( 6 , 7 ).…”

Local hardware hypothermia influence on the physiological processes

“…The origin of cold-induced vasodilation (CIVP) is still a matter of discussion [4]. CIVP can be mediated either centrally through the sympathetic nervous system [5,6] or locally through cold-induced direct peripheral vascular paralysis [7]; authors would like to note the role of arteriovenous anastomoses [8]. The regulation of skin blood flow occurs due to a complex and dynamic interaction of thermal effects emanating from the depths of the body (core) and skin (shell).…”