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Influence of Ischaemia‐Reperfusion Injury on the Subsequent Response to Local Heating in Non‐Glabrous and Glabrous Skin of the Index Finger
Author(s) -
McGarr Gregory W.,
Hodges Gary J.,
Cheung Stephen S.
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.684.12
Subject(s) - medicine , ischemia , blood flow , vasodilation , frostbite , cuff , anesthesia , laser doppler velocimetry , index finger , hyperaemia , vascular occlusion , blood pressure , neurovascular bundle , axon reflex , nitric oxide , pathophysiology , cardiology , surgery , anatomy
Ischaemia‐reperfusion (I‐R) injury has been implicated in the pathophysiology of many clinical conditions including frostbite and non‐freezing cold injuries. The increased oxidative stress and inflammation associated with I‐R injury may contribute to impaired restoration of blood flow and tissue recovery in the hands and feet during rewarming through alterations in neurovascular and/or endothelial function. This may be reflected in an altered blood flow response to local skin heating, which is characterized by an initial vasodilatory peak that is primarily controlled by an axon reflex, followed by a secondary plateau that is influenced mainly by nitric oxide release from the endothelium. In ten participants we examined the responses to local heating in non‐glabrous and glabrous skin of the index finger following 20 minutes of ischaemia induced by inflating (220 mmHg) a standard blood pressure cuff around the arm and compared these with a time‐matched sham (non‐ischaemia) trial. Red blood cell flux, an index of skin blood flow, was examined using laser‐Doppler probes with integrated local heating units. Flux values were then divided by mean arterial pressure and reported as cutaneous vascular conductance (CVC). Local heating was initiated prior to ischaemia and 20 minutes after the release of cuff occlusion at separate skin sites. At each site local temperature was controlled at 33°C and then increased (3°C min −1 ) to 42°C and held for ~30 min. Following this, local temperature was increased to 44°C for 20 min. No changes were found in CVC for the initial peak and plateau phases or when heating to 44°C following ischaemia in either skin type (all P>0.05). However, the kinetics of the response were significantly altered by I‐R. Vasodilatory onset was delayed by 24% and 19% for non‐glabrous and glabrous skin, respectively (both P<0.05). Time to initial peak was also delayed by 17% and 11% in non‐glabrous and glabrous skin, respectively, although only the delay in non‐glabrous skin was significant (P<0.05). We conclude that 20 minutes of I‐R injury significantly impairs the kinetics of the response to a rapid, non‐painful local heating stimulus in both non‐glabrous and glabrous skin of the index finger, suggesting an alteration in neurovascular control. This delayed response may be associated with a higher temperature threshold for initiating vasodilation post‐ischaemia and could lead to persistent hypoxic stress during rapid rewarming in association with an increase in local skin temperature, coupled with insufficient tissue perfusion. Support or Funding Information Natural Sciences and Engineering Research Council of Canada: Discovery Grant (227912‐12, S.S. Cheung)