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Cold induced vasoconstriction (CIVC) is a way for mammals to reduce heat loss in an effort to maintain body core temperature. As blood flow to a cooled extremity is reduced, the amount of body heat lost at the cooled location is minimised. However, when the extremity temperature gets below a certain threshold, Cold induced vasodilatation (CIVD) occurs, a phenomenon that is believed to reduce the risk of local cold injuries. Many theories explaining the mechanism of the CIVD reaction have been postulated, but no consensus has been found. One of these theories is that the CIVD reaction is controlled neurally. To study the effect of neural influence on the vascularisation and rewarming patterns a new experimental set-up was designed. This set-up is able to measure responses in both hind paws simultaneously, creating the opportunity to study the effect of nerve injury on one limb and use the contralateral limb as a control. Ten rats received a sciatic nerve transection and repair of either the left (n=5) or the right (n=5) hind limb. Measurements were performed, 1 day pre-operatively, directly post-operatively, and at days 1, 7, 14, 21, 35 and 49 post-operatively. Although results are not significant, there is a tendency for the CIVD reaction to be reduced in the nerve injured paw until the nerve is regenerated around day 35. Further investigation of neural influence on the CIVD reaction will be necessary; this set-up may prove to be useful in future experiments to elucidate the mechanism of the CIVD reaction., (Copyright © 2010 Elsevier B.V. All rights reserved.)

Purpose: This study evaluated the values of transcutaneous oxygen tension (TcPo(2)) measurement in diabetic patients compared with nondiabetic patients and assessed its reproducibility., Methods: In 60 diabetic patients (type 1 and type 2 diabetes mellitus) without signs of peripheral arterial disease or neuropathy, we measured TcPo(2) at the chest and foot and compared these measurements with 60 age- and sex-matched nondiabetic patients in a cross-sectional fashion. The reproducibility of TcPo(2) in terms of interobserver variability was also assessed., Results: Diabetic patients had a mean +/- SD TcPo(2) value at the foot of 50.02 +/- 8.92 mm Hg, which was significantly lower compared with 56.04 +/- 8.80 mm Hg in nondiabetic patients (P < .001). At the chest wall, values for TcPo(2) were 51.77 +/- 11.15 mm Hg, and 58.22 +/- 12.47 mm Hg for diabetic patients and nondiabetic patients, respectively (P = .003). Regression analysis showed that TcPo(2)was significantly associated with diabetes mellitus (coefficient = -0.258; P = .004), and with having a first-degree relative with diabetes mellitus (coefficient = -0.265; P = .003). Furthermore, the interobserver variability showed a substantial correlation for both measurements at the chest (P < .001; r = 0.654; intraclass correlation coefficient [ICC] = 0.79) and at the dorsum of the foot (P < .001; r = 0.426; ICC = 0.60)., Conclusion: Diabetic patients without signs of peripheral disease or neuropathy had significantly lower TcPo(2) values compared with age- and sex-matched nondiabetic patients. The influence of the examiner on the variance in TcPo(2) measurements was relatively small. We advocate the use of TcPo(2) measurement in diabetic patients to detect subclinical microvascular impairment as an additional tool to assess peripheral vascular disease.