Vascular responses to local cold injury.
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In 45 subjects, 154 frostnips of the finger were induced by cooling in air at -15 degrees C with various wind speeds. The mean supercooled skin temperature at which frostnip appeared was -9.4 degrees C. The mean skin temperature rise due to heat of fusion at ice crystallization was 5.3 degrees C. The skin temperature rose to what was termed the apparent freezing point. The relation of this point to the supercooled skin temperature was analyzed for the three wind speeds used. An apparent freezing point for a condition of no supercooling was calculated, estimating the highest temperature at which skin freezes at a given wind speed. The validity of the obtained differences in apparent freezing point was tested by an analysis of covariance. Although not statistically significant, the data suggest that the apparent freezing point with no supercooling decreases with increasing wind velocity. The highest calculated apparent freezing point at -15 degrees C and 6.8 m/s was 1.2 degrees C lower than the true freezing point for skin previously determined in brine, which is a statistically significant difference.
We tested the hypothesis that blocking neutrophil adherence and/or aggregation reduces tissue injury that results when tissue is frozen and rewarmed. The left hindlimbs of three groups of New Zealand White rabbits were immersed in a -15 degrees C salt water bath for 30 min to freeze the foot. The foot was rewarmed in a 39 degrees C water bath. In two groups, adherence and aggregation were blocked with monoclonal antibody (MAb) 60.3, and the third group was treated with saline. Two of the groups were treated at the time of rewarming with either saline or MAb 60.3, and the third group received MAb 60.3 at the conclusion of rewarming. Tissue edema and tissue loss were significantly less in the two groups receiving MAb 60.3 than in the control group. Rabbits treated at the time of rewarming had less edema and tissue loss than those treated at the completion of rewarming. These studies indicate that a substantial component of severe cold injury is neutrophil mediated and occurs after rewarming.
To assess the presence and magnitude of the effect of skin blood flow on finger skin cooling on contact with cold objects against the background of circulatory disorder risks in occupational exposures, this study investigates the effect of zero vs. close-to-maximal hand blood flow on short-term (< or =180 s) skin contact cooling response at a contact pressure that allows capillary perfusion of the distal pulp of the fingertip. Six male volunteers touched a block of aluminium with a finger contact force of 0.5 N at a temperature of -2 degrees C under a vasodilated and an occluded condition. Before both conditions, participants were required to exercise in a hot room for > or = 30 min for cutaneous vasodilation to occur (increase in rectal temperature of 1 degrees C). Under the vasodilated condition, forearm blood flow rate rose as high as 16.8 ml.100 ml(-1).min(-1). Under the occluded condition, the arm was exsanguinated, after which a blood pressure cuff was secured on the wrist inducing arterial occlusion. Contact temperature of the finger pad during the subsequent cold contact exposure was measured. No significant difference was found between the starting skin temperatures for the two blood flow conditions, but a distinct difference in shape of the contact cooling curve was apparent between the two blood flow conditions, with Newtonian cooling observed under the occluded condition, whereas a rewarming of the finger skin toward the end of the exposure occurred for the vasodilated condition. Blood flow was found to significantly increase contact temperature from 40 s onward (P < 0.01). It is concluded that, at a finger contact force compatible with capillary perfusion of the finger pad ( approximately 0.5 N), circulating blood provides a heat input source that significantly affects finger skin contact cooling during a vasodilated state.
The effects of a mild freeze injury to the skin on responses of nociceptive dorsal horn neurons to cold and heat stimuli were examined in anesthetized rats. Electrophysiological recordings were obtained from 72 nociceptive spinal neurons located in the superficial and deep dorsal horn. All neurons had receptive fields (RFs) on the glabrous skin of the hindpaw, and neurons were functionally divided into wide dynamic range (WDR) and high-threshold (HT) neurons. Forty-four neurons (61%) were classified as WDR and responded to both innocuous and noxious mechanical stimuli (mean mechanical threshold of 12.8 +/- 1.6 mN). Twenty-eight neurons (39%) were classified as HT and were excited only by noxious mechanical stimuli (mean mechanical threshold of 154.2 +/- 18.3 mN). Neurons were characterized for their sensitivity heat (35 to 51 degrees C) and cold (28 to -12 degrees C) stimuli applied to their RF. Among WDR neurons, 86% were excited by both noxious heat and cold stimuli, while 14% responded only to heat. For HT neurons, 61% responded to heat and cold stimuli, 32% responded only to noxious heat, and 7% responded only to noxious cold. Effects of a mild freeze injury (-15 degrees C applied to the RF for 20 s) on responses to heat and cold stimuli were examined in 30 WDR and 22 HT neurons. Skin freezing was verified as an abrupt increase in skin temperature at the site of injury due to the exothermic reaction associated with crystallization. Freezing produced a decrease in response thresholds to heat and cold stimuli in most WDR and HT neurons. WDR and HT neurons exhibited a mean decrease in response threshold for cold of 9.0 +/- 1.3 degrees C and 10.0 +/- 1.6 degrees C, respectively. Mean response thresholds for heat decreased 4.0 +/- 0.4 degrees C and 4.3 +/- 1.3 degrees C in WDR and HT neurons, respectively. In addition, responses to suprathreshold cold and heat stimuli increased. WDR and HT neurons exhibited an 89% and a 192% increase in response across all cold stimuli, and a 93 and 92% increase in responses evoked across all heat stimuli, respectively. Our results demonstrate that many spinal neurons encode intensity of noxious cold as well as noxious heat over a broad range of stimulus temperatures. Enhanced responses of WDR and HT neurons to cold and heat stimuli after a mild freeze injury is likely to contribute to thermal hyperalgesia following a similar freeze injury in humans.
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