! 334 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



29 C 



2000 

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mi 



42 C 



Hi in 



60 O 



INUTES 6 ° ° 



60 



fig. ~. Heat loss in cal/ioo ml of finger/min to water in the range o-6 C from the L (anesthetic) 

 and R (normal) 5th fingers, the observations being made between the 30th and 40th days after di- 

 vision of the L ulnar nerve. In the denervated finger, cold vasodilatation is extremely small or absent 

 after preliminary immersion in water at 1 5 C, small but definite after 2Q C, and considerable after 

 42 C. [From Greenfield et al. (109).] 



dilatation is delayed, sometimes for as much as 90 

 min from the time of immersion, and it is reduced 

 in size sometimes to less than one-tenth (127). The 

 response continues in the early days after interruption 

 of the somatic nerves, but becomes difficult to elicit 

 later when the separated distal parts of the nerves 

 have degenerated. This led Lewis (140) to conclude 

 that the response depends on a local axon reflex from 

 cutaneous receptors to the blood vessels. If, however, 

 the chronically denervated limb is warmed for some 

 time before the digits are immersed in cold water 

 (109), a reduced (to 20-90 Tr) but definite vasodilator 

 response is seen (fig. 7). It is always difficult to be 

 certain that denervation is complete, but the observa- 

 tions probably indicate that the axon reflex pathway- 

 is not essential for the response. This view is strength- 

 ened by the finding of a vasodilator response in a 

 finger tip locally injected with anesthetic solution 

 (110). Other vascular responses which appear to be 

 depressed in the chronically denervated limb are 

 improved if the limb is first warmed for an hour or 

 two. 



A chemical stimulus to cold vasodilatation has not 

 been identified. Acetylcholine and histamine in- 

 jected intra-arterially or introduced by electrophoresis 

 during the first few minutes of immersion of a finger 

 in ice water do not provoke an earlier vasodilatation, 

 but it is possible that at this time of intense vasocon- 

 striction they do not reach the blood vessels. Cold 

 vasodilatation, however, is not reduced by atropine 

 nor by antihistamine (188). The mechanism of the 

 response remains obscure. 



The effect of the dilatation is to raise the tempera- 

 ture of the exposed extremities at the expense of a 

 considerable loss of heat from the bodv. Even while 



immersed in stirred water near the freezing point, 

 the average internal temperature of a finger may be 

 raised to as much as 30 C, and in the central parts 

 must presumably be only slightly below the tempera- 

 ture of the body core (107). In a warm person the 

 heat loss per minute from a whole hand and from the 

 distal half of a foot may be 800 and 407 cal per min, 

 respectively (104). These figures are similar to total 

 resting heat production, and the loss of heat from one 

 hand can cause a fall in esophageal temperature 

 of 0.6 C in 9 min (106). When plenty of heat is 

 available, the reaction keeps fingers exposed to 

 reasonable cold sufficiently warm to preserve move- 

 ment and sensation. Dwellers in cold climates nor- 

 mally wear clothing which provides their body with 

 a warm microclimate, and are able to afford some 

 heat loss. When there is a need to conserve heat, 

 the reaction is greatly diminished and the fingers are 

 only slightly warmed by it. For example, Australian 

 aborigines are able, by restricting the peripheral 

 circulation, to retain sufficient heat to sleep naked 

 through the night in a temperature which may fall 

 to o C (177). 



Several observations suggest that the extremities 

 can become acclimatized to cold (44). Local pain, 

 and the reflex increases in arterial pressure and pulse 

 rate are reduced after repeated immersion in water 

 at 4 C (92). Exposure of the fingers to severe cold 

 causes less numbness in persons habitually exposed 

 than in others. Such observations suggest that there 

 may be a local adaptation of the circulation in the 

 exposed parts but the evidence for this is not strong. 

 Repeated exposure of the hands to cold, as in Nor- 

 wegian and Lapp fishermen, leads to a more rapid 

 onset of cold vasodilatation (135) but to no increase 



