<b>Studies on the Reactions of the Cutaneous Vessels to Cold Exposure</b>

Folkow, Björn; Fox, R. H.; Krog, John; Odelram, H.; Thorén, O.

doi:10.1111/j.1748-1716.1963.tb02656.x

Cited by 67 publications

(16 citation statements)

References 16 publications

(5 reference statements)

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“…That in the range between 7 and 11 0C small oscillations in temperature imposed during stimulation of the sympathetic nerves result in large oscillations in contractile response can be attributed to the fact that minimal changes in the amount of noradrenaline released are amplified markedly by the augmented responsiveness of the vascular smooth muscle cells. Earlier work on isolated arteries, as well as in the intact organism, showed that precapillary cutaneous vessels usually fail to respond to noradrenaline at 5 C (Keatinge, 1958;Folkow, Fox, Krog, Odelram & Thoren, 1963;Patton & Wallace, 1978), although strong direct myogenic activation still can cause a certain degree of contractile activity (Keatinge, 1964). The reason for the different behaviour between arteries and veins is uncertain, but it probably reflects the different ways in which cutaneous arterial and venous smooth muscle handle activator Ca2+, with the former relying more on the influx ofextracellularly available ions than the latter (Vanhoutte, 1976;Vanhoutte, Verbeuren & Van Nueten, 1980).…”

Section: Unstimulated Preparationsmentioning

confidence: 99%

The effect of profound cooling on adrenergic neurotransmission in canine cutaneous veins.

Rusch¹,

Shepherd²,

Vanhoutte³

1981

The Journal of Physiology

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1. Experiments were performed to investigate how profound cooling affects adrenergic neurotransmission and vascular smooth muscle reactivity in isolated saphenous veins of the dog. 2. Cooling from 37 to 5 degrees C caused progressive depression of the contractile responses to high K+ solutions, illustrating the direct inhibitory effect of cooling on depolarization‐induced contraction of the venous smooth muscle cells. 3. During prolonged cooling to 20, 15 and 10 degrees C, the contractile response to exogenous norepinephrine (10(‐8)‐10(‐6) M) was augmented compared to that at 37 degrees C. At 5 degrees C responses up to 10(‐7) M were also augmented, but those at higher concentrations were depressed. When veins contracted with 2 x 10(‐6) M‐norepinephrine were cooled to 20, 15, 10 and 5 degrees C, there was a further increase in tension; this increase slowly subsided to control values at 5 degrees C but was sustained at the other temperatures. 4. Cooling to 20 and 15 degrees C augmented the contraction caused by low but not high frequencies of electrical stimulation of the adrenergic nerve endings. Further cooling to 10 degrees C depressed, and at 5 degrees C abolished the response, demonstrating that profound cooling interrupted adrenergic neurotransmission. 5. In rings stimulated electrically at a low frequency (0.5 Hz), warming from 7 to 9 degrees C or from 9 to 11 degrees C, caused marked increases in tension. This may be explained by the combination of resumption of adrenergic neurotransmission and the increased responsiveness of the cutaneous venous smooth muscle cells to adrenaline. 6. The combination of enhanced affinity for noradrenaline combined with inhibition of neurotransmitter disposition probably permits the cutaneous veins to remain constricted during exposure to severe cold.

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Section: Unstimulated Preparationsmentioning

confidence: 99%

The effect of profound cooling on adrenergic neurotransmission in canine cutaneous veins.

Rusch¹,

Shepherd²,

Vanhoutte³

1981

The Journal of Physiology

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“…It has previously been suggested that such a cold-induced ''indirect'' vasoconstriction is orchestrated either by the reflex response to a noxious stimulus and/or the action of a central mechanism excited by the cold blood returning from the skin (Folkow et al, 1963;Kregel et al, 1992;Pickering, 1932). The increased adrenal secretion triggered by the prolonged cold application constitutes an additional mechanistic explanation to the phenomenon (Freeman, 1935).…”

Section: Temperature Response Of the Non-immersed Regionsmentioning

confidence: 99%

Acute Effects of Normobaric Hypoxia on Hand-Temperature Responses During and After Local Cold Stress

Keramidas

Kölegård

Mekjavic

et al. 2014

High Altitude Medicine & Biology

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Keramidas, Michail E, Roger Kölegård, Igor B. Mekjavic, and Ola Eiken. Acute effects of normobaric hypoxia on hand-temperature responses during and after local cold stress. High Alt Med Biol. 15:183-191, 2014.-The purpose was to investigate acute effects of normobaric hypoxia on hand-temperature responses during and after a cold-water hand immersion test. Fifteen males performed two right-hand immersion tests in 8°C water, during which they were inspiring either room air (Fio 2 : 0.21; AIR), or a hypoxic gas mixture (Fio 2 : 0.14; HYPO). The tests were conducted in a counterbalanced order and separated by a 1-hour interval. Throughout the 30-min cold-water immersion (CWI) and the 15-min spontaneous rewarming (RW) phases, finger-skin temperatures were measured continuously with thermocouple probes; infrared thermography was also employed during the RW phase to map all segments of the hand. During the CWI phase, the average skin temperature (Tavg) of the fingers did not differ between the conditions (AIR: 10.2 -0.5°C, HYPO: 10.0 -0.5°C; p = 0.67). However, Tavg was lower in the HYPO than the AIR RW phase (AIR: 24.5 -3.4°C; HYPO: 22.0 -3.8°C; p = 0.002); a response that was alike in all regions of the immersed hand. Accordingly, present findings suggest that acute exposure to normobaric hypoxia does not aggravate the cold-induced drop in hand temperature of normothermic males. Still, hypoxia markedly impairs the rewarming responses of the hand.

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“…17 Studies measuring tissue oxygen tension in nonfreezing cold injury models have demonstrated hypoxia and local tissue anoxia, both subcutaneously and intramuscularly, during cooling. 7,23 Cold injury is also known to reduce blood flow, induce vasopressor changes, 8 increase the viscosity of the blood, 24 and cause platelet aggregation. 10,33 It has also been pointed out that, although hypothermia reduces the rate of cellular metabolism, the poor perfusion of capillaries results in insufficient oxygen being released to meet the needs of surrounding tissues.…”

Section: Discussionmentioning

confidence: 99%

Cold nerve injury is enhanced by intermittent cooling

Jia

Pollock

1999

Muscle Nerve

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Studies on the Reactions of the Cutaneous Vessels to Cold Exposure

Abstract: FOLKOW, B., K. H. Fox, J. KROG, H. ODELRAM and 0. THoRks. Studies on the reactions of the cutaneous vessels to cold exposure. Acta physiol. scand. 1963. 58. 342-354. -Some inter-relationships between the

Cited by 67 publications

References 16 publications

The effect of profound cooling on adrenergic neurotransmission in canine cutaneous veins.

The effect of profound cooling on adrenergic neurotransmission in canine cutaneous veins.

Acute Effects of Normobaric Hypoxia on Hand-Temperature Responses During and After Local Cold Stress

Cold nerve injury is enhanced by intermittent cooling

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