The Effect of Temperature on the Rate of Blood Flow in the Normal and in the Sympathectomized Hand

Freeman, Norman E.

doi:10.1152/ajplegacy.1935.113.2.384

Cited by 162 publications

(54 citation statements)

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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). In the present study, despite the increased general sympathetic discharge during the HYPO test, no differences in Tforearm and Tavg of the non-immersed thumb were detected between the tests.…”

Section: Temperature Response Of the Non-immersed Regionscontrasting

confidence: 49%

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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Section: Temperature Response Of the Non-immersed Regionscontrasting

confidence: 49%

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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show abstract

“…The heart rate was counted by arterial palpation. The blood flow in the hand, foot, forearm, and calf was measured by the plethysmographic methods previously described (14,15,16). When measurements were made on the forearm and calf, the circulation to the hand and foot distal to them was occluded by pressure cuffs below the plethysmographs (16,17).…”

Section: Methodsmentioning

confidence: 99%

MECHANISM OF THE ARTERIAL HYPERTENSION INDUCED BY PAREDRINOL (α-N-DIMETHYL-p-HYDROXYPHENETHYLAMINE

Stead¹,

Kunkel²

1939

J. Clin. Invest.

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In arterial hypertension the cardiac output, the metabolic rate, and the usual blood chemical constituents are essentially normal. Experimental hypertension in man, however, is usually attended by alterations in some of these measurements. Epinephrine produces hypertension in normal subjects, but at the same time it usually increases the heart rate and cardiac output. It elevates the basal metabolism, the blood flow in the muscles, the blood sugar and the blood lactic acid, and also causes great vasoconstriction in the skin vessels. This hypertension is therefore in no way comparable to that observed in disease. The study to be reported indicates that in normal subjects paredrinol sulphate 1 (a-N-dimethyl-p-hydroxyphenethylamine sulphate) produces a type of hypertension which has many features in common with clinical hypertension. For this reason the circulatory adjustments following the administration of this drug are of particular interest.The pharmacology of paredrinol, a sympathomimetic drug closely allied in structure to ephedrine, has been studied extensively in animals. Rein (1, 2), in an investigation of the action of paredrinol on dogs anesthetized with morphine and pernocton, found that both the arterial pressure and the minute volume output of the heart were elevated. The drug acted first on the venous side of the circulation, and produced a greater venous return to the heart by increasing the venous tone and probably by emptying out the liver. This was followed in a few seconds by a slow increase in arterial tone and, shortly thereafter, by a powerful discharge of blood from the abdominal organs, particularly the spleen. Rein claimed that this intense 'discharge of blood from 1 The paredrinol sulphate used in this study was obtained through the courtesy of the Smith, Kline, and French Laboratories. This drug has been reported in the German literature under the trade names "veritol" and " H 75 " (Knoll).the abdominal venous reservoirs indicated that the main cause for the rise in arterial pressure was an increase in venous return to the heart, rather than an increase in peripheral resistance. He demonstrated that the blood flow in the extremities and in the abdominal viscera was never greatly decreased and at times was increased. Since the drug did not cause blanching when introduced into the human skin, he concluded that the capillaries were not constricted and that the arterial tone was increased in the larger vessels.Heymans and Bayless (3), on the basis of experiments conducted on anesthetized dogs, concluded that the vascular effect of the drug was characterized by slight peripheral vasoconstriction and pronounced splanchnic vasoconstriction. When the physiological reflexes for the proprioceptive regulation of blood pressure were depressed by means of barbiturates, they were not restored by paredrinol, even though the blood pressure was raised. Lindner (4), working with isolated cats'-hearts, demonstrated that paredrinol in concentrations of 1 to 1,000,000 increased the frequency and strength of ...

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“…The blood flow in the hand and forearm was measured by plethysmographic methods (5,6). When the blood flow in the forearm was determined, the circulation to the hand was occluded by a tourniquet, distal to the forearm plethysmograph (7,8).…”

Section: Methodsmentioning

confidence: 99%

“…Other investigators have not produced as great a degree of vasodilatation from paravertebral block as they have from heating the body (6,11). They made no attempt, however, to determine whether the injection of novocain had completely destroyed all evidences of sympathetic activity.…”

Section: Commentmentioning

confidence: 99%

Blood Flow in the Hand and Forearm After Paravertebral Block of the Sympathetic Ganglia. Evidence Against Sympathetic Vasodilator Nerves in the Extremities of Man

Warren¹,

Walter²,

Romano³

et al. 1942

J. Clin. Invest.

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The Effect of Temperature on the Rate of Blood Flow in the Normal and in the Sympathectomized Hand

Cited by 162 publications

References 0 publications

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

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

MECHANISM OF THE ARTERIAL HYPERTENSION INDUCED BY PAREDRINOL (α-N-DIMETHYL-p-HYDROXYPHENETHYLAMINE

Blood Flow in the Hand and Forearm After Paravertebral Block of the Sympathetic Ganglia. Evidence Against Sympathetic Vasodilator Nerves in the Extremities of Man

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