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KMID : 0383119660140020001
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Journal of Aerospace Medicine
1966 Volume.14 No. 2 p.1 ~ p.16
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The role of catecholamines on the acceleration tolerance
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Abstract
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It has been well documented that striking functional alterations are brought about when the living organisms are exposed to high acceleratory forces in widely different aerial activities, and by the sequence of functional alterations the development of tolerance to acceleration is also produced. The numerous efforts have been made to protect the individual by increasing the tolerance to acceleratory forces, however none of the apparent mechanism for increasing the tolerance to acceleration has been established. Wood et al. (1946) and Brown et al. (1949) reported that effective protection was developed in the form of the antigravity or G-suit and this was attributed in, at least in part, its increasing effect on peripheral vascular resistance. Maciolek (1955) supported this findings in his experiment which indicated that this improvement was due to a compensatory reflex constriction of peripheral arteries and veins. Gauer (1945) suggested that the favorable effect of carbon dioxide to increase the tolerance could easily be ascribed to the increase of the peripheral vasculartonus. Subsequent studies have shown that pitrossin (Britten et al. , 1946), metaraminol (Greiner 1956) and pitressin plus atropine (Lamport et al. , 1945) could protect from the lethal effect of acceleration forces. These observations appear to indicate that increase in peripheral resistance might be pertinent for an increase in the development of tolerance to acceleration. This concept is further. supported by Brown et aL (1946) who observed that tetramethyl ammonium chloride blocks the compensatory vasomotor- reflex and thus no recovery follows. In contrast to the above results, Schock (1964) , proposed that the effectiveness in increasing acceleration tolerance related closely to function of "general adaptation mechanisms," Polls reported that 2-dimethyl-aminoethyl-p-chlorophen-oxyacetate (Lucidril) was effective to increase in tolerance and it facilitated.hypothalamic mechanism for maintaining cerebral circulation.
Although numerous factors have been reported to play an important role, in development of acceleration tolerance, the initiating mechanism is still ilnknown. Itis´ obvious, however, that the. compensatory vasoconstriction is a prominent feature -of the early stage of tolerance in experimental animals. Most authorities agree that this is protective mechanism mediated through the sympatho-adrenal system to maintain a ,blood pressure. Euler and Lundberg (1954) reported that the excretion of, epinephrine and norepinephrine in urine of human volunteers was significantly increased after exposure of g-force. Recently Goodall and Berman (1960) and Goodall (1962) strongly ;.postulated the activation of sympatho-adrenal system is most important for the development of "acceleration tolerance in animals.
In view of the. controversial reports concerning the mechanism for the increase in tolerance, the studies of the relationship between sympathetic nervous system and the development of tolerance would lead to a great, help in protecting living organismf from acceleration force. It is thus attempt to gain insight into the role of sympathetic neinous system in the development of acceleration tolerance.
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