(The) role of catecholamine on the acceleration tolerance
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 the effective protection was developed in the form of the antigravity or G-suite 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 vascular tonus. Subsequent studies have shown that pitressin (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." Polis 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 unknown.
It is 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
organism from acceleration force. It is thus attempt to gain insight into the role of sympathetic nervous system in the development of acceleration tolerance.
Male albino rats, weighing approximately 150 grams, were used throughout this experiment. The animals were maintained in a controlled environment (25℃) and were given basal diet for a period of two week to acclimatize them to their environment.
Tolerance to acceleration stress (+15G) was evaluated using a medium animal centrifuge. The end point for tolerance to +15G was ECG monitoring as described by Sipple and Polis(1959). The catecholamine contents of various organs were determined by the Aminco-Bowman spectrophotofluorometirc procedure described by
Shore and Olin (1958).
1. The intraperitoneal injection of reserpine (0.4mg/100g) deplets almost completely the myocardial catecholamines of rats within 24 hours. At the end of 24 hours after the injection of reserpine, the animals were exposed to positive acceleration force. The survival time of these animals was significantly reduced to 228.75 seconds by the pretreatment of reserpine.
2. Rats were pretreated with bretylium which interferes selectively the release of catecholamines from sympathetic nerve endings. Four hours after being given in intramusculary injection of bretylium (2.0 mg/100g) the animals were exposed to positve acceleration by the procedure described previously. The heart rate of these animals was also markedly reduced to one fourth of normal animals at the end of two minutes after beginning of experiment, however this is not so pronounced as that of guanethidine treated animals. Although, the pretreatment of bretylium hastened the death of animal, the survival time of guanethidine treated animals was far below than that of bretylium treated animals.
3. Rats were premedicated with guanethidine (25 mg/100g) which blocks initially the release of catacholamine and later depletes catecholamine from sympathetic nerve endings. At the end of 20 hours after the injection of guanethidine, the animals were exposed to positive acceleration force. The heart rate of these
animals was most markedly decreased to almost one sixth of initial heart rate at the end of two minutes and thereafter heart rate was declined gradually until death. The average survival time for these animals was 144.44 seconds, indicating that the pretreatment of guanethidine hastens the death due to exposure of
4. The injection of norepinephrine (0.1 mg/100g) markedly elevated the concentration of myocardial catecholamines in rats. At the end of one hour after injection of norepinephrine, the animals were exposed to the positive acceleration force by the procedure described previously. Heart rate was rapidly reduced to one third of initial rate at two minutes after exposure, but this decrease in heart rate was not significantly different from that of normal animals. The average survival time for normal animals and norepinephrine treated animals were 267.38 seconds and 350 seconds, respectively. This indicates that pretreatment of
norepinephrine appears to prolong the death due to exposure of acceleration force. The myocardial catecholamine content of these animals was markedly depleted as those of normal animals at the end of death.
5. SKF-385(2.0 mg/100g) as a potent monoamine oxidase inhibitor was injected intraperitoneally into the rats. Marked decrease in heart rates of these animals was similar to those seen in normal animals, thereafter the heart rate was gradually decreased until death. The average survival time for these animals was 255.00 seconds which is not significantly different from the noraml animals.
6. Rats were given norepinephrine (0.1 mg/100g) intraperitoneally 16 hours afer the administration of SKF-385 (2.0mg/100g). At the end of one hour after injection of norepinephrine, the animals were exposed to the positive acceleration force.
Marked decrease in heart rates of these animals was similar to those seen in norepinephrine, thereafter the heart rates were gradually decreased until death.
The average survival time for these animals was 278.90 seconds which is not significantly different from the normal animals.
Form the above results, it is reasonable to assume that the intact sympathetic nervous system plays an important role in the development of acceleration tolerance.