(The) influence of rotatory movement on the tissue catecholamines in rats
It has been well established that motion sickness is a symptom complex resulted from generalized responses of organisms to certain characteristic forms of motion. The main symptoms are characterized by epigastric distress, drowsiness, dizziness, nausea, vomiting and headache. The extensive studies have been reported concerning the protection of the individual aganist motion sickness; however, the mechanism for the development of motion sickness has not been established. Floureas (1828) reported that the disturbance of equilibrium in the body was probably attributed in the stimulation on a certain portion of inner ears.
Kreidl (1902) further suggested that bilateral section of the auditory nerve rendered animals immune to motion sickness. Subsequently, other investigators (Johnson et al., 1962; Babkin and Bornstein, 1943; wang and Chinn, 1956) have reported experiments in which animals were found to be immune to motion sickness following bilateral labyrinthectomy. Furthermore, it has been demonstrated that the experimental motion sickness is produced by stimulating on the otolith organs (Egmond et al., 1954; Morton et al., 1947) and on the semicircular canals (Johnson, et al., 1951; Johnson and Taylor, 1961) in labyrinth.
On the basis of these observations, it has been generally accepted that the labyrinth contains the receptor(s) which, when stimulated appropriately, give rise to motion sickness.
Recently Hasegawa (1949) and others postulated that motion sickness is the secondary phenomenon resulted in the activation of sympathetic nervous system mediated through the labyrinthine stimulation and further suggested that the role of sympathetic nervous system is more important in the development of motion
sickness rather than a generalized imbalance of the autonomic nervous system. This concept is supported by Mood (1966) who observed that the intact sympathetic nervous system plays a important role in the development of acceleration tolerance and concomitantly showed that the tissue catecholamines were significantly reduced following exposure of animals to rotatory acceleration.
In an attempt to explore the mechanism responsible for the depletion of tissue catecholamines in motion sickness, the present study was designed to examine the possible relationship between the function of labyrinth and the role of sympathetic nervous system in the experimental motion sickness produced by rotatory movement.
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 weeks to acclimatize them to their environment. The rat was accelerated on the electrically driven turntable to a
constant angular velocity of 80 r.p.m. which was maintained for 60 minutes. The nature of the postrotatory motion sickness was observed visually. Caloric-test was performed according to the Herniksson (1962) method to confirm whether the function of labyrinth is intact or not at the end of two months after daily injection of streptomycin (15mg/100g). The catecholamine contents of various organs were determined by the Aminco-Bowman spectrophotofluorometric procedure described by Shore and Olin(1958).
1. The catecholamine content was examined in the brain, heart and adrenal gland of rats exposed to the rotatory movement for a various length of time. The catecholamines in brain, heart and adrenal gland rapidly reduced to 60%, 63% and 46% below normal, respectively, at the end of following one hour the exposure to
rotatory movement and returned to normal level within three hours. Concomitantly the main symptoms including drowsiness, nystagmus, ataxia, vomiting and diarrhea which were associated with the rotatory movement were most intensive at the end of
one hour after the begining of rotation.
2. Rats were pretreated with streptomycin which interferes selectively with the function of labyrinth. Two months after the intramusculary injection of streptomycin (15mg/100g), the animals were exposed to rotatory movement by the procedure described previously. The pretreatment of streptomycin prevented completely from the depletion of tissue catecholamines in brain, heart and adrenal gland and also abolished the symptoms associated with the rotatory movement.
3. Rats were pretreated with dramamine which is known to interfere with the function of labyrinth. The pretreatment of dramamine (10mg/100g) also blocked completely the depletion of tissue catecholamines. However, the postrotatory nystagmus and atatxia were temporarily appeared after the terminal of rotation.
4. Rats were premedicated with scopolamine which blocks peripheral cholinergic receptors. At the end of one hour after the injection of scopolamine (0.1mg/100g) the animals were exposed to the rotatory movement. The pretreatment of scopolamine
did not prevent the reduction of tissue catecholamines in brain, heart and adrenal gland. All the symptoms of motion sickness, except nystagmus and diarrhea which, were somewhat alleviated, persisted as those observed in normal animals.
5. Rats were pretreated with bretylium which interferes selectively with the release of catecholamines from sympathetic nerve endings. Thirty minutes after the intramuscular injection of bretylium (20.mg/100g) the animals were exposed to the
rotatory movement. The reduction of tissue catecholamines in both of brain and heart was markedly inhibited, but not that of adrenal gland by the pretreatment of bretylium. The symptoms presented were generally mild and vomiting was completely
6. The intravenous administration of chlorpromazine (0.1mg/100g) slightly but significantly prevented the reduction of tissue catecholamines in brain and heart without affecting the release of catecholamines from adrenal gland. All the symptoms associated with rotatory movement were moderately suppressed as those observed in bretylium-pretreated animals. From the above results, the reduction of tissue catecholamines is presumed to be caused largely by activation of sympathetic nervous system mediated through the labyrinthine stimulation in rotatory movement.