intestinal peristalsis, fatigue, malaise and mental depression. In general, the
emesis among the symptoms is often left as the only simple and objective criterion
in detecting motion sickness in experimental pleasures. For this reason, the
effectiveness of prophylaxis or therapy is generally based upon a decrease in
emesis although vomiting is not a necessary consequence of motion sickness.
Nevertheless, very few studies of gastric secretion in relation to motion
sickness, have been made in recent years. Gastric juice is difficult to collect
during motion sickness, because of vomiting behavior. In early Rosenbach (1896) and
Pincussen (1912) reported gastric inhibition was observed during motion sickness.
However, the findings of Havelburg (1921) and Saito (1930) are cantradictory.
Present study is undertaken to determine response of gastric secretion to
rotatory stimulus in rats and explore some insight of the sickness with drugs used
in motion sickness as well as labyrinthine interferences.
Methods:
1) Experimental materials
Male albino its, weighing approximately 250 grams, were used throughout this
experiment. The animals were maintaind in a controlled environment (20℃) and were
given basal diet for a period of two weeks to acclimatize them to their
environment.
Throughout the experimental period the animals were housed singly in cages with
raised bottoms of wide mesh to avoid coprophagy.
2) Experimcntal group
The animals were starved for twenty-feur and forty-eieht hours depending upon the
etperimental schedule.
The pyloric ligature was placed by the procedure described by Shay et al. (1945).
Under the light ether anesthesia, ligation of the pylorus was done through a
midline incisien of 2-3 cm inferior to the xiphoid process. In the first series of
experimental group, responses of gastric secretion during and after exposure to
rotatory stimuli were observed. In the second series of the experiment, effect of
several agents or maneuvers in the response of gastric secretion in rats expgsed
rotatory stimuli for 5 hrs following 24 hrs starvation were observed.
In obis sub-groups of this experiment, the vagotomy was performed in the
following procedure, e.g., the thoracic wall was incised and the pleural cavity
opened. The vagus nerve, which with the associated vessels runs along the right and
left border of the esophagus, was cut. In these associnated, the occurence of
vagotomy was confirmed by talc observation of dyspnes.
Labyrinthectomy was performed in some of the experimental groups. After the skin
incision was made the auricular attachment the auricle was retracted forward.
Incision was then made into the cartilaginous portion of the external auditory
meatus and the area from the oval window to the vestibule was curetted. Under the
anesthesia, the rats were killed by exanguination from the femoral artery. The
stomach was removed, timmed free of adipose tissue, and then opened by cutting
along the greater curvature.
3) Rotatory procedure
The albino rat was accelerated on the electrically driven turntable to a constant
angular velocity of 80 r.p.m. which was maintained for 60 min. The nature of the
postrotatory motion sickness was observed visually.
4) Caloric test
Caloric test was performed according to the Herniksson'a method (1962) to confirm
whether the function of labyrinth is intact or not at the end of 45 days after
daily injection of streptomycin(1.5mg/kg).
5) Gastric juice analysis
The gastric juice was collected. The specimens were then washed under tap water.
The volumes of solid matter and juice were noted. Free and total acid of the juice
were titrated in the usual manner using Topfer's an? phenolphthalein as the
indicators and N/2O NaOH for titration. Amount of pepsin out put was measured by
Anson's method (1938) that was used to measure the amount(mg) of tyrosine derived
frets hemoglobin.
Summary and Conclusion:
Experimental motion sickness was induced in rata exposing to rotatory stimulus
(80 r.p.m. for 5 hrs) and the influence of the stimuli upon gastric secretion was
investigated with and without drugs using motion sickness or labyrinthine
interferences and obtained following results.
1) Gastric secretion was inhibited in rats exposed to rotatory stimulus, e. g.,
both the volume and acidity were reduced significantly and pepsin content was
reduced but little when comparing to unexposed control animals.
2) Bretylium which is known to interfere selectively the release of catecholamine
from sympathetic ending, was blocked but less extent the inhibitory response of
gastric secretion to rotatory stimulus. Epinephrine alone exerted an inhibition of
gastric secretion in an unexposed control animal.
3) Vagotomy as well as pretreatment of scopolamine or dipbenhydramine, an
anticholinergic agent used in motion sickness, was resulted in an inhibition of
gastric secretion, and abolished the symptoms and gastric response to rotatory
movement, however, the rata exposed to the stimulus were showed a slight increase
of the secretion comparing to the unexposed animals.
4) Pretreatment of chlorpromazine was little effective to block the symptoms and
response of gastric secretion to rotatory movement.
5) The symptoms and response of gastric secretion to rotatory movement were
completely abolished following labyrinthectomy or when labyrinthine function was
destroyed by streptomycin.
These data indicate that exposure to rotatory stimulus bring an inhibition of
gastric secretion via stimulation of beth sympathetic and parasympathetic nerves
through directly emetic center which is excited by labyrinthine stimulation in
response of rotatory movement.
[영문]
Motion sickness is a syndrome consisting anorexia, drowsiness, pallor, epigastric discomfort, cold sweat, nausea, salivation, vomiting, headache, increased intestinal peristalsis, fatigue, malaise and mental depression. In general, the emesis among the symptoms is often left as the only simple and objective criterion
in detecting motion sickness in experimental pleasures. For this reason, the effectiveness of prophylaxis or therapy is generally based upon a decrease in emesis although vomiting is not a necessary consequence of motion sickness.
Nevertheless, very few studies of gastric secretion in relation to motion sickness, have been made in recent years. Gastric juice is difficult to collect during motion sickness, because of vomiting behavior. In early Rosenbach (1896) and Pincussen (1912) reported gastric inhibition was observed during motion sickness.
However, the findings of Havelburg (1921) and Saito (1930) are cantradictory.
Present study is undertaken to determine response of gastric secretion to rotatory stimulus in rats and explore some insight of the sickness with drugs used in motion sickness as well as labyrinthine interferences.
Methods:
1) Experimental materials
Male albino its, weighing approximately 250 grams, were used throughout this experiment. The animals were maintaind in a controlled environment (20℃) and were given basal diet for a period of two weeks to acclimatize them to their environment.
Throughout the experimental period the animals were housed singly in cages with raised bottoms of wide mesh to avoid coprophagy.
2) Experimcntal group
The animals were starved for twenty-feur and forty-eieht hours depending upon the etperimental schedule.
The pyloric ligature was placed by the procedure described by Shay et al. (1945).
Under the light ether anesthesia, ligation of the pylorus was done through a midline incisien of 2-3 cm inferior to the xiphoid process. In the first series of experimental group, responses of gastric secretion during and after exposure to rotatory stimuli were observed. In the second series of the experiment, effect of
several agents or maneuvers in the response of gastric secretion in rats expgsed rotatory stimuli for 5 hrs following 24 hrs starvation were observed.
In obis sub-groups of this experiment, the vagotomy was performed in the following procedure, e.g., the thoracic wall was incised and the pleural cavity opened. The vagus nerve, which with the associated vessels runs along the right and left border of the esophagus, was cut. In these associnated, the occurence of
vagotomy was confirmed by talc observation of dyspnes.
Labyrinthectomy was performed in some of the experimental groups. After the skin incision was made the auricular attachment the auricle was retracted forward.
Incision was then made into the cartilaginous portion of the external auditory meatus and the area from the oval window to the vestibule was curetted. Under the anesthesia, the rats were killed by exanguination from the femoral artery. The stomach was removed, timmed free of adipose tissue, and then opened by cutting along the greater curvature.
3) Rotatory procedure
The albino rat was accelerated on the electrically driven turntable to a constant angular velocity of 80 r.p.m. which was maintained for 60 min. The nature of the postrotatory motion sickness was observed visually.
4) Caloric test
Caloric test was performed according to the Herniksson'a method (1962) to confirm whether the function of labyrinth is intact or not at the end of 45 days after daily injection of streptomycin(1.5mg/kg).
5) Gastric juice analysis
The gastric juice was collected. The specimens were then washed under tap water.
The volumes of solid matter and juice were noted. Free and total acid of the juice were titrated in the usual manner using Topfer's an? phenolphthalein as the indicators and N/2O NaOH for titration. Amount of pepsin out put was measured by Anson's method (1938) that was used to measure the amount(mg) of tyrosine derived frets hemoglobin.
Summary and Conclusion:
Experimental motion sickness was induced in rata exposing to rotatory stimulus (80 r.p.m. for 5 hrs) and the influence of the stimuli upon gastric secretion was investigated with and without drugs using motion sickness or labyrinthine interferences and obtained following results.
1) Gastric secretion was inhibited in rats exposed to rotatory stimulus, e. g., both the volume and acidity were reduced significantly and pepsin content was reduced but little when comparing to unexposed control animals.
2) Bretylium which is known to interfere selectively the release of catecholamine from sympathetic ending, was blocked but less extent the inhibitory response of gastric secretion to rotatory stimulus. Epinephrine alone exerted an inhibition of
gastric secretion in an unexposed control animal.
3) Vagotomy as well as pretreatment of scopolamine or dipbenhydramine, an anticholinergic agent used in motion sickness, was resulted in an inhibition of gastric secretion, and abolished the symptoms and gastric response to rotatory
movement, however, the rata exposed to the stimulus were showed a slight increase of the secretion comparing to the unexposed animals.
4) Pretreatment of chlorpromazine was little effective to block the symptoms and response of gastric secretion to rotatory movement.
5) The symptoms and response of gastric secretion to rotatory movement were completely abolished following labyrinthectomy or when labyrinthine function was destroyed by streptomycin.
These data indicate that exposure to rotatory stimulus bring an inhibition of gastric secretion via stimulation of beth sympathetic and parasympathetic nerves through directly emetic center which is excited by labyrinthine stimulation in response of rotatory movement.