naloxone and Motion-Sickness

This study evaluated the time course to Malaise III in human subjects given naloxone and placebo with a double-blind cross-over protocol in the prevention of motion sickness induced by exposure to coriolis stimulation in a rotating chair. During naloxone tests, subjects reached the designated level of sickness sooner than during the placebo testing (significance greater than 0.05) and their discomfort lingered for up to 3 d--a feature not seen with the placebo. This implicates endogenous opiates with an endogenous protective or adaptive role in the control of motion sickness. It is suggested that when subjects experience endogenous opioid withdrawal, such as post exercise, they could be in a state of neuron hypersensitivity, and thus more prone to any form of exogenous emetic stimuli. Greater tolerance to motion stresses could be experienced in subjects whose endorphins were repeatedly elevated, thus avoiding a hypersensitivity state from endogenous opiate withdrawal. Subjects whose endorphins have not been elevated in the first instance cannot secondarily suffer opioid abstinence.

Topics: Adult; Double-Blind Method; Endorphins; Humans; Male; Motion Sickness; Naloxone; Random Allocation; Regression Analysis; Rotation

Doses of naloxone far below those which elicit emesis increase the sensitivity to motion sickness. In order to evaluate the possible interaction with broad spectrum antiemetics, low doses of naloxone were tested alone and in combination with 8-hydroxy-2-(di-n-propylamine)tetralin (DPAT), fentanyl and the NK1 antagonist CP-99994. A modified autonomic symptom rating scale was unaffected by any drug and thus considered of little value. Fentanyl and NK1 antagonists decreased the duration of the retch/vomit sequence. Naloxone alone and in combination with each of the drugs increased the duration of retching/vomiting. Naloxone also increased the number of vomiting sequences. The results are interpreted in terms of possible site(s) of action of the antiemetic drugs.

Topics: 8-Hydroxy-2-(di-n-propylamino)tetralin; Animals; Antiemetics; Cats; Dose-Response Relationship, Drug; Drug Interactions; Emetics; Female; Fentanyl; Models, Animal; Motion Sickness; Naloxone; Neurokinin-1 Receptor Antagonists; Physical Stimulation; Piperidines; Vomiting

The aim of the present study was to investigate an opioid receptor involvement in the adaptation response to motion sickness in Suncus murinus. Different groups of animals were treated intraperitoneally with either saline, morphine (0.1 and 1.0 mg/kg), naloxone (1.0, 10.0 and 5.0 mg/kg) or a combination of naloxone plus morphine in the absence or 30 min prior to a horizontal motion stimulus of 1 Hz and 40 mm amplitude. For the study of adaptation, different groups received saline on the first trial, and in subsequent trials (every 2 days) they received either saline, naloxone (1.0 and 10.0 mg/kg, i.p.) or morphine (0.1 mg/kg, i.p.) 30 min prior to the motion stimulus. Pretreatment with morphine caused a dose-related reduction in emesis induced by a single challenge to a motion stimulus. Pretreatment with naloxone alone did not induce emesis in its own right nor did it modify emesis induced by a single challenge to a motion stimulus. However, pretreatment with naloxone (5.0 mg/kg, i.p.) revealed an emetic response to morphine (P<.001) (1.0 mg/kg, i.p.) and antagonised the reduction of motion sickness induced by morphine. In animals that received saline or naloxone (1.0 mg/kg), a motion stimulus inducing emesis decreased the responsiveness of animals to a second and subsequent motion stimulus challenge when applied every 2 days for 11 trials. However, the animals receiving naloxone 10.0 mg/kg prior to the second and subsequent challenges showed no significant reduction in the intensity of emesis compared to the first trial. The data are revealing of an emetic potential of morphine when administered in the presence of a naloxone pretreatment. The administration of naloxone is also revealing of an additional inhibitory opioid system whose activation by endogenous opioid(s) may play a role in the adaptation to motion sickness on repeated challenge in S. murinus.

Topics: Adaptation, Psychological; Analgesics, Opioid; Animals; Female; Ganglionic Stimulants; Male; Morphine; Motion Sickness; Naloxone; Narcotic Antagonists; Nicotine; Receptors, Opioid; Shrews; Vomiting

The effects of body rotation in a horizontal plane and the opiate antagonist, naloxone, on the nociceptive responses and the feeding behavior of male mice were examined. In the first experiment the mice were rotated (70 rpm, schedule of 15 sec on; 5 sec off) for 60 minutes or exposed to sham rotation for the same duration. Midway through the rotation or sham procedure the mice were either injected with naloxone (1 mg/kg) or isotonic saline. At the end of the 60-minute treatment period the animals were placed on a warm surface (47.5 degrees C) and their latency to show a foot-licking response was measured. The rotation procedure produced a significant (p less than 0.01) increase in response latency in the saline-injected mice and the naloxone injections blocked this analgesic effect. This finding provides evidence for opioid involvement in the rotation-induced analgesia. In Experiment 2 mice on a food restriction schedule were rotated (70 rpm, 15 sec on; 5 sec off) or sham exposed for 60 minutes. Midway through this treatment period the mice were either injected with naloxone (1 mg/kg) or isotonic saline. Following the treatment period the mice were given access to food for 2 hours. The rotation procedure produced a significant (p less than 0.01) reduction in feeding (anorexia) in the first 30 minutes of food access for the saline-injected mice. Injections of naloxone significantly (p less than 0.05) enhanced the rotation-induced anorexia. These experiments demonstrate that rotation-induced analgesia in mice is blocked by the opiate antagonist, naloxone, whereas rotation-induced anorexia is not.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Analgesia; Animals; Anorexia; Feeding and Eating Disorders; Feeding Behavior; Male; Mice; Motion Sickness; Naloxone; Rotation

Investigations were performed with 19 healthy male volunteers to specify a possible role of endogenous opioid peptides in the pathogenesis of motion sickness. For this purpose the test subjects were administered naloxone, a specific antagonist of opiates and opioids, before rotation and during rotation in a BU-4 armchair at a rate of 30 rpm. In addition, the content of beta-endorphin in blood plasma was measured. It was discovered that naloxone exerts both prophylactic and therapeutic effects as regards the simulated motion sickness. In this respect it was more efficacious than the reference drug scopolamine. After rotation there was a significant increase in the beta-endorphin content in the blood plasma of the test subjects. It is assumed that endogenous opioid peptides (in particular beta-endorphin) may be directly involved in the genesis of vestibulo-vegetative disorders in motion sickness.

Topics: Acceleration; Adult; beta-Endorphin; Blood Pressure; Coriolis Force; Endorphins; Heart Rate; Humans; Male; Middle Aged; Motion Sickness; Naloxone; Respiration; Rotation; Scopolamine; Time Factors

Subcutaneous injections of naloxone in a total dose of 0.4 mg or greater one hour before a swing stimulus increased the frequency of motion sickness symptoms and shortened the latency of retching and vomiting.

Topics: Animals; Cats; Female; Motion Sickness; Naloxone; Reaction Time