| Animal restraint can be considered as a form of motor restriction, which enables containment of the animal for the purpose of preventing injury when administering medications or performing other procedures. During one form of restraint in neonatal foals a profound change in mentation and physical tone has been noted. The purpose of this study was to evaluate what had been initially called "the flopping reaction in neonatal foals". This phenomenon frequently occurs in response to firm body pressure restraint, the physiologic mechanisms of which are incompletely understood.;Upon application of a restraint device the phenomenon was propagated and following habituation measurements were made before and during restraint to investigate changes in physiological parameters including: vital signs, blood gas parameters; blood levels of cortisol, neurosteroids, adrenocorticotropic hormone and beta-endorphin. Electroencephalographic evaluations were performed in order to determine brain activity. A square pulse stimulator was used to quantify changes in pain threshold.;With this restraint foals lay down and stayed in lateral recumbency while exhibiting relaxed, somnolent behavior. Electroencephalographic recordings revealed wave patterns consistent with non-rapid eye movement sleep. Vital parameters uniformly decreased during the procedure and foals exhibited significantly lower heart, respiratory rates and rectal temperatures. Venous blood gas profiles did not show significant changes in either the partial pressure of carbon dioxide, oxygen or venous blood pH, and values remained within reference ranges. Foals had significantly elevated plasma adrenocorticotropic hormone, dihidroepiandrostenedione-sulphate and androstenedione levels during restraint compared to levels at rest. Foals exhibited significantly increased tolerance to noxious stimuli during the restraint, however correlation with increased levels of circulating beta-endorphin was not found.;We conclude that restraint activated the hypothalamo-pituitary-adrenal axis and favored non-rapid eye movement sleep with decreased vital parameters and lower metabolic rate. The squeeze induced somnolence (SIS), as we named it, may be a remnant of an autonomic signal originating from parturition, where compression of the fetus in the birth canal likely initiates hypotonia and activation of hypothalamo-pituitary-adrenal-axis in order to prevent damage and prepare newborns for extrauterine life. Further studies are warranted to elucidate exact receptor pathways that may be involved in SIS. |
