Participation of VEM and VDM Mechanisms in Drum Shock and in Development of ‘Resistance’ to Drum Trauma

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Abstract
Rats were made resistant to trauma in the Noble-Collip drum by repeated sublethal exposures. Such animals can withstand 1000 drummings without fatal outcome, whereas normal rats, subjected to 650 turns, in the drum, invariably go into fatal shock(85%). A study was made of the mechanisms of the angiotropic principles, VEM and VDM, in such animals to determine whether these factors undergo changes which are compatible with the development of resistance to trauma. In rats made resistant to the drum procedure there occurs, in association with the development of resistance, specific alterations in the hepatic VDM mechanisms which differentiate the response of these animals from those of control rats. There is a virtual absence of VDM in the blood following 1000 drummings, a minimal amt. of VDM in the liver, a persistence of an effective hepatic VDM inactivation system and a normal or slightly increased reactivity of the mesenteric vascular bed. In vitro studies indicate that the resistant rat liver can inactivate larger amts. of VDM in an equal period of time. Also, the liver of resistant rats inactivates VDM more rapidly than livers of control animals. In contrast with the deterioration of the VDM inactivation mechanisms of control rats following 2 hrs. of anoxia in vitro, the resistant rat livers preserve their capacity to inactivate VDM on restoration to aerobic conditions. The renal VEM component does not appear to play a significant role in the development of resistance to drum trauma.