ROLE OF ADRENALS IN PRODUCTION OF TRAUMATIC SHOCK IN RATS1

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Abstract
The development of shock in rats as a result of trauma to hind legs occurs when there is a quantitative insufficiency of adrenal function (since both unilaterally and bilaterally adrenalectomized rats are sensitive to this type of shock) and when the rate of fluid loss from the vascular system is rapid. When the loss of fluid into the area of injury is sufficiently slow, adrenalectomized rats may withstand trauma without mishap. If the rate of fluid loss is rapid, a quantitatively adequate degree of adrenal function is necessary to set protective compensatory reactions into motion. Studies of the capillary permeability changes associated with shock in injured adrenalectomized rats revealed that capillary porosity to trypan blue was normal in all tissues except in the damaged limb and possibly in skin. This increased capillary permeability in the local area of injury, however, was manifest for only a short period of time, presumably because the injured capillaries were blocked mechanically. Reinvestigation of the effect of anoxia upon capillary porosity revealed that generalized asphyxia (produced by rebreathing air) terminating in death was without effect on the permeability of the capillaries of any tissue. Studies in skin and muscle revealed that the capillaries in these tissues are able to withstand severe local anoxia for prolonged periods of time without permeability increase. Only by local asphyxiation for 4 or more hrs. was it possible to demonstrate that anoxia increases capillary permeability.

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