Lipoid and Hemorrhagic Changes in Adrenal Cortex Following Traumatic Shock. ∗

It has been shown that if profound and fatal shock is to be obtained in the intact dog by traumatization, the severity of tissue injury must be very much greater than is required to induce shock symptoms in the equally healthy and vigorous animal lacking adrenal glands. 1 Evidence is presented indicating that the extreme susceptibility of the adrenalectomized dog to shock following trauma is largely due to the absence of one of the mechanisms concerned with the maintenance of normal blood volume, namely, the adrenal cortex. Data are presented here which show that the adrenal cortex of intact dogs dying from traumatic shock presents histological evidence of considerable impairment.

The lipoid studies were made on frozen sections of the adrenals variously stained with 2% osmic acid, Scharlach R, and Sudan III. For the study of adrenal cortical hemorrhages and other histological details, paraffin sections were stained with iron hematoxylin and eosin.

The dogs in both the normal and experimental groups were rigorously selected and only mature, well-nourished animals were employed. Deep nembutal and ether anesthesia was used and care was taken that the animals suffered no pain. Shock was induced by traumatization of the muscles of the hind limbs. 1 Periodic blood-pressure readings were taken by direct needle-puncture into the femoral artery and used as a criterion for the presence and duration of shock. 2 Following the temporary fall and rise of blood-pressure characteristic of primary shock, a subsequent and more gradual fall in pressure to 50 mm., or less, indicated the unquestioned presence of secondary shock.

A definite depletion in adrenal cortical lipoid occurs in dogs dying from traumatic shock as shown in Table I. Three dogs (11T, 12T, 13T), whose blood-volumes were temporarily increased and survival periods lengthened by single intravenous injections of saline showed marked lipoid depletion of the adrenal cortex at autopsy.