Abstract
The circulation in the everted, transillumined cheek pouch of adrenalectomized hamsters and the microscopic appearance of the small blood vessels remained essentially normal until twenty-four hours before death at five to seven days. The rate of blood flow then diminished and stasis developed. In terminal stages of adrenal insufficiency, the arterioles were frequently constricted. The threshold of the vascular smooth muscle to direct electrical stimulation with a microelectrode remained low as compared with normal values, but the threshold to topically applied nor-epinephrine increased slightly. An increased susceptibility to petechial formation from negative pressure occurred at one to three days after adrenalectomy, but an increased resistance developed terminally, paralleling the onset of vasoconstriction. Cortisone acetate (5 mg. daily doses) produced arterial vasoconstriction in the cheek pouch of normal hamsters with intact adrenal glands, persisting from an early period until death at fourteen to thirty days. The threshold of the vascular smooth muscle to the microelectrode test and also to the norepinephrine test was elevated. The persistent vasoconstriction may explain clinical findings such as the tendency for infection to occur. Furthermore, vasoconstriction may also explain the increased resistance to petechial formation induced by negative pressure. A significant finding may be the sticking of leukocytes to the endothelial lining of venules and the concomitant leukocytosis during prolonged cortisone treatment. DCA (1 mg. daily plus 1 per cent saline) produced no significant changes in the microscopic appearance of cheek pouch blood vessels until the period of severe weight loss prior to death. An increased vascular fragility persisted during DCA administration as indicated by the negative pressure test. Although vascular spasm was observed occasionally, DCA did not produce vasoconstriction comparable to that caused by cortisone.
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