Absence of Adrenocortical Stress Responses in Experimental Pyelonephritis. ∗

Abstract

Infection is a primary threat to life and higher organisms have developed an intricate set of responses to combat invaders and repair resultant tissue damage. By their very nature such responses represent homostatic disturbances likely to elicit corresponding compensatory physiological reactions. Despite the relevance of such a disturbance and response to the theory of stress as an adaptive mechanism, adrenocortical activation has been studied in relatively few diseases and little is known about the adrenocortical stress response in various stages of infection. As Selye(1) has pointed out, such studies are of particular theoretical interest because of the ambiguous survival value of the adrenocortical response in the infectious process. Indeed, the very anti-inflammatory properties of the adrenal corticoids which facilitate tissue repair and alleviate attendant symptomatology also are actions permitting spread of the infection and accentuate the danger to the host.

As part of a larger survey on enzymic and hormonal responses to stress, the present study concerns the endogenous adrenocortical response during stages of an infectious process. Experimental pyelonephritis was selected in this study for several reasons. The disease is readily produced in the laboratory rat by intravenous injection of Str. faecalis and its natural history has been studied by bacteriological (2), immunological (3), histochemical (4), and physiological (5) techniques. In-jected bacteria are rapidly cleared from the blood by the liver and spleen and are destroyed in these organs. The renal microbial population, however, increases shortly after infection and then remains relatively constant throughout the life of the animal (2+ years). During this time, the infection evolves histo-logically from an acute phase with abscesses, tissue destruction and polymorphonuclear cell infiltration, through a subacute, to a chronic stage with tissue repair, scarring and mono-nuclear cell infiltration.