Acute Inflammatory Edema Research Articles

Quantitative Investigations on the Composition of Acute Inflammatory Edema

Quantitative Investigations on the Composition of Acute Inflammatory Edema

An experimental model illustrating the pathogenesis of the diseases of adaptation.

WHEN the pituitary-adrenocortical axis is activated during the general adaptation syndrome, various types of inflammatory responses are suppressed. This had been demonstrated first for the so-called histamine appendicitis (1, 2), several varieties of acute inflammatory lung edema (3, 4) and the anaphylactoid inflammation caused by egg-white in the rat (5, 6). It undoubtedly holds true also for many other experimental and clinical instances of inflammation. However, subsequently it was noted that—at least under certain “conditioning” circumstances—systemic stress can also facilitate the production of inflammatory lesions (e.g., nephritis and myocarditis after exposure to cold). The adrenals were thought to play an important part in both these responses, since adrenalectomy prevented the inhibition, as well as the stimulation of inflammation by systemic stress (7). Later, when pure adrenal corticoids became available, it was observed that some, the so-called mineralo-corticoids (e.g., desoxycorticosterone) ...