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At least 703 records · Page 39Linked to original sources
PubMed1964

ACUTE INFLAMMATION IN THE RENAL CORTEX AND MEDULLA FOLLOWING THERMAL INJURY.

As determined by serial histologic study, the leukocyte component of the acute inflammatory response to thermal injury in the medulla of the kidney of rabbits was markedly delayed and diminished in intensity when compared with the response of the cortex. Similar differences in granulocyte mobilization between cortex and medulla were seen following the inoculation of bacteria. Hydronephrosis produced by ureteral ligation had no discernible effect upon the inflammatory response in either cortex or medulla following thermal burns. The susceptibility of the cortex to E. coli infection was markedly enhanced during leukopenia induced by nitrogen-mustard. These results suggest that deficiencies in granulocyte mobilization play an important role in the increased susceptibility of the renal medulla to bacterial infection.

Animals↗
PubMed1965

ENDOTOXEMIA AND ADRENAL HEMORRHAGE. A MECHANISM FOR THE WATERHOUSE-FRIDERICHSEN SYNDROME.

An experimental model that produces adrenal cortical hemorrhage with endotoxin has been described. When stimulated by thorotrast, endotoxin, or its tropic hormone (ACTH), the adrenal cortex is susceptible to the development of a hemorrhagic reaction during endotoxemia. The hemorrhagic reaction resembles that described in the Waterhouse-Friderichsen syndrome. A pathophysiologic mechanism for the occurrence of adrenal hemorrhage occurring during acute sepsis is presented. Increased metabolic activity associated with the production of corticosteroids seems to make the adrenal cortex susceptible to endotoxin-induced hemorrhage. Adrenal hemorrhage observed during sepsis, as in the Waterhouse-Friderichsen syndrome, may be attributable to endotoxemia occurring during or shortly after stimulation of the adrenal cortex by infection. Significant differences between adrenal cortical hemorrhage and the Shwartzman phenomenon are described.

Adrenal Gland Diseases↗
PubMed1965

THE PRESENCE OF ENDOGENOUS PYROGEN IN NORMAL RABBIT TISSUES.

Saline extracts of homogenized, uninfected, rabbit tissues produced febrile responses when injected intravenously into rabbits. Extracts of muscle, lung, and heart evoked fevers that were similar to those induced by leucocyte pyrogen; extracts of spleen, liver, and kidney caused more sustained fevers. The minimal pyrogenic dose appeared to be between 1.5 and 3 gm wet weight of tissue. Evidence is presented that neither Gram-negative bacterial endotoxin nor polymorphonuclear leucocytes (circulating or sequestered in the tissues) can be implicated as the source of pyrogen in tissue extracts. It seems likely, therefore, that a pyrogenic material of truly endogenous origin is widely distributed in tissues. Tissue pyrogen appears to be a large molecule which is relatively resistant to treatment with acid but not with alkali. Possible pathological roles for this endogenous agent (or agents) are briefly indicated.

Animals↗
PubMed1965

A ROLE OF POLYMORPHONUCLEAR LEUKOCYTES AND COMPLEMENT IN NEPHROTOXIC NEPHRITIS.

In acute nephrotoxic nephritis, polymorphonuclear leukocytes (polymorphs) accumulated in large numbers in the glomeruli in the first 12 hours. The endothelial cells were dislodged by the polymorphs which then came to lie immediately adjacent to the glomerular basement membranes. Ultrastructural changes in neither polymorphs nor basement membranes were observed. Depletion of polymorphs in both rats and rabbits prevented the development of proteinuria. This occurred when doses of nephrotoxic globulin were employed that produced proteinurias of as much as 1800 mg/kg/24 hours in intact rabbits, or enough to yield near maximal immediate proteinuria in intact rats. In addition, measurable glomerular damage was frequently averted until the onset of the secondary stage of NTN. Controls indicated that the polymorph depleted animals exhibited minimal non-specific changes in the blood, that the ability of their vascular beds to react to stimuli was not affected, and that deposition of nephrotoxic antibody and C' in the glomeruli was not inhibited. Elimination of polymorphs from the circulation was only partially effective in preventing glomerular damage when large doses of nephrotoxic globulin were used. This indicated that under these circumstances, a polymorph independent glomerular injury may also take place in first stage nephrotoxic nephritis. An indirect role of C', i.e., the accumulation of polymorphs, in bringing about glomerular injury in first stage nephrotoxic nephritis was apparent. When rabbit nephrotoxic globulin was injected into rats depleted of C', or when duck nephrotoxic globulin that fixed C' poorly was injected into normal rats, C' failed to bind with the antibody along glomerular basement membranes and polymorphs did not accumulate.

Animals↗