- 1 9 5 1 - 



who were receiving adequate hemotherapy and fluids, the renal 

 plasma flow, glomerular filtrate rate and fraction excretion were 

 determined. An analysis of both arterial and venous blood was 

 added. There were changes in plasma protein concentration. The 

 possibility that there is increased thyroxine production in burns 

 was suggested, and certain similarities to results obtained through 

 DOCA were noted. In fevers, the maintenance of glomerular fil- 

 tration is accompanied by effective increases in blood plasma flow. 

 Reduction of filtration factors has been reported. Pyrogen, 

 without actual production of fever, increases the renal plasma 

 flow but does not affect glomerular filtration. Filtration 

 fractions are decreased, 



715. KIRKENDALi, W. M,, HODGES, R, E, and JANUARY, L. E. 



The ACTH-like effect of fever in man 



Jo Lab, & Clin, Med, 37,' 771-779, 1951 ^ 



In studies planned to determine whether or not eosinopenia ob- 

 served after induced fever is caused by liberation of ACTH, 

 elevation of temperature was induced in 27 afebrile patients, 

 all with normally-functioning adrenal and pituitary glands. 

 Fever was Induced by either (1) I5 to 100 million typhoid or- 

 ganisms in vaccine (2) moist air fever cabinet or (3) an endo- 

 genous polysaccharide of Proteus vulgaris (PV PYROMEN) . The 

 last-named was administered intravenously in 25 to 100 gamma 

 doses. 



The effects of aspirin, dibenamlne and chlor-trimeton before and 

 after injection of Pv PYROMEN were observed in four patients. 

 Determinations of uric acid/creatinine ratios, circulating leuko- 

 cytes, corticosteroid excretion and rectal temperatures were em- 

 ployed in evaluating the results obtained. 



The blood leukocyte changes following fever induced by all of 

 the methods employed simulated those produced by ACTH with three 

 major differences (1) neutrophilia and lymphopenia were greater 

 after induced fever (2) eosinopenia occurred later than when 

 ACTH was administered, particularly when typhoid vaccine was the 

 pyrogenic agent, (3) leukopenia produced by typhoid vaccine was 

 prolonged to 48 hours. The leukocyte response following fever 

 cabinet pyrexia most nearly resembled that seen in ACTH therapy. 

 Aspirin minimized the pyretic effects of Pv PYROMEN but did not 

 affect leukocyte changes. Neither dibenamlne or chlor-trimeton 

 had capacity to alter febrile or leukocytic responses. None of 

 the agents provoked consistent Increases in uric acid/creatinine 

 ratios or corticosteroid excretion. 



Pv PYROMEN gave a 210^ increase in leukocytes within 8 hours; 

 levels returned to normal in 24 hours. There was a sharp rise in 



