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FERRIS ET AL.--DATA ON PULMONARY FUNCTION
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asthma showed signs of returning to its pretreatment status (chart 2, column 4). The maximum breathing capacity showed the same sequence--a fall during the asthmatic attack, a rise after ACTH, (but not to normal), and a fall within one week after cessation of therapy. Chart. 3 A represents the changes in vital capacity and expiratory air velocity. The improve ment following epinephrine (adrenalin) during his asthmatic attack is apparent, as is the marked improvement following ACTH therapy. The expiratory tracing of March 22 (chart 3 A) demonstrates regression.
The eosinophil count showed fairly good fall under ACTH therapy, but the 17-ketosteroids excretion remained unchanged.
N.A.o* AGED 16. ASTHMA RESPONSE TO ACTH Ifc
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MAR. 6
5? ASTHMA ATTACK
MAR. 16
MAR. 22
M.B.C. 16 L./rnin(BTPS)
10 79 41
ACTH MAR. II - SS MG. MARIE-16 -40M0./DAY
EXP. NORM.
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Chart 2 (case 2).--The patient's pulmonary volume subdivisions and maximum breathing capacity in relation to his treatment with ACTH. See chart 1 for key to the subdivisions. The last column on the right Indicates by broken lines (-------) the limits of normal for the residual volume and the total lung capacity. Columns 1' and 2 are the subdivisions before and during ari acute attack of asthma which happened to develop during the study. Adrenal response: The eosinophil count fell from 980 to 288/mm.3; the 17-ketosteroids excretion was
4.8 mg./24 hr.
Case 3 (E. R., P.B.BiH. No. 4B-527).--This 40 year old man was a shoe cutter, and for a six year period before 1942 was exposed to inhalation of talcum powder. He had no previous exposure to dusts nor any history of pulmonary disease.'. Eight years before admission a pro gressive cough and dyspnea developed.
Cardiac catheterization in 1948 showed pulmonary hypertension. Vital capacity and maximum breathing capacity at that time wete lower than expected. Between this period and the next admission, in March 1950 right heart failure developed, which responded to digitalis,
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