Among the complications of this medical therapy, the authors include 5 episodes of infection associated with open lung biopsy, leptomeningeal biopsy, bowel resection necessitated by mesenteric infarction, and antibiotic therapy-related Clostridium dificile enterocolitis. It is not possible to determine in such complex cases whether these infections might also have occurred in the absence of any immunosuppressive medications.We remain concerned about any infectious complications of cyclophosphamide and glucocorticosteroid therapy. However, we believe that Bradley et al have observed an unusually high incidence of such problems because they did not adhere to our guidelines for reduction of glucocorticosteroid therapy, and they included 5 sequential complications of intestinal infarction and surgery in 1 patient. Reply To the Editor:Hoffman et a1 correctly identified several important features of our series of patients: 1) many infections occurred as complications of the underlying vasculitis (e.g., bowel infarction) or of procedures performed (e.g., placement of an indwelling catheter, thoracotomy); 2) the mode of corticosteroid therapy (every other day versus daily) appeared to be related to the incidence of infection; and 3) the duration of corticosteroid therapy, and particularly, daily corticosteriod therapy, was longer than that previously recommended (Cupps TR, Fauci AS: The Vasculitides. Philadelphia, WB Saunders, 1981).While we could not determine a causal relationship with infection for either corticosteroid or cyclophosphamide therapy, in 6 of 10 patients in our series who became infected, infection occurred within 4 weeks of the initiation of cyclophosphamide therapy. Only 2 of 10 developed an infection within the first month of corticosteroid therapy.While the average daily corticosteroid dosage at the onset of the first infection was >40 mg, it was consistent with the guidelines promulgated by Cupps and Fauci for the administration of concomitant corticosteroids during the first month of cyclophosphamide therapy. As stated in our report, infection did not correlate with the dosage or duration of corticosteroid therapy, but seemed more closely associated with the initiation of cyclophosphamide therapy. We agree with Hoffman et al that in the complicated cases we reported, it is difficult to determine the cause(s) of the infections observed. Our report explored a number of probable factors in addition to those mentioned herein. It would be as much an oversimplification to attribute these infections entirely to the corticosteroid component as it would be to single out the cyclophosphamide component of the therapeutic regimen.

Reflex respiratory responses to increased and decreased tracheal pressure have been studied at bilateral local vagus temperatures between 30 degrees C and 0 degrees C in anaesthetized spontaneously breathing rabbits. The temperature of each cervical vagus nerve was governed by separate thermodes, which were cooled by Peltier elements and heated by transistors. In this study, the lowest activity level of the diaphragm during expiration was considered to reflect tonic inspiratory activity. As an indicator for this level, the longest interspike interval in the electromyogram of the diaphragm during a breath was used. Tonic inspiratory activity at tracheal pressures below -1.2 kPa was higher with vagi intact than after vagotomy. This observation indicates that disinhibition, due to the decreased activity of pulmonary stretch receptors, occurring during the Hering-Breuer deflation reflex, is an insufficient explanation for the facilitation of tonic inspiratory activity. When local vagus temperatures are 8 degrees C, and tracheal pressure has been increased or decreased, tonic inspiratory activity is higher than it would be with vagi at 0 degrees C or cut. Two reflex mechanisms that might explain the observed high tonic inspiratory activity are discussed.

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In ten vagus nerves the effect of local cooling on the compound action potential was studied in the temperature range of 34 to 0 degrees C in spontaneously breathing, anaesthetized rabbits. The mean temperature at which the myelinated (A) fibres were completely blocked, was 10.2 +/- 2.4 degrees C (mean +/- S.D.). In nine nerves, local vagus cooling to 0 degrees C failed to block all non-myelinated (C) fibres. In one nerve, total blocking occurred at 2.0 degrees C. We conclude that in the rabbit, the earlier found increase in tonic activity of the diaphragm following lung inflation or deflation during bilateral local vagus cooling to a temperature between 8 and 0 degrees C is due to afferent impulses in vagal C fibres.