The effects of synthetic platelet-activating factor (PAF) on guinea pig lung were examined in isolated lungs perfused with platelet-free Krebs-Ringer solution. When PAF (1 microgram) was injected into the pulmonary artery (PA), it markedly increased airway pressure (maximal increase, 84.7%) and moderately raised PA pressure (maximal increase, 22.8%). The same dose also provoked a massive (29-fold) release of thromboxane B2 (TXB2), the stable metabolite of TXA2, into the perfusate, beginning before the increases in airway and PA pressures. The concentration of 6 keto-PGF1 alpha, the stable metabolite of prostacyclin, also increased (to 5 times control levels) about 70 s after peak release of TXB2. Indomethacin completely blocked TXB2 release, reduced the magnitude of airway pressure increase by 79%, and shortened its duration, as well as the duration of the PA pressure rise. Larger concentrations of PAF (3 and 10 micrograms) produced even greater increments in airway and PA pressures, but these were only moderately attenuated by indomethacin. Also, PAF increased extravascular lung water, as evidenced by increases in wet/dry lung weight and lung/body weight ratios. In a concentration of 0.1 microgram, PAF had no effects on airway or PA pressures, nor did it stimulate TXB2 or 6-keto-PGF1 alpha release. Lyso-PAF was similarly ineffective. We conclude that PAF induces airway constriction, pulmonary hypertension, and pulmonary edema in guinea pig lung independently of platelets. These effects are associated with stimulated synthesis of TXA2, but the mechanisms of their production remain to be determined.

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An unusual radiographic sign of crescentic cavitation appeared in a case of invasive pulmonary mucormycosis complicating the treatment of a patient with acute myelogenous leukemia and having a normal admission chest radiograph. The first manifestation was a large, wedge‐shaped pleural‐based consolidation, which evolved about 10 days later into a fungus ball‐like lesion, usually known as the air crescent sign. Amphotericin B and 5‐fluorocytosine, which were initiated immediately after appearance of the sign, proved to be effective, probably in association with hematologic improvement. Transbronchial lung biopsy was not only helpful in establishing a definitive diagnosis, but also suggested that an intracavitary mass could have resulted from pulmonary infarction. This experience thus showed that the sign may appear in greater frequency in mucormycosis as well as in aspergillosis, and may be useful as a clinical index for initiating antifungal therapy in immunocompromised patients.

A case of adrenocortical adenoma containing small adipose foci is presented. A small amount of fat within the mass led to an erroneous preoperative diagnosis of myelolipoma. Adrenal adenoma should be included in the differential diagnosis of adrenal mass containing fat.

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