Weevaluated pulmonary vascular permeability In 15patients after lung transplantation (21 allografts) by measuring the pUlmonary transcapiilary escape rate (PTCER) for Ga· 68· labeled transferrin, using positron emission tomography. Seven recipients (four unilateral, three bilateral lung transplants) were studied within 3 days of transplantation, and each developed hypoxemia and allograft Infiltrates consistent with the" relmplantatlon response." PTCERwas higher In subjects studied within 1 day than In those studied at a later time, and fell In seven allografts studied serially. The initial PTCER also correlated (r= 0.77) with length of Ischemic (preservation) time, even In the three subjects with bilateral allografts. Eight other recipients (five unilateral, three bilateral transplants) were evaluated for possible organ rejection at least 1 wk after transplantation. PTCER was normal In patients without clinical or histologic evidence of rejection, and It was elevated In recipients with rejection. PTCER fell each time after treatment for rejection with IncreasedImmunosuppression In the three patients studied serially. These data suggest that positron emission tomography measurements of PTCER might be a useful way to evaluate both the relmplantation response and organ rejection after lung transplantation. AM REV RESPIR DIS 1992; 145: 954-957

During the past 10yr, human lung transplantation has rapidly become a valuable therapeutic option for end-stage lung disease. Among many important issues, the so-called" reimplantation response" and allograft rejection stand out as two processes of particular importance. Although both are characterized by histologic evidence of lung injury, each process has a distinctive clinical course (1). The reimplantation response has been defined as the" morphologic, roentgenographic, and functional changes that occur in a lung transplant in the early postoperative period as a result of surgicaltrauma, ischemia, denervation, lymphatic interruption, and other injurious processes (exclusiveof rejection)"(2). This response is usually diagnosed by exclusion, ie, when basal or perihilar infiltrates occur in the early postoperative period and cannot be attributed to rejection, infection, mucus plugging, or cardiogenic pulmonary edema. The severity of the response usually reaches a maximum by Day 4, and clears rapidly thereafter (3). The diagnosis is often confirmed retrospectively when the observed abnormalities resolve without specific therapy. In contrast, allograft rejection rarely occurs during these first few days after transplantation. After the first week, rejection is suspected when fever, dyspnea, malaise, leukocytosis, hypoxia, or new infiltrates occur, and the diagnosis is confirmed clinically by a prompt response to intravenously administered corticosteroids and/or histologically by a perivascular lymphocytic infiltrate in transbronchiallung biopsies (4). Interestingly, surveillance transbronchial biopsy studies after lung transplantation indicate that unsuspected allograft rejection can frequently be present without clinical signs and symptoms (5). Despite these distinctive features, these two complications of transplantation have been remarkably difficult to evaluate clinically using currently available noninvasive methods (1). Wehave developed a means to noninvasively evaluate pulmonary vascular permeability using the quantitative nuclear medicine imaging technique of positron emission tomography (PET)(6). This technique has been used to evaluate lung injury as a result of the adult respiratory distress syndrome (7), lobar pneumonia (8), chronic cigarette smoke exposure (9), and interstitial lung disease (10). Because