No abstract

Tumor necrosis fattor a (TNF-a) mediates components of the acute-phase response, stimulates granulocyte metabolism, and induces endothelial cell surface changes. We studied whether human recombinant TNF-a (rTNF-a) could. increase pulmonary edema formation and pulmonary vascular permeability. Rabbits preinfused with '251-albumin were administered rTNF-a or saline. Animals were sacrificed, and lung wet/dry weight ratios as well as bronchoalveolar lavage fluid and plasma 125I activities were determined. rTNF-a increased lung wet/dry weight ratios by 151% (P < 0.02) and bronchoalveolar lavage fluid/plasma 1251 activity ratios by 376% (P < 0.01) compared with values for saline controls. Electron microscopy of lung sections demonstrated endothelial injury, perivascular edema, and extravasation of an ultrastructural permeability tracer. To demonstrate that rTNF-a could directly increase pulmonary vascular endothelial permeability in vitro, we studied albumin transfer across cultured porcine pulmonary artery endothelial cell monolayers. rTNF-a induced time-dependent dose-response increments in transendothelial albumin flux in the absence of granulocyte effector cells. These observations suggest that rTNF-a can provoke acute pulmonary vascular endothelial injury in vivo as well as in vitro.

An SO-year-old man who initially presented with a left hemiparesis rapidly developed right-sided heart failure and died. Although an echocardiogram suggested the presence of a tumor, the diagnosis of a primary cardiac lymphoma was made only at autopsy. The tumor involved a leaflet of the tricuspid valve, a finding not previously reported in the literature. In 1977, the Armed Forces Institute of Pathology defined a primary malignant lymphoma of the heart as that involving only the heart and pericardium. Many reports of primary cardiac malignant lymphomas have been published, however, most of which mention the presence of metastases. We have reviewed the world literature to determine the number of actual cases of primary malignant lymphoma of the heart. Only 15 reported cases, including the current case, were found to meet the current criteria. Accepted for publication December 26, 1988. medications), hyperuricemia (treated with allopurinol), supraventricular tachycardia, and a normochromic normocytic anemia. Admission physical examination revealed a pulse of 100 beats per minute, respirations of 22 per minute, and a blood pressure of 160/100 mm Hg. He was afebrile. His head and eyes were deviated to the right, with intact doll's eyes and a questionable left field cut. He had a left central fifth and seventh nerve deficit. The chest was symmetrical without bony abnormality. There were bibasilar rales without evidence of consolidation or wheezes.A cardiac examination revealed a rocking motion on palpation with a summation gallop and a holosystolic murmur at the left lower sternal border. Carotid pulses were 2+ without bruits. There was no jugular venous distention. Abdominal, genitourinary, and rectal examination were unremarkable. The extremities were without clubbing, cyanosis, or edema. Motor examination revealed 5/5 strength on the right side. On the left, there was 3/5 strength in both upper and lower extremities, and muscle development was appropriate for age. There was increased muscle tone ofthe left upper and lower extremities. His reflexes were brisk and symmetric. There were crossed adductor responses bilaterally as well. Coordination, station, and gait were not tested.The admission computed tomography scan (CT scan) of the head showed only moderate cortical atrophy, as seen on CT scan performed 1 year previously. An elecrocardiogram (EKG) revealed sinus tachycardia, first degree atrioventricular block, and nonspecific ST-T changes. A chest radiograph showed prominent pulmonary vasculature and blunting of the right a stovertebral angle. There was a marked increase in the sue of the heart since the most recent film was taken 1 year earlier. Liver function tests were elevated with an aspartate aminotransferase (AST) of 406 U/1 (normal, 26-88); alanine aminotransferase (ALT) of 197 U/1 (normal, 10-60), and alkaline phosphatase of 52 1

Pneumocystis carinii was tightly attached to host alveolar type I cells, as judged by freeze-fracture electron microscopy. In contrast to other organisms studied by this technique, no changes in the cell membranes of P. carinii or the host cells could be demonstrated. These data suggest that P. carinii attaches in an unusual manner.