Showing papers by "Giuseppe G. Pietra published in 1980"

Alveolar response to experimental Pneumocystis carinii pneumonia in the rat.

Abstract: In order to characterize the alveolar response to Pneumocystis carinii pneumonia, light and electron miscropy were used to trace the development of experimental infections with P carinii in rats treated with cortisone acetate and a low-protein diet. The first changes were found by the eighth day of treatment and consisted of the selective attachment of Pneumocystis organisms, mostly trophozoites, to alveolar Type 1 pneumocytes; the host cells were undamaged, and no inflammatory response was seen. After approximately one month of treatment, the seemingly innocuous host-parasite interaction was succeeded by focal necrosis of the Type 1 pneumocytes adjacent to organisms; hyperplasia of nearby Type 2 pneumocytes also occurred, to replace the dead Type 1 pneumocytes. Even at this stage, inflammatory reaction was conspicuously absent except for occasional alveolar macrophages in the diseased alveoli; in addition, all cells of the alveolar-capillary membrane other than Type 1 pneumocytes appeared entirely normal. Not only does the present study clarify the nature of alveolar injury caused by Pneumocystis carinii, but it also provides an experimental animal model in which selective injury of the alveolar lining cells occurs.

PRIMARY PULMONARY HYPERTENSIONl

Abstract: The designation "primary pulmonary hypertension" is generally used as a synonym for "unexplained pulmonary hypertension" (1, 2). Both clinicians and pathologists have adopted this term. Unfortunately, despite this appar­ ent concurrence, not all who use the term have in mind the same disorders, etiologies, pathogenetic mechanisms, or anatomic lesions. For the clinician, the syndrome of primary pulmonary hypertension has three essential features: (a) clinical, x-ray, and electrocardiographic evi­ dence of pulmonary hypertension, (b) abnormally high pulmonary arterial pressures and pulmonary vascular resistance in the face of a normal pulmo­ nary wedge pressure and a nearly normal cardiac output, and (c) insufficient cause for the pulmonary hypertension either in the lungs or heart (3). Since the advent of cardiac catheterization (4), the pathologist has partic­ ipated in the search for etiology by seeking to establish the extent and nature of the widespread pulmonary vascular disease, and by excluding cardiac or pulmonary causes of diffuse pulmonary vascular involvement. Indeed, re­ cently a few pathologists assumed the lead in attempting to sort out primary pulmonary hypertension when they proposed that a distinctive vascular lesion, i.e. "plexogenic arteriopathy," is prerequisite for the diagnosis of primary pulmonary hypertension (1). But, as indicated below, this proposi­ tion has not been universally accepted (5-7).