Pulmonary hypertension is a common and serious condition, either as a primary event or secondary to other injury. In its clinical form there is always a restrictive lesion caused by vascular cell proliferation. This narrows the lumen of vessels throughout the lung but especially ones forming the microcirculation, the smallest vessels that lie adjacently to the capillaries. In addition, contractile cells develop in segments where normally these cells are absent (neomuscularization). As these cells form elastic laminae and organize into intimal and medial layers, microvascular segments that resemble capillaries in wall structure are converted into thick-walled vessels. To analyze the cellular basis of this we have developed a model of restrictive pulmonary hypertension in the rat breathing high oxygen at normobaric pressure. Vascular changes begin within hours of injury and progress until virtually all microvessels are affected. Currently, little is known of the mediators that act as signal molecules but it is likely that ones released by inflammatory and vascular cells stimulate chemotaxis, proliferation and expression of contractile organelles, as well as secretion of the matrix proteins. Light microscopy studies and quantitative methods of analysis provide a broad understanding of the nature and extent of wall reorganization within the microvessel network. High resolution studies, including the use of immunogold techniques, are critical to identify cell phenotype during the early stage of wall changes, and, later, the type of filament proteins expressed as cells switch phenotype by acquiring contractile organelles.
Biomedical Reviews 1995; 4: 47-59.
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