Objective:

Intimal venous endothelial hyperplasia is one of the main causes of thrombosis in vascular reconstructions. This pathological process is defined as the cellular and molecular response characterized by an abnormal proliferation of smooth muscle cells. An important association of intimal hyperplasia with trophic signals has been described, some associated with growth factors such as growth factor derived from platelet-derived growth factor platelets. Such initiating mechanisms have not yet been well characterized. Intimal hyperplasia generally includes the presence of alpha-actin positive smooth muscle cells, extracellular matrix, inflammatory cellular components such as macrophages, leukocytes and a wide variety of mediators and cytokines. The objective of this study was to develop an experimental model for the study of the pathophysiology of venous intimal hyperplasia in the first 7 days.

Methods:

Our study included 12 rabbits. 6 of these patients underwent an injury by balloon angioplasty in the femoral vein (tension force by barotrauma), the remaining were controls.

Results:

Using a model of endothelial lesion through barotrauma, we were able to reproduce the detonating events of the early stages in the development of venous intimal hyperplasia. These changes were reflected at the systemic and histopathological level.

Conclusions:

The experience of rabbit management as an experimental model met the technical expectations for the evaluation of the pathophysiology of venous intimal hyperplasia and this coupled with the absence of complications (0% mortality, 0% morbidity).

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