Angiogenesis occurs rarely in normal adult tissues. The female reproductive tract, however, provides several exceptions, including the endometrium during early pregnancy. The aim of this study was to quantify endothelial cell proliferation (a component of angiogenesis) in the rat endometrium at about the time of implantation, using immunohistochemistry with a double staining technique. Proliferating cells were stained using an antibody against proliferating cell nuclear antigen (PCNA; clone PC10), and endothelial cells were stained with a lectin from Griffonia simplicifolia. Results showed that the endothelial cell proliferative index in the endometrium rose significantly from approximately 1% on the first 2 days of pregnancy to 13% on day 3; and continued to rise to 28% on day 5. After embryo implantation, the endometrial endothelial cell proliferative index rose further to 71% on day 7 at embryo sites only; but significantly decreased to basal values at intersites. The endothelial cell proliferative indices in the myometrium and mesometrial triangle remained at basal values during the first 5 days, but increased to approximately 22% at embryo sites only by day 7. We conclude that in the rat: (1) endometrial angiogenesis may be occurring before embryo implantation; (2) endometrial endothelial and stromal cell proliferation occurs concomitantly, except on day 3 when endothelial cell proliferation begins in advance of other stromal cell proliferation; and (3) there are two separate mechanisms controlling uterine endothelial cell proliferation during early pregnancy. The first mechanism is maternally controlled and is apparent throughout the entire endometrium from day 3; and the second mechanism is apparent after implantation in the vicinity of the embryo.

Angiogenesis, or formation of new blood vessels by sprout formation from existing vessels, is generally considered to be the only mechanism by which blood vessel growth occurs. This traditional concept of angiogenesis has been derived largely from observations of experimental systems. Relatively fewer studies on angiogenesis have been carried out using normal angiogenic situations where vessel growth occurs in a controlled three-dimensional fashion throughout the tissue. Recent advances in the treatment of infertility and outpatient gynecological procedures have led to greater accessibility to normal human endometrium, thus providing new opportunities to study the process of angiogenesis in a physiological context. However, to date, it appears that very little work had been done in relation to endometrial angiogenesis apart from the location of numerous angiogenic and other growth factors with potential to influence angiogenesis in the endometrium, and here there have been few attempts to link these observations with actual angiogenic events. The purpose of this review is to summarize the literature regarding angiogenesis in the endometrium, including work from our own laboratory, and to suggest that blood vessel growth in the endometrium may occur by a mechanism that differs from classical angiogenesis.

We have studied the kitten model of oxy en induced retinopathy by the technique of corrosion vascular casting/scanning electron microscopy ?he predominant morphologmcal features of the kitten model are preretinal and intraretinal neovascularization with a minor component of arterievenous shunting This is contrasted with the actwe phase of the blinding disease in the human neonate which is characterised predominantly by so called mesenchymal arterio venous shunting' A failure to appreciate fundamental differences in the nature of oxygen induced retinopathy between the human infant and its kitten model we believe has led to erroneous concluslons about pathogenesis in the human neonate Key words Retrolental fibroplasta human kitten model corrosion vascular casting, scanning electron microscopy neovascularization arterio venous shunting

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