title: Changes of ovarian microvasculature in hCG stimulated rabbits. A scanning electron microscopic study of corrosion casts.
abstract: The microvasculature of the ovarian cortex was studied by means of scanning electron microscopy of vascular corrosion casts in estrous and hCG stimulated rabbits in order to establish a better understanding of the structural as well as functional vascular changes which accompany the evolution of the luteofollicular complex. According to the various shape and size seven different morphological types of vascular plexuses corresponding respectively to antral follicles (Types 1-2), atretic follicles (Types 3-4), periovulatory follicles (Type 5), growing pseudopregnant corpora lutea (Type 6) and regressing pseudopregnant corpora lutea (Type 7) were identified. Growing to mature cycling type follicles (Types 1-2) showed a gradual enlargement and proliferation of the theca capillaries. These changes, associated with capillary hyper-permeabilization were observed in ovulatory and post-ovulatory follicles (Types 5), after hCG stimulation. The corpus luteum formation (Types 6) was accompanied by additional capillary dilatation, diffuse angiogenetic sprouts and organization of a more conspicuous venous drainage. The regression of the corpus luteum (Type 7) was characterized by the appearance of avascular areas within the glandular tissue and by regression of vascular dilatation. The atretic follicle (Types 3-4) wall showed large interruptions (avascular areas) and focal invasion of the central cavity by newly formed capillaries randomly arranged. The hCG stimulation did not affect consistently the atretic follicle microvasculature. The present observation shows that both thecal capillary vasodilatation and angiogenetic processes support the gradual increase of ovarian blood flow during follicle growth and corpora lutea formation and that microvascular changes of atretic follicles are possibly related to a type of inflammatory reaction since they seem to be a consequence rather than a primary cause of atresia.
authors.affiliation: Department of Human Anatomy, University of Rome La Sapienza, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Macchiarelli
authors.forename: S A
authors.initials: SA
authors.lastname: Nottola
authors.forename: E
authors.initials: E
authors.lastname: Vizza
authors.forename: S
authors.initials: S
authors.lastname: Correr
authors.forename: P M
authors.initials: PM
authors.lastname: Motta
mesh_terms: D000818:Animals; D006063:Chorionic Gonadotropin / Q000494:pharmacology*; D003338:Corpus Luteum / Q000098:blood supply / Q000187:drug effects / Q000648:ultrastructure; D016319:Corrosion Casting / Q000379:methods*; D004971:Estrus / Q000502:physiology; D005260:Female; D008833:Microcirculation / Q000187:drug effects* / Q000648:ultrastructure*; D008855:Microscopy, Electron, Scanning; D023421:Models, Animal; D006080:Ovarian Follicle / Q000098:blood supply / Q000187:drug effects / Q000648:ultrastructure; D010053:Ovary / Q000098:blood supply* / Q000187:drug effects / Q000648:ultrastructure*; D011247:Pregnancy; D011555:Pseudopregnancy / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology; D011817:Rabbits
chemical_list: D006063:Chorionic Gonadotropin