兽医产科学2.ppt

* * * * * * * * * * * * * * * * * * * It wasn’t until 1969 that a compound call prostaglandin F2a was proposed as the uterine luteolysine because: Prostaglandin F2a has been isolated from endometrial tissue of several species, and its concentration in maximal during the period of luteal regression. Also it extremely labile in circulation, it is totally destroyed by the lungs. Infusion of PGF2alpha to pregnant rats caused a dramatic decrease in the ovarian progesterone content. This key finding in the regulation of the corpus luteum function was extended to other species and PGF2a has been shown to exert a luteolytic effect in cattle, sheep, guinea pig, goats, horses, pseudopregnant mice, hamsters and rabbits. What It was not known was the mechanism. Think of another mechanism to prove that PGF2a in a luteolytic agent. * However when PGF2a was administered systemically to seep no regression of the LC was observed, but when it was injected in the arterial supply of the ovary corpus luteum regression occurs. * The uterine luteolytic factor appears to pass directly from the uterine vein to the ovarian artery in the ewe. Although there do not appear to be vascular connections between the uterine vein and ovarian artery; In sheep, the ovarian artery in closely attached to the surface of the utero-ovarian vein. So, The possibility was considered that substances might diffuse from the utero vein to the ovarian artery. To demonstrated that what you can do?? * In 1972 was demonstrated the countercurrent transfer mechanism by injecting Labeled PGF2a in the uterine vein and collecting blood from the ovarian artery. The author demonstrated that 1 % of the PGF2a injected appears in the ovarian vein. So, PGF2a from the uterus is transported to the ipsilateral ovary through a vascular countercurrent exchange mechanism. PGF2a from the endometrium enters the uterine vein and by countercurrent exchange diffuses across the wall of the uterine vein into the blood of the ovar