Ovulation and the role of the ovarian surface epithelium.

Epon sections from all tissue layers of the rabbit ovary, including the often neglected surface or germinal epithelium, were studied to elucidate the mechanism of follicle rupture. Scanning electron microscopy showed cells covering preovulatory follicles increased clearly in size up to 8 hours after human chorionic gonadotropin (HCG) injection. These showed an increasing number of large, intracellular structures with prominent rounded contours. Transmission electron microscopy showed large, electron dense, lysosomelike bodies in some cells 4 hours after HCG. These membrane-surrounded structures increased in size up to 8 hours after HCG, then decreased markedly. These obviously corresponded to the bodies found by light microscopy and scanning electron microscopy. Histochemistry revealed many represent lysosomes. During the last 2 hours before rupture, the dense bodies of the surface epithelium considerably decrease, signs of material emptying into vacuoles is found, and sometimes there is open communication from vacuoles towards the unerlying tunica albuginea. An extracellular edema appeared under the epithelium with degenerated fibroblasts and disintegrated collagen; these changes gradually proceeded inwards. Blood capillaries close to the membrana granulosa gradually showed small pores and close to ovulation the endothelial cells had gaps up to 3 mcm in diameter. The preovulatory follicles grew rapidly and an augmenting edema occupied the whole ovary. In the last hours before ovulation the membrana granulosa gradually dissociated. Whatever the net effect of the prostaglandins, prostaglandin F2alpha appears to be essential for follicle rupture since intrafollicular injections of antiserum blocked ovulation. Prostaglandin E1 promotes vascular permeability and lysosommal enzymes released extracellularly may be coupled to collagen degration. The enzyme synthesis and lysosomal growth in the surface epithelium of preovulatory follicles may be due to the high local concentration of sex steroids.     

Lead potentiation of endotoxin lethality in rats: lack of effect of kininase inhibition.

Although lead and SQ20881 are potent in vitro inhibitors of kininase II activity, SQ20881 does not alter the sensitivity of rats to endotoxin. These results indicate that marked changes in plasma kininase activity do not contribute to endotoxin morbidity and that kininase inhibition is not the mechanism whereby lead ions sensitize rats to endotoxin.