Summary. Metabolism of PGE-2 and PGF-2α by cytosolic fractions (100 000 g supernatant) of the uterus, oviduct and lung of rabbits treated with hCG and endotoxin (20 μg/kg) was measured. Endotoxin caused immediate decreases in metabolism of both PGs by uterus at 1 h, and these decreases became significant at 2 h for PGE-2 and 6 h for PGF-2α. The metabolism of both PGs remained depressed throughout the 24 h study. Metabolism by oviduct tissue differed in that at 1 h metabolism of both PGs increased but then remained depressed between 2 and 24 h. Metabolism of PGs by lung also showed a different pattern: that of PGE-2 was depressed only briefly (at 2 h), while that of PGF-2α was consistently depressed between 2 and 24 h. Pre-treatment with hCG did not affect the response: tissues from animals killed 6 h after endotoxin but not given hCG responded like those from animals treated with endotoxin 24 h after hCG and killed 6 h later. Much of the increased PG levels in venous drainage after endotoxin treatment can be explained by depressed ability of cells to metabolize PGs.
M. J. K. Harper, R. R. Bodkhe and W. E. Friedrichs
M. J. K. Harper, Catherine J. Norris, W. E. Friedrichs and A. Moreno
Summary. Administration of poly I:C (1 mg/kg i.v.) to rabbits 24 h after an ovulating injection of hCG caused accelerated ovum transport; only 30% of the ova were still found in the oviducts 24 h later compared with 79% of ova in control animals. This action of poly I:C was prevented by concomitant administration of indomethacin. Poly I:C (0·5 mg/kg i.v.) given to anaesthetized rabbits produced significantly increased levels of prostaglandins (PGs) E and F in uterine vein blood up to 2 h later. Production of PGs by lung, oviduct and myometrium was unaffected 2 h after poly I:C administration, but production of both PGE and PGF by endometrium was significantly elevated at the same time. Metabolism of PGs by cytosols of lung, oviduct and uterus was inhibited to various degrees at 2 h after poly I:C (1 mg/kg i.v.), but by 4 h after treatment this process was reduced to 70–80% of pretreatment values. It is concluded that poly I:C accelerates ovum transport through the oviduct by a PG-mediated mechanism, and that elevated levels of PGs in oviduct are due to inhibition of metabolism of PGs.
AM Petrunkina, J Friedrich, W Drommer, G Bicker, D Waberski and E Topfer-Petersen
On reaching the oviduct, spermatozoa are retained in the isthmic region of the oviduct until ovulation occurs. The essential steps of capacitation are co-ordinated in this region. In this study, a primary cell culture system of oviductal epithelial cells was established to investigate sperm binding to oviductal epithelium and modulation of sperm function during incubation under capacitating conditions in co-culture with oviductal epithelial cells. Epithelial cells were stripped from the oviducts of sows and cultivated for 5-7 days on Lab-Tek Chamber slides on Matrigel. The preparations on chamber slides and suspensions of control spermatozoa were incubated for 3 h in Tyrode's albumin lactate pyruvate (TALP) medium. At 3, 30, 60, 90 and 180 min the free-swimming spermatozoa were collected by washing, and membrane integrity, tyrosine phosphorylation patterns and [Ca(2+)](i) of bound, unbound and control spermatozoa were assessed with fluorescent probes (propidium iodide, Cy-3 and fluo-3-AM). The cells bound to oviductal epithelial cells showed reduced cytosolic Ca(2+) concentration, reduced and almost absent tyrosine phosphorylation of membrane proteins and higher viability at the time of the first sampling. Increases in Ca(2+) concentration and cell death occurred much more slowly during incubation in cells bound to oviductal epithelial cells compared with free-swimming spermatozoa, and no changes in tyrosine phosphorylation were observed. The preferential binding of viable, low-Ca(2+) cells with suppressed tyrosine phosphorylation and slower functional modulation of boar spermatozoa attached to oviductal epithelial cells might represent a mechanism for selecting functionally competent spermatozoa and prolonging their lifespan by delaying capacitation in the oviductal reservoir.