Malayer J R, Hansen P J, Gross T S, Thatcher W W
Dairy Science Department, University of Florida, Gainesville, FL 32611-0701, USA.
Theriogenology. 1990 Aug;34(2):219-30. doi: 10.1016/0093-691x(90)90516-v.
Maternal heat stress in cattle may disrupt pregnancy by elevating uterine prostaglandin F(2 alpha) (PGF(2 alpha)) secretion. The objectives of this study were to determine the effects of elevated temperature (42 degrees C) in vitro upon 1) prostaglandin secretion by endometrial tissue; 2) the actions of extracellular regulators of uterine PGF [conceptus secretory proteins (bCSPs) and platelet-activating factor, (PAF)]; 3) the activity of the cyclooxygenase-endoperoxidase enzyme complex (PG synthetase); and 4) the activity of the endometrial PG synthesis inhibitor present in the endometrium from pregnant cattle. Endometrial explants at Day 17 of the estrous cycle produced more PGF than PGE(2) while elevated temperature caused increased PGF secretion but did not affect PGE(2) secretion. Elevated temperature did not reduce the ability of bCSPs or PAF to suppress release of PGF. The heat shock-induced increase in PGF at Day 17 was not due to the direct effects on PG synthetase, because PGF production from a cell-free cotyledonary microsomal enzyme preparation was reduced at elevated temperature. The activity of the cytosolic inhibitor of cyclooxygenase present in the endometrium of Day-17 pregnant cows could be reduced but not eliminated at 42 degrees C. We conclude that in vitro heat stress induces PGF secretion from the bovine uterine endometrium at Day 17 after estrus. This increase is not accompanied by the loss of regulatory capacity of conceptus products or increased activity of PG synthetase.
母牛的母体热应激可能通过提高子宫前列腺素F(2α)（PGF(2α)）的分泌来干扰妊娠。本研究的目的是确定体外高温（42摄氏度）对以下方面的影响：1）子宫内膜组织的前列腺素分泌；2）子宫PG的细胞外调节剂[孕体分泌蛋白（bCSPs）和血小板活化因子（PAF）]的作用；3）环氧化酶-内过氧化物酶复合物（PG合成酶）的活性；4）妊娠母牛子宫内膜中存在的子宫内膜PG合成抑制剂的活性。发情周期第17天的子宫内膜外植体产生的PGF比PGE(2)多，而高温导致PGF分泌增加，但不影响PGE(2)的分泌。高温并没有降低bCSPs或PAF抑制PGF释放的能力。热休克诱导的第17天PGF增加并非由于对PG合成酶的直接影响，因为在高温下无细胞的子叶微粒体酶制剂产生的PGF减少。在42摄氏度时，发情周期第17天妊娠母牛子宫内膜中存在的环氧化酶胞质抑制剂的活性可能降低，但不会消除。我们得出结论，体外热应激在发情后第17天诱导牛子宫内膜分泌PGF。这种增加并没有伴随着孕体产物调节能力的丧失或PG合成酶活性的增加。
