Waterman R A, Guthrie H D
Prostaglandins. 1984 Jan;27(1):131-46. doi: 10.1016/0090-6980(84)90227-2.
The effects of Cloprostenol administration on porcine luteal lipid metabolism, progesterone production, and prostaglandin F production were examined in 32 pigs at day 12 of the estrous cycle. Pigs were killed between 0 and 18 hours after treatment. Recovered luteal tissue was incubated at 0 C and at 37 C in the absence and presence of dibutyryl cyclic AMP and indomethacin. Net in vitro release of progesterone from luteal tissue was depressed within 1 hour after Cloprostenol treatment whereas net in vitro release of prostaglandin F was accelerated 4 hours after Cloprostenol treatment. Inclusion of dibutyryl cyclic AMP in the incubation media did not alter progesterone production but did enhance prostaglandin F production at 0 and 1 hour after Cloprostenol treatment. Inclusion of indomethacin in the incubation media completely inhibited the Cloprostenol-induced acceleration of in vitro luteal PGF production. Cloprostenol treatment increased luteal triglycerides and decreased luteal free cholesterol and cholesterol esters within 1 hr after treatment. Arachidonic acid percentages in free fatty acids and triglycerides were also increased within 1 hr after treatment. When 37 C and 0 C incubations were compared, in vitro luteal accumulation of free fatty acids was maximum at 1 hr after Cloprostenol treatment. In vitro accumulation of triglycerides in luteal tissue was comparatively uniform at all times examined during the first 18 hr after Cloprostenol treatment. Comparison of 37 C and 0 C incubations further revealed that luteal triglycerides were active in accumulation of arachidonic acid. Inclusion of dibutyryl cyclic AMP and/or indomethacin in the incubation media did not alter luteal lipid contents or fatty acid compositions. Blood plasma progesterone was depressed at 4 hours after Cloprostenol whereas 13,14-dihydro-15-keto-prostaglandin F2a was elevated at 18 hours after treatment. Blood plasma free fatty acids increased 330 percent at 4 hours and free fatty acid compositions also changed at this time. In both luteal tissue and blood plasma, changes in steroid and fatty acid metabolism occurred prior to changes in prostaglandin metabolism, suggesting that Cloprostenol induced functional luteal regression prior to altering prostaglandin metabolism.
在发情周期第12天，对32头母猪研究了氯前列醇给药对猪黄体脂质代谢、孕酮生成及前列腺素F生成的影响。在治疗后0至18小时内宰杀母猪。将回收的黄体组织在0℃和37℃下，分别于不存在和存在二丁酰环磷腺苷及吲哚美辛的情况下进行孵育。氯前列醇治疗后1小时内，黄体组织孕酮的体外净释放量降低，而前列腺素F的体外净释放量在氯前列醇治疗后4小时加快。孵育培养基中加入二丁酰环磷腺苷不会改变孕酮生成，但在氯前列醇治疗后0和1小时会增强前列腺素F生成。孵育培养基中加入吲哚美辛可完全抑制氯前列醇诱导的黄体体外前列腺素F生成加速。氯前列醇治疗后1小时内，黄体甘油三酯增加，黄体游离胆固醇和胆固醇酯减少。治疗后1小时内，游离脂肪酸和甘油三酯中的花生四烯酸百分比也增加。比较37℃和0℃孵育时，氯前列醇治疗后1小时黄体游离脂肪酸的体外积累量最大。在氯前列醇治疗后的前18小时内，所检测的所有时间点，黄体组织中甘油三酯的体外积累相对均匀。37℃和0℃孵育的比较进一步显示，黄体甘油三酯在花生四烯酸积累中起作用。孵育培养基中加入二丁酰环磷腺苷和/或吲哚美辛不会改变黄体脂质含量或脂肪酸组成。氯前列醇治疗后4小时，血浆孕酮降低，而治疗后18小时，13,14-二氢-15-酮-前列腺素F2a升高。治疗后4小时，血浆游离脂肪酸增加330%，此时游离脂肪酸组成也发生变化。在黄体组织和血浆中，类固醇和脂肪酸代谢的变化先于前列腺素代谢的变化，这表明氯前列醇在改变前列腺素代谢之前诱导了功能性黄体退化。
