Roth Z, Wolfenson D
Department of Animal Sciences, Faculty of Agriculture, Food and Environment, The Hebrew University, Rehovot 76100, Israel.
Department of Animal Sciences, Faculty of Agriculture, Food and Environment, The Hebrew University, Rehovot 76100, Israel.
Domest Anim Endocrinol. 2016 Jul;56 Suppl:S218-27. doi: 10.1016/j.domaniend.2016.02.013.
Reduced reproductive performance of lactating cows is strongly associated with environmental and pathogenic stressors. This review summarizes the most recent knowledge on the effects of acute or chronic heat stress (HS) and acute or chronic intramammary infection (IMI) on ovarian function. It also offers various approaches for improving the fertility of cows under chronic HS or IMI. Comparing the 2 stressors reveals a few similarities in the mode of alteration in the hypothalamus-pituitary-ovarian axis, in particular, in the follicle and its enclosed oocyte. Both HS and IMI cause a reduction in the preovulatory LH surge, with a pronounced effect in cows with IMI, and consequently, ovulation is being delayed or inhibited. Both stresses induce changes in follicular growth dynamics, reduce follicular steroidogenesis, and disrupt follicular dominance. Unlike their effects on follicular function, the effects of mastitis and HS on corpus luteum (CL) function are debatable. Under chronic summer thermal stress, several, but not all, studies show reduced progesterone secretion by the CL. Subclinical mastitis does not affect CL function, whereas the effect of clinical mastitis is controversial; some show a reduction in progesterone, whereas others do not. Both stresses have been found to impair cytoplasmic and nuclear maturation of oocytes, associated with reduced embryonic development. These findings have provided insights into the mechanism by which HS and IMI compromise fertility, which enable developing new strategies to mitigate these effects. For instance, treatment with GnRH and PGF2α to induce follicular turnover successfully improved conception rate in subpopulations of HS cows during the summer, in particular, primiparous cows and cows with high BCS. The "Ovsynch" program, also based on the use of GnRH and PGF2α, has been shown to improve conception rate of subclinical mastitic cows, most likely due to better synchronization of timing of ovulation with that of AI. Supplementing progesterone after AI improves conception rate of HS cows, particularly those with postpartum uterine disease and low BCS. It should be noted that similarities between the 2 stressors do not necessarily suggest a shared mechanism. Although not clear enough, an additive deleterious effects of HS and IMI on reproduction is suggested.
泌乳奶牛繁殖性能下降与环境和致病应激源密切相关。本综述总结了关于急性或慢性热应激（HS）以及急性或慢性乳房内感染（IMI）对卵巢功能影响的最新知识。它还提供了改善处于慢性热应激或乳房内感染状态下奶牛繁殖力的各种方法。比较这两种应激源可以发现，下丘脑 - 垂体 - 卵巢轴的改变模式存在一些相似之处，特别是在卵泡及其包裹的卵母细胞方面。热应激和乳房内感染均会导致排卵前促黄体生成素（LH）高峰降低，对患有乳房内感染的奶牛影响尤为显著，进而导致排卵延迟或受到抑制。两种应激都会引起卵泡生长动态变化，降低卵泡类固醇生成，并破坏卵泡优势。与它们对卵泡功能的影响不同，乳腺炎和热应激对黄体（CL）功能的影响存在争议。在夏季慢性热应激下，一些（但并非所有）研究表明黄体分泌的孕酮减少。亚临床乳腺炎不影响黄体功能，而临床乳腺炎的影响存在争议；一些研究显示孕酮减少，而另一些则没有。已发现两种应激都会损害卵母细胞的细胞质和核成熟，这与胚胎发育减少有关。这些发现为热应激和乳房内感染损害繁殖力的机制提供了见解，从而有助于制定减轻这些影响的新策略。例如，在夏季，用促性腺激素释放激素（GnRH）和前列腺素F2α（PGF2α）诱导卵泡更替的治疗方法成功提高了热应激奶牛亚群的受孕率，特别是初产奶牛和体况评分（BCS）高的奶牛。同样基于使用GnRH和PGF2α的“同期发情”程序已被证明可提高亚临床乳房炎奶牛的受孕率，这很可能是由于排卵时间与人工授精（AI）时间更好地同步。人工授精后补充孕酮可提高热应激奶牛的受孕率，特别是那些患有产后子宫疾病和体况评分低的奶牛。需要注意的是，这两种应激源之间的相似性并不一定意味着存在共同机制。虽然尚不够明确，但提示热应激和乳房内感染对繁殖具有累加有害作用。
