Dobson H, Smith R F
Department of Veterinary Clinical Science and Animal Husbandry, University of Liverpool, Leahurst, Wirral, Neston, UK.
Anim Reprod Sci. 2000 Jul 2;60-61:743-52. doi: 10.1016/s0378-4320(00)00080-4.
Stress is revealed by the inability of an animal to cope with its environment, a phenomenon that is often reflected in a failure to achieve genetic potential. Field data from dairy cows show that stressors such as milk fever or lameness increase the calving to conception interval by 13-14 days, and an extra 0.5 inseminations are required per conception. We suggest that a variety of endocrine regulatory points exist whereby stress limits the efficiency of reproduction. Transport produces an immediate constant increase in arginine vasopressin (AVP) and corticotrophin-releasing hormone (CRH) secretion in ewes, but adrenocorticotrophic hormone (ACTH) reaches a maximum in the first hour while cortisol is highest during the second hour. In contrast, after an insulin injection, the hypothalamo-pituitary-adrenal (HPA) response is delayed occurring only after glucose decreases below a threshold. Changes in AVP, CRH and ACTH each follow a similar time course, but eventually the secretion of AVP and CRH decreases while glucose is still at a nadir. Negative feedback effects appear to operate mainly at the pituitary level during transport but at the hypothalamus during hypoglycaemia. We also have endocrine evidence to show that stressors interfere with precise timings of reproductive hormone release within the follicular phase. Transport, or insulin, reduce the frequency and amplitude of gonadotrophin-releasing hormone and LH pulses, suggesting that these stressors exert effects at the hypothalamus or higher centres in the brain. Both stressors also delay the onset of the luteinising hormone (LH) surge. Preliminary results suggest that opioids mediate these effects but progesterone/glucocorticoid receptors are not involved because the antagonist, RU486, is unable to reverse insulin-induced delays in the LH surge. There is also evidence to support effects at pituitary level because exogenous ACTH, or transport, reduce the amount of LH released by challenges with GnRH. The reduction in endogenous GnRH/LH secretion ultimately deprives the ovarian follicle of adequate gonadotrophin support leading to reduced oestradiol production by slower growing follicles. Thus, there is a level of interference by stressors at the ovary. Reproduction is such an important physiological system that animals have to ensure that they can respond to their surroundings; thus, it is advantageous to have several protein mechanisms, i.e. at higher brain, hypothalamus, pituitary and target gland levels. However, when pushed too far, subfertility occurs.
动物无法应对其环境就表明其处于应激状态，这种现象通常表现为无法发挥遗传潜力。奶牛的田间数据显示，诸如产乳热或跛足等应激源会使产犊至受孕间隔延长13 - 14天，每次受孕需要额外进行0.5次授精。我们认为存在多种内分泌调节点，应激通过这些调节点限制繁殖效率。运输会使母羊体内的精氨酸加压素（AVP）和促肾上腺皮质激素释放激素（CRH）分泌立即持续增加，但促肾上腺皮质激素（ACTH）在第一小时达到峰值，而皮质醇在第二小时最高。相比之下，注射胰岛素后，下丘脑 - 垂体 - 肾上腺（HPA）反应会延迟，仅在血糖降至阈值以下后才会出现。AVP、CRH和ACTH的变化各自遵循相似的时间进程，但最终AVP和CRH的分泌会减少，而此时血糖仍处于最低点。负反馈效应在运输过程中似乎主要作用于垂体水平，而在低血糖期间作用于下丘脑。我们还有内分泌学证据表明，应激源会干扰卵泡期生殖激素释放的精确时间。运输或胰岛素会降低促性腺激素释放激素和促黄体生成素（LH）脉冲的频率和幅度，这表明这些应激源在大脑的下丘脑或更高中枢发挥作用。这两种应激源还会延迟促黄体生成素（LH）高峰的出现。初步结果表明，阿片类物质介导了这些效应，但孕酮/糖皮质激素受体未参与其中，因为拮抗剂RU486无法逆转胰岛素诱导的LH高峰延迟。也有证据支持在垂体水平的作用，因为外源性ACTH或运输会减少GnRH刺激释放的LH量。内源性GnRH/LH分泌的减少最终使卵巢卵泡得不到足够的促性腺激素支持，导致生长较慢的卵泡产生的雌二醇减少。因此，应激源在卵巢水平存在一定程度的干扰。繁殖是如此重要的生理系统，以至于动物必须确保它们能够对周围环境做出反应；因此，拥有多种蛋白质机制是有利的，即在大脑高级中枢、下丘脑、垂体和靶腺水平。然而，当压力过大时，就会出现生育力低下的情况。
