Effects of tachykinins on uterine contractility

一组神经，称为感觉神经，供应包括子宫在内的大多数身体器官，并众所周知地向大脑传递信息。现在已经知道，这些神经也能够从这些身体器官内的末端释放出化学物质(神经肽)来影响它们的功能。在子宫中，这些化学物质会导致子宫收缩。我们已经证明，与应用于剖宫产孕妇的类似子宫标本相比，在子宫切除术中应用于非妊娠妇女的小样本时，被称为速激肽的神经肽在较低浓度下有效。这个项目的目的有两个。首先，我们想知道为什么速激肽在非怀孕妇女的子宫组织中更有效。我们将研究的可能解释是，非怀孕妇女的组织包含更多的作用部位，这些肽可以在其中发挥作用，或者，非怀孕妇女子宫组织中这些速激肽的分解减少。如果一种已知的分解子宫中速激肽的物质在怀孕期间比女性未怀孕时表现出更大的活动，就可能发生这种情况。其次，我们希望找出其他化学物质(可以产生炎症反应的物质，特别是一组被称为前列腺素的化学物质)是否可以导致我们正在研究的神经肽的释放，这些化学物质已知在痛经等疾病状态下存在于女性组织中的数量更多。如果它们确实导致了速激肽的释放，这可能是导致疾病状态的一个重要因素。我们的假设是，速激肽和能够分解它们的物质可能在调节未怀孕妇女的子宫收缩能力方面发挥重要作用，在怀孕妇女中可能起到较小的作用。

A group of nerves, called sensory nerves, supply most body organs including the uterus, and are well known to transmit information to the brain. It is now known that these nerves are also capable of releasing the chemicals (neuropeptides) from their endings within these body organs to affect their function. In the uterus these chemicals cause the uterus to contract. We have shown that neuropeptides known as tachykinins are effective in lower concentrations when applied to small specimens of uterine tissue taken from non-pregnant women at hysterectomy than when applied to similar uterine specimens taken from pregnant women at caesarean section. The aim of this project is twofold. Firstly, we want to know why the tachykinins are more potent in uterine tissue from non-pregnant women. Possible explanations that we will examine are that tissues from non-pregnant women contain more sites of action at which the peptides can act, or alternatively, that there is decreased breakdown of these tachykinins in uterine tissue from non-pregnant women. This could occur if a substance known to break down the tachykinins in the uterus shows greater activity during pregancy than when a woman is not pregnant. Secondly, we wish to find out if other chemicals (substances that can produce inflammatory responses, and in particular a group of chemicals known as prostaglandins), that are known to be present in greater amounts in the tissues of women during disease states such as dysmenorrhoea, can cause the release of the neuropeptides that we are studying. If they do cause such a release of tachykinins, this could be an important factor contributing to the disease state. Our hypothesis is that tachykinins and the substances which can break them down may play an important role in regulating uterine contractility in non-pregnant and to a lesser degree in pregnant women.