Say you're at the beach, and you get sand in your eyes. How do you know the sand is there? You obviously can't see it, but if you are a normal, healthy human, you can feel it, that sensation of extreme discomfort, also known as pain. Now, pain makes you do something, in this case, rinse your eyes until the sand is gone. And how do you know the sand is gone? Exactly. Because there's no more pain. There are people who don't feel pain. Now, that might sound cool, but it's not. If you can't feel pain, you could get hurt, or even hurt yourself and never know it. Pain is your body's early warning system. It protects you from the world around you, and from yourself. As we grow, we install pain detectors in most areas of our body. These detectors are specialized nerve cells called nociceptors that stretch from your spinal cord to your skin, your muscles, your joints, your teeth and some of your internal organs. Just like all nerve cells, they conduct electrical signals, sending information from wherever they're located back to your brain. But, unlike other nerve cells, nociceptors only fire if something happens that could cause or is causing damage. So, gently touch the tip of a needle. You'll feel the metal, and those are your regular nerve cells. But you won't feel any pain. Now, the harder you push against the needle, the closer you get to the nociceptor threshold. Push hard enough, and you'll cross that threshold and the nociceptors fire, telling your body to stop doing whatever you're doing. But the pain threshold isn't set in stone. Certain chemicals can tune nociceptors, lowering their threshold for pain. When cells are damaged, they and other nearby cells start producing these tuning chemicals like crazy, lowering the nociceptors' threshold to the point where just touch can cause pain. And this is where over-the-counter painkillers come in. Aspirin and ibuprofen block production of one class of these tuning chemicals, called prostaglandins. Let's take a look at how they do that. When cells are damaged, they release a chemical called arachidonic acid. And two enzymes called COX-1 and COX-2 convert this arachidonic acid into prostaglandin H2, which is then converted into a bunch of other chemicals that do a bunch of things, including raise your body temperature, cause inflammation and lower the pain threshold. Now, all enzymes have an active site. That's the place in the enzyme where the reaction happens. The active sites of COX-1 and COX-2 fit arachidonic acid very cozily. As you can see, there is no room to spare. Now, it's in this active site that aspirin and ibuprofen do their work. So, they work differently. Aspirin acts like a spine from a porcupine. It enters the active site and then breaks off, leaving half of itself in there, totally blocking that channel and making it impossible for the arachidonic acid to fit. This permanently deactivates COX-1 and COX-2. Ibuprofen, on the other hand, enters the active site, but doesn't break apart or change the enzyme. COX-1 and COX-2 are free to spit it out again, but for the time that that ibuprofen is in there, the enzyme can't bind arachidonic acid, and can't do its normal chemistry. But how do aspirin and ibuprofen know where the pain is? Well, they don't. Once the drugs are in your bloodstream, they are carried throughout your body, and they go to painful areas just the same as normal ones. So that's how aspirin and ibuprofen work. But there are other dimensions to pain. Neuropathic pain, for example, is pain caused by damage to our nervous system itself; there doesn't need to be any sort of outside stimulus. And scientists are discovering that the brain controls how we respond to pain signals. For example, how much pain you feel can depend on whether you're paying attention to the pain, or even your mood. Pain is an area of active research. If we can understand it better, maybe we can help people manage it better.
假设你在海滩上,沙子进了眼睛 你怎么知道有沙子呢? 显然你看不到 但若你是个正常、健康的人 你可以感觉到有沙子 这种极不舒服的感觉叫做「疼痛」 疼痛要你采取行动 此例中是要你 冲洗眼睛,直到沙子消失 你怎么知道沙子不见了? 没错,因为不痛了 有人感觉不到疼痛 听起来很酷,但其实一点也不酷 如果感觉不到疼痛 你可能会受伤,甚至可能伤到自己 而完全不知道 疼痛是你身体的早期预警系统 可保护你不受到 周围世界或自己的伤害 随着我们长大,疼痛感测器 会安装在身体的大多数地方 这些感测器是特殊的神经细胞 称为「痛觉感受器」 分布在脊髓、皮肤、肌肉、关节 牙齿和一些内脏 就像所有的神经细胞 它们传送电信号 从它们所在之处传送讯号回大脑 但是,不像其他神经细胞 痛觉感受器在身体可能或正在收到伤害时 才会作用 所以,轻摸针尖 你可以感觉到金属 一般神经细胞给你这种感觉 但是你不会感到任何疼痛 但你越用力推针尖 越接近痛觉感受器的极限值 很用力的话,就会超过极限值 痛觉感受器会启动 并告诉身体停止目前的行为 痛觉感受器的门槛,并非一成不变 某些化学物质可以调节感受器 降低痛觉的阈值 细胞受损时,受损细胞及邻近细胞 开始疯狂生产这些调节化学物质 降低痛觉感受器的门槛,直到 连触摸都会疼痛 这时非处方的止痛药 可以大展身手了 阿斯匹灵和布洛芬 可阻止一种调节化学物质的生产 称为「前列腺素」 我们来探讨一下原理 当细胞损伤,会释放一种化学物质 叫做「花生油酸」 有两种酵素 COX-1 和 COX-2 可将花生油酸转换成前列腺素 H 2 再将其转换成一系列化学物质 产生一连串效果 包括升高体温、引起发炎、 降低疼痛阈值 所有的酵素有特定的活性部位 也就酵素反应发生的地方 COX-1 和 COX-2 的活性部位 非常适合花生油酸 正如你看到的,也没有多余的空间 阿斯匹灵和布洛芬,就是在这个 活性部位发挥作用 它们的工作原理不同: 阿斯匹灵像豪猪的刺 进入活性部位,然后脱落 留下一半在那里 完全阻断通道,让花生油酸进不来 这会永久停用 COX-1 和 COX-2 另一方面,布洛芬 进入活性部位 但不破坏或改变酵素 COX-1 和 COX-2 可把它再吐出来 但布洛芬在那里的期间 酵素无法结合花生油酸 因此无法进行正常的化学反应 阿斯匹灵和布洛芬 怎么知道哪里痛? 噢,它們並不知道 一旦药物进入血液中 就会被带往全身 不但会到疼痛部位 也会到正常部位 这就是阿斯匹灵和布洛芬的原理 还有其他种类的疼痛 例如神经性疼痛 是神经系统本身受损 所引起的疼痛 这种疼痛不需要任何形式的外界刺激 科学家们发现,大脑控制了 我们对疼痛信号的反应 例如,疼痛的程度取决于 你对疼痛的在意程度 甚至是你的心情 疼痛是个活跃的研究领域 如果我们能更了解疼痛 或许我们就更能有效的管理疼痛