(音樂)
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.
假設你在海灘上,沙子進了眼睛 你怎麼知道有沙子呢? 顯然你看不到 但若你是個正常、健康的人 你可以感覺到有沙子 這種極不舒服的感覺叫做「疼痛」 疼痛要你採取行動 此例中是要你 沖洗眼睛,直到沙子消失 你怎麼知道沙子不見了? 沒錯,因為不痛了 有人感覺不到疼痛 聽起來很酷,但其實一點也不酷 如果感覺不到疼痛 你可能會受傷,甚至可能傷到自己 而完全不知道 疼痛是你身體的早期預警系統 可保護你不受到 周圍世界或自己的傷害 隨著我們長大,疼痛感測器 會安裝在身體的大多數地方 這些感測器是特殊的神經細胞 稱為「痛覺感受器」 分布在脊髓、皮膚、肌肉、關節 牙齒和一些內臟 就像所有的神經細胞 它們用電傳送信號 從它們所在之處,送訊號回大腦 不像其他神經細胞 痛覺感受器只在 可能、或正在造成傷害時 才會作用 所以,輕摸針尖 你可以感覺到金屬 一般神經細胞給你這種感覺 不會感到任何疼痛 但你越用力推針尖 越接近痛覺感受器的閾值 (譯註:閾值指的是生物上產生神經脈衝的門檻。) 很用力的話,就會超過閾值 痛覺感受器啟動 告訴身體停止目前的行為 痛覺感受器的門檻,並非一成不變 某些化學物質可以調節感受器 降低痛覺的閾值 細胞受損時,受損細胞及鄰近細胞 開始瘋狂生產這些調節化學物質 降低痛覺感受器的門檻,直到 連觸摸都會疼痛 這時非處方的止痛藥 可以大展身手了 阿斯匹靈和布洛芬 可阻止一種調節化學物質的生產 稱為「前列腺素」 我們來探討一下原理 當細胞損傷,會釋放一種化學物質 叫做「花生油酸」 有兩種酵素 COX-1 和 COX-2 可將花生油酸轉換成前列腺素 H 2 再將其轉換成一系列化學物質 產生一連串效果 包括升高體溫、引起發炎、 降低疼痛閾值 所有的酵素有特定的活性部位 也就酵素反應發生的地方 COX-1 和 COX-2 的活性部位 非常適合花生油酸 正如你看到的,也沒有多餘的空間 阿斯匹靈和布洛芬,就是在這個 活性部位發揮作用 它們的工作原理不同: 阿斯匹靈像豪豬的刺 進入活性部位,然後脫落 留下一半在那裡 完全阻斷通道,讓花生油酸進不來 永久停用 COX-1 和 COX-2 另一方面,布洛芬 進入活性部位 但不破壞或改變酵素 COX-1 和 COX-2 可把它再吐出來 但布洛芬在那裡的期間 酵素無法結合花生油酸 因此無法進行正常的化學反應 阿斯匹靈和布洛芬 怎麼知道哪裡痛? 噢,它們並不知道 一旦藥物進入血液中 就會被帶往全身 不但會到疼痛部位 也會到正常部位 這就是阿斯匹靈和布洛芬的原理 還有其他種類的疼痛 例如神經性疼痛 是神經系統本身受損 所引起的疼痛 不需要任何形式的外界刺激 科學家們發現,大腦控制了 我們對疼痛信號的反應 例如,疼痛的程度取決於 你對疼痛的在意程度 甚至是你的心情 疼痛是個活躍的研究領域 如果能更了解疼痛 或許就更能有效的管理疼痛