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.
Estás na praia e éntrache area nos ollos. Como sabes que tes area neles? Obviamente non podes vela, pero se es unha persoa sa normal, podes sentila, esa sensación de incomodidade extrema, tamén chamada dor. Entón, a dor impúlsate a facer algo, neste caso, lavar os ollos ata que a area se vaia. E como sabes que xa non está? Exacto: porque xa non hai dor. Hai persoas que non senten dor. Iso pode soar ben, pero non o está. Se non sentes dor, podes mancarte, incluso a ti mesmo, e nunca te darías conta. A dor é un sistema de aviso rápido. Protexe o teu corpo do entorno que o rodea e de ti mesmo. A medida que medramos, instálanse detectores da dor por todo o corpo. Estes son células nerviosas especializadas chamados nociceptores que se estenden desde a medula espiñal ata a pel, os músculos, as articulacións, os dentes e algúns órganos internos. Igual que as neuronas, conducen sinais eléctricos e envían información desde a súa localización ata o cerebro. Porén, a diferenza doutras neuronas, os nociceptores só se activan se algo causa ou está causando un dano. Se tocas con coidado a punta dunha agulla, sentirás o metal. Esas son as células nerviosas normais. Pero non sentirás dor. Se premes con forza contra a agulla, acercaraste ao limiar da dor. Premendo coa forza suficiente, pasarás o límite e activaranse os nociceptores, que avisan o corpo de que pare o que está a facer. Pero este límite non é fixo. Algúns compostos poden afectar aos nociceptores e baixar o limiar da dor. Cando se danan as células, estas, xunto con outras próximas, comezan a liberar estes compostos coma tolas e a baixar o limiar dos nociceptores ata o punto en que o mero contacto produce dor. E aquí é onde entran en xogo os analxésicos comúns. A aspirina e o ibuprofeno bloquean a produción dun destes compostos, chamados prostaglandinas. Botemos unha ollada a como o fan. Cando hai un dano celular, libérase un composto chamado ácido araquidónico. Dous enzimas denominados COX-1 e COX-2 converten este ácido araquidónico en prostaglandina H2, que se pode transformar nunha chea de compostos con diferentes accións, como aumentar a temperatura corporal, causar unha inflamación e baixar o limiar da dor. Todos os enzimas teñen un sitio activo. Este é o lugar do enzima onde ten lugar a reacción. Os sitios activos de COX-1 e COX-2 axústanse ao ácido araquidónico á perfección. Como se pode ver, non sobra sitio. E é neste sitio onde a aspirina e o ibuprofeno fan o seu traballo, pero de diferente forma. A aspirina actúa como unha espiña dun ourizo. Entra no sitio activo, rompe e deixa unha parte dentro, que bloquea o sitio e fai imposible que encaixe o ácido araquidónico. Isto desactiva de forma permanente COX-1 e COX-2. Por outra banda, o ibuprofeno entra no sitio activo, pero non rompe nin cambia o enzima. COX-1 e COX-2 son capaces de librarse del, pero, mentres o ibuprofeno estea unido, o ácido araquidónico non se une ao enzima, polo que non funciona de forma normal. Pero como saben a aspirina e o ibuprofeno onde se localiza a dor? Ben, non o saben. Unha vez os medicamentos chegan ao sangue, transpórtanse por todo o corpo, e acaban chegando ás zonas doridas igual que ao resto. Esta é a forma en que funcionan a aspirina e o ibuprofeno. Pero hai outras dimensións de dor. A dor neuropática, por exemplo, débese a un dano no propio sistema nervioso; non necesita ningún estímulo externo e os científicos están descubrindo que o cerebro controla como respondemos á dor. Por exemplo, a cantidade de dor que sentes depende de se lle estás a prestar atención ou incluso do teu estado de ánimo. A dor é unha grande área de estudo. Se a entendemos mellor, quizais poidamos axudar as persoas a levala mellor.