Pain, Anaesthesia & Inflammation

prostaglandin

Prostaglandins are short-lived chemical messengers that tissues make on the spot, in response to injury or stress, to coordinate the local response. They are not stored and shipped around like hormones; instead each cell brews them as needed and they act right where they are made, then break down within seconds. They are the local foremen of inflammation, pain, and fever.

Chemically they are lipid mediators built from arachidonic acid by the cyclooxygenase enzymes. Different prostaglandins do different jobs: some widen blood vessels and make tissue red and swollen, some sensitise nerve endings so that touch becomes painful, and one acting on the brain's temperature centre raises the body's thermostat to cause fever. The same family also protects the stomach lining, maintains kidney blood flow, and regulates platelet clumping and uterine contractions.

Because prostaglandins sit at the heart of pain, fever, and inflammation, they are the target of some of the most-used drugs in the world. NSAIDs and aspirin work by cutting off prostaglandin production at the cyclooxygenase step, and that single intervention explains both their benefits and their characteristic harms — relief of pain alongside stomach ulcers, kidney stress, and altered bleeding. Naming a culprit molecule like this is what lets one drug class treat so many seemingly different complaints.

Prostaglandins do not directly cause pain so much as turn up the gain: they sensitise nociceptors so that ordinary stimuli are felt as painful (a state called hyperalgesia).