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Heparin: Mechanism of Action

Instructor: Amanda Robb

Amanda holds a Masters in Science from Tufts Medical School in Cellular and Molecular Physiology. She has taught high school Biology and Physics for 8 years.

In this lesson, we'll be learning about the anticoagulant drug, heparin. Here, you'll discover how heparin works and why it is used for certain medical treatments.

What Is Heparin?

Everything has been quiet on the night shift in the emergency department so far. But suddenly, you hear ambulance sirens approaching. The EMTs rush an unresponsive patient, who is suffering from a heart attack, into the waiting area. The arteries carrying blood to their heart are clogged and their heart is not receiving oxygen. Every moment the blood clot clogging their artery stays put is another moment heart tissue continues to die.

To save them, you administer an anti-coagulant drug called heparin intravenously. Heparin should quickly dissolve the blood clot, helping your patient get the oxygen they need. Your patient may also stay on heparin to prevent further clots from forming.

Heparin is an anti-coagulant drug. This type of drug interferes with the body's blood clotting process, preventing blood clots from forming. Heparin is sometimes called a blood thinner, but it doesn't actually thin your blood. Rather it prevents clots from forming, keeping the blood liquid. Today, we're going to learn how heparin works at the molecular level and why it is used as an anticoagulant drug.

Coagulation Cascade

Based on this scenario you might assume that blood clots are a problem in the body, but really we need blood clot formation to survive, just in the right places. Blood clots are collections of proteins in your blood that prevent blood from flowing. If you've ever scraped your knee you know that the cut eventually stops bleeding. That's because the cut itself triggers blood clots to form. They stop the cut from bleeding, so your cut closes up and eventually heals.

Blood clots can also form in places they are not supposed to, like when you have a blood clot inside your blood vessels. This can lead to blocked blood flow to important organs like the heart in a heart attack, or the brain during a stroke.

To understand how heparin prevents blood clots from forming, we first need to understand how they form in the first place. The sequence of events to create blood clots is called the coagulation cascade. The coagulation cascade is initiated either by external factors like a wound, or internal factors like a trauma. The pathway that involves external damage to the body is called the extrinsic pathway. Whereas pathways that stem from trauma inside the body are called the intrinsic pathway.

Both pathways start with platelets sticking together, slowing blood flow. After that, other proteins in the blood become activated. These proteins usually exist in an inactive form called a zymogen. Zymogens get cut, or cleaved, to become active once coagulation starts.

All parts of the coagulation cascade end in one common sequence of events called the common pathway. First, factor Xa is activated. Factor Xa cleaves another protein called prothrombin to its active form, thrombin. Thrombin then cleaves another protein fibrinogen into its active form fibrin. Fibrin is a long stringy protein that forms a mesh-like covering in the blood vessel or over the wound. This covering traps more platelets forming blood clots, which stop any blood flow.

The common pathway of the coagulation cascade ending in fibrin activation
coagulation cascade

Mechanism of Action

We know that heparin interferes with the blood clotting process, but how does it do so? Our bodies have ways of keeping itself in balance or homeostasis. Our body has ways to turn on the coagulation cascade, and also ways to turn it off.

A natural inhibitor of thrombin in the body is called antithrombin. Heparin binds to antithrombin, which changes the shape of antithrombin. Heparin is able to bind to antithrombin because of its structure as one of the most negatively charged molecules in the body. Heparin's extensive negative charges located on sulfate groups on the molecule are necessary for its high-affinity binding to antithrombin. Once heparin binds to antithrombin, its new shape allows it to be more biologically active and bind to thrombin faster, thus inhibiting thrombin better than without heparin.

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