It had been three years since I had arrived in Germany and only a few months since I began working as an assistant doctor. It had been a long and tiring day. I had breakfast early in the morning before heading out, and my lunch was just a banana and a cup of coffee. By the time I got home late in the evening, I was both very hungry and tired. The past few years had been challenging and weighed heavily on me. I was no longer as young as I used to be, nor was I a specialist doctor, as I had been back home. I was trying to survive in a foreign culture, struggling to communicate in a language I barely knew. To the many wounds in my body and soul, aching and waiting to heal with hope, was now added the stress of an unfamiliar work environment.
When I stepped into the kitchen to quickly prepare something, I accidentally cut my left index finger. Although the cut wasn’t very deep, it started bleeding right away. “Here’s another wound to wait patiently to heal,” I thought to myself. I looked closely at my bleeding finger. The blood trickled slowly down into my hand like a tiny red spring, accumulating over the cut before finally stopping after about three minutes. From the outside, it seemed very simple, but it wasn't like that at all.
Repairing a hole in a ship floating in water is extremely challenging. High-pressure water outside meets low-pressure air inside, and this significant pressure difference causes seawater to continuously rush in. Similarly, repairing a hole deep in a dam wall is also difficult. Due to gravity and pressure differences, water tries to gush out of the hole, potentially bursting through the solid walls around it. While repairs are straightforward when the dam is empty, fixing a damaged area when the dam is full of water is much harder, as neither iron nor cement can easily hold under these conditions. How is it that the bleeding can be stopped so quickly when the vessels that carry our life-sustaining blood are damaged? With certain pressure in our vascular network, estimated to be 90,000-120,000 kilometers long, our blood flows continuously, delivering essential nutrients and oxygen to the tissues and removing byproducts of cellular metabolism. Blood pressure, regulated by the contraction and relaxation of the heart, is considered normal if below 140/90 mmHg, with an ideal reading below 120/80 mmHg. Yet, we have no advanced machines, nor any extraordinary bricks or superglues in our blood to repair vessel damage. So, which craftsman, and with what materials, stops this bleeding?
In a healthy individual, bleeding time ranges between two and nine minutes, with an average around five minutes. The blood flowing in the vascular network of tens of thousands of kilometers in our body contains coagulation factors and coagulation cells (called platelets or thrombocytes), whose role is repairing the vessel wall when it is harmed. The coagulation process, also called hemostasis, takes place in two stages: primary and secondary. This process activates immediately upon bleeding, both on our skin and within our body, where even a small injury can trigger major reactions.
One of the most crucial roles in the coagulation process is assigned to coagulation cells, known as platelets. These are actually cell fragments, not complete cells, and are named platelets because of their flat, plate-like shape. Measuring 1.5–3 μm (micrometers) in diameter, these fragments are produced in the bone marrow from large, multinucleated cells called megakaryocytes. After production, platelets have a lifespan of 9–10 days and are then broken down in the spleen once their role is complete. Although they lack a nucleus, platelets contain numerous vesicles (granules) filled with various substances. Through channels formed by inward extensions of their cell membrane, they are kept informed of changes in external tissues and developments in the blood.
As I pondered these mechanisms within the blood, I thought of the massive devices in the laboratory at the hospital where I work—machines required for measuring even the simplest blood tests. Yet these minuscule cells in our bodies, far too small to be seen with the naked eye, are endowed with far greater abilities than those large machines. Not only do they function like tiny laboratories, but they also sense alarms in the blood, rushing to the rescue like soldiers awaiting orders. We are remarkably well-equipped, with between 150,000 and 450,000 platelets in just one milliliter of blood, and around 5 liters of blood in total. Primary coagulation, the initial stage of stopping bleeding, begins as soon as there is a vascular injury. When the endothelial cells lining the inner surface of the vessels are damaged, the underlying connective tissue is exposed. Platelet “soldiers,” alerted by certain molecules released from this tissue, spring into action. Blood clotting involves a chain of reactions occurring in sequence, with various factors contributing at each step. Each of the approximately 16 factors have a specific task. In the coagulation process, which functions like a row of dominoes, each factor has been precisely chosen, appreciated, and positioned with boundless knowledge and wisdom. If even one factor is missing, the chain breaks, and coagulation is disrupted. Therefore, an event as complex as blood clotting could not arise randomly through mutations or chaotic chemical reactions. This phenomenon, called platelet activation, is like a commander's declaration of mobilization. Platelets adhere to the damaged area with the help of “Von Willebrand factor”—a protein that binds platelets to collagen exposed in the tissue when a vessel is injured. The ADP (adenosine triphosphate) secreted by platelets discharges the messenger molecule, signaling other “soldiers” to come help. Arachidonic acid is secreted from the cell membrane of the platelets adhering to the injured wound, leading to the production of two molecules: thromboxane A2 and PGI2 (prostacyclin). These two molecules work together to stop the bleeding.
The task of thromboxane A2, which is synthesized from arachidonic acid in coagulation cells, is to skillfully arrange platelet bricks, allowing them to cluster and form plugs. Additionally, coagulation cells secrete serotonin, which helps the vessel wall to constrict, reducing the bleeding surface and thus the amount of blood loss. The actin and myosin strands in coagulation cells contract and shrink further strengthening the platelet plug.
The second stage, known as secondary coagulation, activates later and makes the platelet plug—initially fragile and weak—much more stable and stronger. During this stage, fibrinogen molecules in the blood bond together, transforming into a sticky, thread-like protein called fibrin. Fibrin fibers act like a powerful adhesive, binding to the platelet plug and, along with red blood cells, weaving into solid layers. As with any biological system, there is a need for some agents to oversee and regulate the process. The endothelial cells lining the vessel’s inner surface monitor the events with the meticulousness of an inspector, as if they had studied biochemistry. When the time comes, these cells secrete prostacyclin (PGI2), synthesized from arachidonic acid taken from platelets. This prevents platelet aggregation and expands the vessel wall, confining the plug to the damaged area and ensuring uninterrupted blood flow to distant regions.
Limiting coagulation is just as vital as stopping bleeding. Without molecules such as prostacyclin, clots formed in a period of seconds would extend along the vessel for meters, and organs deprived of blood flow would face gangrene. Meanwhile, a separate clot-dissolving system has been established to ensure that vessels supplying vital organs, such as the brain, heart, and lungs, are not blocked. Again, the enzymes in this system, created with endless knowledge, mercy and wisdom, dissolve unnecessary clots and prevent blockages.
“Another wound has been bandaged and is now waiting to heal,” I thought. The Almighty, who heals even the smallest and seemingly insignificant wounds in this way, is surely able to heal all wounds in a way we never expected – as long as we are patient.
