Why vasodilation in inflammation

As a person ages, their baroreceptors become less sensitive. This can reduce their ability to maintain steady blood pressure levels. Blood vessels also become stiffer and less elastic with age. This makes them less able to constrict and dilate as needed. The air at high altitudes contains less available oxygen.

A person at high altitude will therefore experience vasodilation as their body attempts to maintain oxygen supply to its cells and tissues.

Although vasodilation decreases blood pressure in major blood vessels, it can increase blood pressure in smaller blood vessels called capillaries. This is because capillaries do not dilate in response to increased blood flow. Increased blood pressure within the capillaries of the brain can cause fluid to leak into surrounding brain tissue. This results in localized swelling, or edema. Medical professionals refer to this condition as high-altitude cerebral edema HACE.

People at high altitudes may also experience vasoconstriction within the lungs. This can cause a buildup of fluid within the lungs, which medical professionals refer to as high-altitude pulmonary edema HAPE. In some cases, a doctor may induce vasodilation as a treatment for certain conditions.

In other cases, vasodilation may be what requires treatment. Vasodilators are medications that cause the blood vessels to widen. Doctors may use these drugs to reduce blood pressure and ease any strain on the heart muscle.

There are two types of vasodilator: drugs that work directly on the smooth muscle, such as that in the blood vessels and heart, and drugs that stimulate the nervous system to trigger vasodilation.

The type of vasodilator a person receives will depend on the condition they have that needs treatment. Vasodilation is an important mechanism. However, it can sometimes be problematic for people who experience hypotension or chronic inflammation.

People with either of these conditions may require medications called vasoconstrictors. These drugs cause the blood vessels to narrow. For people with hypotension, vasoconstrictors help increase blood pressure. For people with chronic inflammatory conditions, vasoconstrictors reduce inflammation by restricting blood flow to certain cells and body tissues. Vasodilation refers to the widening, or dilation, of the blood vessels.

It is a natural process that increases blood flow and provides extra oxygen to the tissues that need it most. In some cases, doctors may deliberately induce vasodilation as a treatment for certain health conditions. In other cases, doctors may work to reduce vasodilation, as it can worsen conditions such as hypotension and chronic inflammatory diseases.

Doctors sometimes use drugs called vasoconstrictors to help treat these conditions. Learn about healthy blood pressure ranges and when to see a doctor in this…. Women can experience health problems and complications during pregnancy, and one such condition is eclampsia. Repeated bouts of acute inflammation, known as chronic inflammation, leads to a progressive shift in the type of cells present at the site of inflammation and is characterized by simultaneous destruction and healing of the tissue from the inflammatory process.

In particular, fibrosis scarring and tissue necrosis are common outcomes of chronic inflammation. Learning Objectives Describe the biological mechanisms of inflammation and its role in innate immunity. Key Points Acute inflammation occurs due to infection, injury, or irritation, and is an essential part of the healing process to remove pathogens and start the wound-healing process.

During inflammation, vasodilation occurs, the endothelium becomes more permeable as exudate leaks into the tissues, and neutrophils migrate to the site of inflammation. Acute inflammation is initiated by cells already present in all tissues, such as mast cells that recognize pathogen-associated molecular patterns PAMPs with toll-like receptors, but other cells like natural killer NK cells can trigger inflammation as well.

Acute inflammation is characterized by pain, redness, immobility loss of function , swelling, and heat. Neutrophils migrate to inflamed tissues by rolling onto the endothelium with selectins, adhering to it with integrins, and sliding through its gaps with PECAM Then they follow chemokines to the tissues to find pathogens to destroy. Repeated bouts of acute inflammation lead to chronic inflammation, a process of constant healing and inflammation-induced damage as the initial problem is never truly healed.

Allergic reactions are the result of an inappropriate immune response that triggers inflammation. Key Terms extravasion : exudate : Protein-rich edema caused by proteins flowing into the tissues during inflammation due to increased vascular permeability and oncotic pressure. Functions and Components of Inflammatory Response The main function of inflammation is to trigger an immune response in an area of the body that needs it to fight off pathogens that may cause an infection or to help heal an injury.

Vasodilation An inflammatory response can be caused by any of numerous inflammatory mediators released from innate immune system cells. Increased Vascular Permeability The next step of acute inflammation is an increase in vascular permeability due to inflammatory mediator activity, which causes the blood vessels to become more permeable.

Leukocyte Migration to the Tissues The next step of the acute inflammatory response is chemotaxis migration of neutrophils to the affected area.

Outcomes of Acute Inflammation Inflammation : Toes inflamed by chilblains When acute inflammation ends typically by release of anti-inflammatory mediators such as IL or an end to the release of inflammatory mediators resolution will occur if the problem is alleviated. Figure 1 illustrates a typical case of acute inflammation at the site of a skin wound. Figure 1. These events result in the swelling and reddening of the injured site, and the increased blood flow to the injured site causes it to feel warm.

Inflammation is also associated with pain due to these events stimulating nerve pain receptors in the tissue. The interaction of phagocyte PRRs with cellular distress signals and PAMPs and opsonins on the surface of pathogens leads to the release of more proinflammatory chemicals, enhancing the inflammatory response.

During the period of inflammation, the release of bradykinin causes capillaries to remain dilated, flooding tissues with fluids and leading to edema.

Increasing numbers of neutrophils are recruited to the area to fight pathogens. As the fight rages on, pus forms from the accumulation of neutrophils, dead cells, tissue fluids, and lymph. Typically, after a few days, macrophages will help to clear out this pus. Eventually, tissue repair can begin in the wounded area. Figure 2. A tubercle is a granuloma in the lung tissue of a patient with tuberculosis.

In this micrograph, white blood cells stained purple have walled off a pocket of tissue infected with Mycobacterium tuberculosis. Granulomas also occur in many other forms of disease. When acute inflammation is unable to clear an infectious pathogen, chronic inflammation may occur.

This often results in an ongoing and sometimes futile lower-level battle between the host organism and the pathogen. The wounded area may heal at a superficial level, but pathogens may still be present in deeper tissues, stimulating ongoing inflammation.

Chronic inflammation may lead to the formation of granuloma s , pockets of infected tissue walled off and surrounded by WBCs. Macrophages and other phagocytes wage an unsuccessful battle to eliminate the pathogens and dead cellular materials within a granuloma.

One example of a disease that produces chronic inflammation is tuberculosis , which results in the formation of granulomas in lung tissues. A tubercular granuloma is called a tubercle Figure 2.

Tuberculosis will be covered in more detail in Bacterial Infections of the Respiratory Tract. Chronic inflammation is not just associated with bacterial infections. Chronic inflammation can be an important cause of tissue damage from viral infections. The extensive scarring observed with hepatitis C infections and liver cirrhosis is the result of chronic inflammation. Figure 3. Elephantiasis chronic edema of the legs due to filariasis.

In addition to granulomas, chronic inflammation can also result in long-term edema. A condition known as lymphatic filariasis also known as elephantiasis provides an extreme example. Lymphatic filariasis is caused by microscopic nematodes parasitic worms whose larvae are transmitted between human hosts by mosquitoes.

Adult worms live in the lymphatic vessels, where their presence stimulates infiltration by lymphocytes, plasma cells, eosinophils, and thrombocytes a condition known as lymphangitis.

Because of the chronic nature of the illness, granulomas, fibrosis, and blocking of the lymphatic system may eventually occur. Over time, these blockages may worsen with repeated infections over decades, leading to skin thickened with edema and fibrosis.

Lymph extracellular tissue fluid may spill out of the lymphatic areas and back into tissues, causing extreme swelling Figure 3. Secondary bacterial infections commonly follow. Because it is a disease caused by a parasite, eosinophilia a dramatic rise in the number of eosinophils in the blood is characteristic of acute infection.

However, this increase in antiparasite granulocytes is not sufficient to clear the infection in many cases.