Vasodilation


Vasodilation

Description, Causes and Risk Factors:

Widening of the lumen of blood vessels.

Vasodilation occurs in superficial blood vessels of warm-blooded animals when their ambient environment is hot; this process diverts the flow of heated blood to the skin of the animal, where heat can be more easily released into the atmosphere. The opposite physiological process is vasoconstriction. These processes are naturally modulated by local paracrine agents from endothelial cells (e.g. nitric oxide, bradykinin, potassium ions and adenosine), as well as an organism's Autonomic Nervous System (ANS) and adrenal glands, both of which secrete catecholamines such as norepinephrine and epinephrine, respectively.

Vasodilation directly affects the relationship between mean arterial pressure (MAP), cardiac output and total peripheral resistance (TPR). The cardiac output (blood flow measured in volume per unit time) is equal to the heart rate (in beats per unit time) multiplied by the stroke volume (the volume of blood ejected during ventricular systole). TPR depends on several factors including the length of the vessel, the viscosity of blood (determined by hematocrit) and the diameter of the blood vessel. The latter is the most important variable in determining resistance, changing by the fourth power of the radius, in accordance with Poiseuille's Law. An increase in either of these physiological components (cardiac output or TPR) cause a rise in the MAP. Vasodilation works to decrease TPR and blood pressure through relaxation of smooth muscle cells in the tunica media layer of large arteries and smaller arterioles.

Vasodilation is the result of relaxation in smooth muscle surrounding the blood vessels. This relaxation, in turn, relies on removing the stimulus for contraction, which depends on intracellular calcium ion concentrations and, consequently, phosphorylation of the light chain of the contractile protein myosin. Thus, vasodilation mainly works either by lowering intracellular calcium concentration or the dephosphorylation of myosin. This includes stimulation of myosin light chain phosphatase and induction of calcium symporters and antiporters that pump calcium ions out of the intracellular compartment. This is accomplished through reuptake of ions into the sarcoplasmic reticulum via exchangers and expulsion across the plasma membrane. There are three main intracellular stimuli that can result in the vasodilation of blood vessels. The specific mechanism to accomplish these effects varies from vasodilator to vasodilator.

Sometimes, vasodilation can result from a medical emergency such as anaphylactic shock, which is a severe or life-threatening allergic reaction to an allergen. Unlike in the case of a cardiac failure, vasodilation in anaphylaxis is not a good thing, because the dilation of the blood vessels can cause a drop in blood pressure severe enough to bring on shock. Just as there are drugs to provoke vasodilation to save lives, there also are drugs to counter it in cases such as anaphylactic shock. Epinephrine is one of those drugs.

Symptoms:

Symptoms may include,

    Decrease arterial blood pressure.

  • Decreased heart rate.

  • Systemic and pulmonary hypertension.

  • Headaches.

  • Angina.

  • Tissue edema.

Diagnosis:

Due to the lack of specific diagnostic tests, the diagnosis of vasodilation is currently based on several diagnostic criteria.A set of examinations is mandatory prior to the intervention such as chest X-ray, ECG, serum creatinine, blood clotting time.The intervention is usually planned on the basis of an MRI or CT scans.

Treatment:

There is no known method of prevention. Wearing specialised venous support stockings may prevent some vasodilation from developing in some people. Maintaining a normal weight and regular exercise, especially walking, may be helpful; also avoiding the wearing of high heeled shoes as these affect the proper functioning of the larger veins by restricting ankle movement.

In the majority of cases, a procedure called sclerotherapy is used. In this a solution, called a sclerosing agent, is injected with a very fine needle directly into the blood vessel. This procedure has been used for spider veins since the 1930s and long before that for larger veins. The solution irritates the lining of the vessel, causing it to swell and stick together. Over a period of weeks the vessel fades from view, eventually becoming barely visible or not visible at all.

NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.

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