Inflammation Vasodilation

Vascular Inflammation, vasodilation, hemorrhage mir-126 miR-17 miR-146a Endothelial cells promote vascular homeostasis, release factors including NO Yamakuchi (2012)... 

Lippe, I.T., Stabentheiner, A. and Holzer, P. (1993a). Role of nitric oxide in the vasodilator but not exudative component of mustard oil-induced inflammation in rat skin. Agents Actions 38, c22-24. 

Histamine, which promotes bronchoconstriction as well as the vasodilation and increased capillary permeability that lead to inflammation... 

Inflammation is a local and early response of a tissue to a noxious stimulus, such as physical injury or infection. It results in an increase in the number of immune cells in the area of damage or infection which kill pathogens, remove damaged or dead cells and initiate the healing process. The well-known characteristics of inflammation are redness, heat, swelling and pain. Redness is due to increased blood flow to the damaged area caused by vasodilation of small arterioles, which facilitates an increase in the number of immune cells in the damaged area and facilitates provision... 

Adenosine 2a receptor ADORA2A Agonism Inhibition of platelet aggregation, anti-inflammation and neuroprotective effects, coronary vasodilation, decreased blood pressure, increased plasma renin activity and sleep induction. Antagonism Increased platelet aggregation, hypertension, nervousness (tremor, agitation), arousal, insomnia, cerebral and coronary vasodilation (in microvessels only). 

The inflammatory response changes with time and can be divided into phases. The rapid phase occurs within seconds to minutes and consists of vasodilation, increased blood flow, edema, and pain. The acute phase is characterized by induction of inflammatory genes by NF-kB and other transcription factors. During this phase, moderate amounts of inflammatory mediators are produced. The chronic phase occurs over months to years and is marked by dramatically increased production of inflammatory mediators. The secondary chronic phase of inflammation occurs after years of oxidative damage has degraded blood vessels and tissues. Such chronic inflammation appears to play a role in many disease states, such as arteriosclerosis and cancer. 

In addition to the phagocytic activity of the leukocytes, small peptide substances, such as the kinins, which are thought to be partially responsible for the local inflammatory response in gouty arthritis, accumulate in the joint space. The inflammation is associated with local vasodilation, increased vascular permeability, and pain. 

Vaginitis. Inflammation of the vagina marked by pain and by a purulent discharge. Vasoconstrictor. An agent that causes blood vessels to constrict, or narrow the caliber. Vasodilator. An agent that causes blood vessels to relax and dilate. 

Endogenous histamine has a modulating role in a variety of inflammatory and immune responses. Upon injury to a tissue, released histamine causes local vasodilation and leakage of plasma-containing mediators of acute inflammation (complement, C-reactive protein) and antibodies. Histamine has an active chemotactic attraction for inflammatory cells (neutrophils, eosinophils, basophils, monocytes, and lymphocytes). Histamine inhibits the release of lysosome contents and several T- and B-lymphocyte functions. Most of these actions are mediated by H2 or H4 receptors. Release of peptides from nerves in response to inflammation is also probably modulated by histamine, in this case acting through presynaptic H3 receptors. 

The stimulation of C fibers by capsaicin causes a subset of sensory airway neurons to release several neuropeptides, which include tachykinin, substance P and neurokinin A. In addition to capsaicin, other endogenous mediators including histamine, prostaglandins and bradykinins can also result in their release. These neuropeptides are responsible for neurogenic inflammation, which is characterized by vasodilation, mucus secretion, plasma protein extravasation, increased expression of the adhesion molecules and bronchoconstriction. 

Besides neuropeptides, nitric oxide is an inflammatory mediator in the airways, which is also a vasodilator and a neurotransmitter. Nitric oxide is produced by the enzymatic action of nitric oxide synthetase on L-arginine. Airways contain this enzyme in three different forms, two of which termed neuronal and endothelial nitric oxide synthetase are constitutive whereas the third form called inducible nitric oxide synthetase is inducible. The inflammatory cytokines including IL-1 and TNF-a augment the expression of inducible nitric oxide synthetase in human airway epithelial cells. Nitric oxide causes bronchodilation as a result of the relaxation of bronchial smooth muscles. It has also been suggested that nitric oxide is the neurotransmitter of the inhibitory NANC bronchodilation. The detrimental effects of nitric oxide include airway inflammation and vasodilation. It causes airway edema by increasing the erudition of plasma due to increased blood flow to postcapillary venules. The increased blood flow may also contribute to an increased mucus secretion. The role of nitric oxide in inflammatory responses has not yet been established. 

Cryotherapy Cold/ice packs Ice massage Cold bath Vapocoolant sprays Decreased pain, edema, and inflammation Muscle relaxation and decreased spasticity Anti-inflammatory steroids (glucocorticoids) nonsteroidal anti-inflammatory analgesics (aspirin and similar NSAIDs) Skeletal muscle relaxants Peripheral vasodilators may exacerbate acute local edema Nonselective cholinergic agonists may stimulate the neuromuscular junction Some forms of cryotherapy may produce local vasoconstriction that temporarily impedes diffusion of drugs to the site of inflammation... 

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