Vascular system, injury

Histamine is a substance present in various tissues of die body, such as die heart, lungs, gastric mucosa, and skin (Pig. 36-1). The highest concentration of histamine is found in die basophil (a type of white blood cell) and mast cells diat are found near capillaries. Histamine is produced in response to injury. It acts on areas such as die vascular system and smooth muscle, producing dilatation of arterioles and an increased permeability of capillaries and venules. Dilatation of die arterioles results in localized redness. An increase in die permeability of... 

Infection 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body s defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the microorganisms gain access to the lymphatic or vascular system. 2. An infectious disease. [EU]... 

The role of the fibrinolytic system is to dissolve any clots that are formed within the intact vascular system and so restrict clot formation to the site of injury. The digestion of the fibrin and hence its lysis is catalysed by the proteolytic enzyme, plasmin, another serine proteinase. Plasmin is formed from the inactive precursor, plasminogen, by the activity of yet other proteolytic enzymes, urokinase, streptokinase and tissue plasminogen activator (tPA) which are also serine proteinases. These enzymes only hydrolyse plasminogen that is bound to the fibrin. Any plasmin that escapes into the general circulation is inactivated by binding to a serpin (Box 17.2). 

Physiologically, the maintenance of blood circulating freely in the vascular system reflects a meticulous balance between coagulation and fibrinolysis. After microvascular injury subendothelial structures are exposed to which platelets adhere. This is followed by their aggregation and activation of the coagulation cascade with the ultimate conversion of fibrinogen to fibrin. 

Exposure to allylamine in industries synthesizing pharmaceuticals and other commercial products is a known occurrence. Allylamines are known to cause adverse effects, especially to the liver, kidney, heart and/or blood vascular systems in experimental humans. It has been reported that exposure to methyl-, ethyl-, heptyl-, and allylamines results in severe pathologic lesions of the above-mentioned vital organs in animals and humans.72 High doses of allylamines are always associated with the induction of fatal cardiovascular injury.72,73... 

Extensive burn injuries produce a systemic response that pulls fluid from the vascular system into the interstitial space. This is exacerbated in burns greater than 20% TBSA by a significant capillary leak into the microvasculature and generalized edema. Without proper treatment, intravascular fluid loss and hypovolemic burn shock result. This is why immediate initiation of fluid resuscitation is important. A successful fluid resuscitation will maintain intravascular volume and organ perfusion until capillary membrane integrity is restored (approximately 24 to 48 hours postinjury). 

CHRONIC HEALTH RISKS damage to kidneys and liver injury to the vascular system changes in olfactory and respiratory systems may alter genetic material. 

Because of negative pressure, the vascular system must be able to support a gas invasion due to injury or cavitation. This is the role of bordered pits or vessel-to-vessel pits. These anatomical features may dramatically inhibit the fluid migration in the wood. 

Immediately following injury, there are changes in vascular flow, caliber, and permeability. Fluid, proteins, and blood cells escape from the vascular system into the injured tissue in a process called exudation. Following changes in the vascular system, which also include changes induced in blood and its components, cellular events occur and characterize the inflammatory response. The effea of the injury and/or biomaterial in situ on plasma or cells can produce chemical factors that mediate many of the vascular and cellular responses of inflammation. 

Selectins are ceU-ceU adhesion molecules, which play a critical role in leukocyte diapedesis through the vascular wall due to inflammation or tissue injury (Table 5.3) (Alberts et al. 2002). The three closely related family members mainly expressed by leukocytes (L-selectin), platelets (P-selectin), and endotheUal cells (E- and P-selectin) contain a characteristic extracellular lectin-domain that binds to carbohydrate ligands (Fig. 5.2). In contrast to other CAMs Hke cadherins or integrins, selectin function is confined to the vascular system. 

On the basis of their location and appearance inside the vascular system, different types of thrombi have been described. The mural thrombus sometimes covers a relatively large surface of the vascular and cardiac wall without altering the lumen or the cavity. Obliterating thrombi occlude the vascular lumen (see Fig. 7-7). Sometimes injuries of the endothelial surface of the valvular structure of the heart lead to the formation of thrombi that are called vegetations. A ball thrombus is a thrombus that comes loose from its mural or valvular attachments and bounces back and forth in the cardiac cavity with the rhythm of the heartbeat. 

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