Changes in Vascular Flow and Caliber in inflammation

Acute InflammationAcute inflammation is a rapid response to an injurious agentthat

serves to deliver mediators of host defenseleukocytes and plasma proteinsto the site of injury. Acute inflammation has three major components:

(1) alterations in vascularcaliber that lead to an increase in blood flow;

(2) structuralchanges in the microvasculature that permit plasma proteins andleukocytes to leave the circulation; and

(3) emigration of theleukocytes from the microcirculation, their accumulation in thefocus of injury, and their activation to eliminate the offending agent ).

The escape of fluid, proteins,and blood cells from the vascular system into the interstitial tissue or body cavities is known as exudation. An exudate isan inflammatory extravascular fluid that has a high proteinconcentration, cellular debris, and a specific gravity above1.020. It implies significant alteration in the normal permeabilityof small blood vessels in the area of injury. In contrast,a transudate is a fluid with low protein content (mostof which is albumin) and a specific gravity of less than 1.012.It is essentially an ultrafiltrate of blood plasma that results from osmotic or hydrostatic imbalance across the vessel wall without an increase in vascular permeability. Edema denotesan excess of fluid in the interstitial or serous cavities; it canbe either an exudate or a transudate. Pus, a purulent exudate,is an inflammatory exudate rich in leukocytes (mostlyneutrophils), the debris of dead cells and, in many cases, microbes.STIMULI FOR ACUTE INFLAMMATION Acute inflammatory reactions are triggered by a variety ofstimuli: Infections (bacterial, viral, parasitic) and microbialtoxins Trauma (blunt and penetrating) Physical and chemical agents (thermal injury, e.g., burnsor frostbite; irradiation; some environmental chemicals) Tissue necrosis (from any cause) Foreign bodies (splinters, dirt, sutures) Immune reactions (also called hypersensitivity reactions)

VASCULAR CHANGES Since the two major mechanisms of host defense againstmicrobesantibodies and leukocytesare normally carriedin the blood stream, it is not surprising that vascular phenomena play a major role in acute inflammation. Normally,plasma proteins and circulating cells are sequestered inside the vessels and move in the direction of flow. In inflammation,blood vessels undergo a series of changes that are designed to maximize the movement of plasma proteins and circulatingcells out of the circulation and into the site of injury or infection.Changes in Vascular Flow and Caliber Changes in vascular flow and caliber begin early after injury and develop at varying rates depending on the severity of the injury.

The changes occur in the following order: Vasodilation is one of the earliest manifestations of acute inflammation; sometimes, it follows a transient constrictionof arterioles, lasting a few seconds. Vasodilation firstinvolves the arterioles and then results in opening of new capillary beds in the area. Thus comes about increased bloodflow, which is the cause of the heat and the redness . Vasodilation is induced by the action of several mediators,notably histamine and nitric oxide, on vascular smooth muscle. Vasodilation is quickly followed by increased permeability, of the microvasculature, with the outpouring of protein rich fluid into the extravascular tissues. The loss of fluid results in concentration of red cells insmall vessels and increased viscosity of the blood, reflectedby the presence of dilated small vessels packed with red cellsand slower blood flow, a condition termed stasis. With mildstimuli, stasis may not become apparent until 15 to 30minutes have elapsed, whereas with severe injury, stasis may occur in a few minutes. As stasis develops, leukocytes, principally neutrophils,accumulate along the vascular endothelium. Leukocytesthen stick to the endothelium, and soon afterward they migrate through the vascular wall into the interstitial tissue.

Changes in Vascular Flow and Caliber in inflammation

By: Dr Izharul Hasan

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