63 - Chapter 63 REACTIONS TO INJURY This chapter provides a...

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Chapter 63 REACT IONS TO INJURY This chapter provides a brief overview of how animals react to an acute cutaneous trauma (e.g. a minor laceration) or a localized infection. As described earlier in Box 34-4, in far more serious trauma such as that involving significant hemorrhage, the immediate responses are aimed at preserving cardiovascular homeostasis. The description here is confined to the relatively nonspecific defenses provided by the innate immune system, described in the preceding chapter. A. Inflammation Many forms of injury provoke a relatively uniform series of reactions by the animal's body. After blood clotting to stem blood loss from ruptured or severed blood vessels, the most important, rapid, response is inflammation . This serves to isolate and destroy noxious agents, to clean up damaged tissue, and to prepare the tissue for healing. Central to inflammatory reactions is the part played by vasoactive substances such as histamine, serotonin, and bradykinin, all of which have been described in previous chapters. Histamine is released from mast cells and basophils in response to a variety of signals. Bradykinin, the end-product of a cascade of events (the kinin cascade), is derived from inactive plasma proteins called kinins. Serotonin, in this instance, is released from platelets when they are provoked into aggregating at a site of injury to the vasculature. Various additional proinflammatory factors act to attract leukocytes to the site of the injury. By way of introduction, the following description applies to the reactions following a cutaneous injury. Exposure of the sub-endothelial materials (e.g. collagen) in the basal lamina of damaged blood vessels causes platelets within the blood to aggregate at the location of endothelial disruption. Platelets change their surface properties so that they become “sticky” and the aggregated platelets form a temporary "plug". The platelets release several factors including serotonin, which triggers a very local vasoconstriction and clotting factors so that blood coagulation, using both of the clotting pathways (Chapter 32), is set in motion. The platelet plug and temporary vasoconstriction is followed by clotting to provide a more rugged mechanism for hemostasis.
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This note was uploaded on 03/23/2009 for the course ANSCI 1110 taught by Professor Brucecurrie during the Fall '08 term at Cornell University (Engineering School).

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63 - Chapter 63 REACTIONS TO INJURY This chapter provides a...

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