lecture 4

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Department
Biological Sciences
Course
BIOC63H3
Professor
Ivana Stehlik
Semester
Fall

Description
10 The Cardiovascular System The BloodHemostasis Hemostasis refers to the stoppage of blood When blood vessels are damaged or ruptured the hemostatic response must be quick localized to the region of damage and carefully controlled Three basic mechanisms reduce blood loss 1 vascular spasm 2 platelet plug formation and 3 blood clotting coagulation These mechanisms are useful for preventing hemorrhage loss of blood in smaller blood vessels but extensive hemorrhage in larger vessels usually requires medicalveterinary intervention Vascular SpasmWhen arteries or arterioles are damaged the circularly arranged smooth muscle in their walls contracts immediately This is called vascular spasm It reduces blood loss for several hours during which time the other hemostatic mechanisms go into operation The spasm is probably caused by damage to the smooth muscle and from reflexes initiated by pain receptors Platelet Plug FormationIn their unstimulated state platelets are discshaped Two types of granules are present in the cytoplasm 1Alpha granules These contain clotting factors and plateletderived growth factor PDGF which can cause proliferation of vascular endothelial cells vascular smooth muscle fibers and fibroblasts to help repair damaged blood vessel walls22 Dense granules These contain ADP ATP Ca and serotonin Also present are enzymes that produce thromboxane A2 a prostaglandin fibrinstabilizing factor which helps to strengthen a blood clot lysosomes some mitochondria membrane systems that take up and store calcium and provide channels for release of the contents of granules and glycogen Platelet plug formation occurs as follows Figure 11 In the first phase of platelet plug formation platelets contact and stick to parts of the damaged bloodvessel such as collagen underlying the damaged endothelium cells This process is called platelet adhesion This requires participation of an endothelial cell secretion of a protein called von Willebrand factor VWF 11Figure 1 2 Adhesion activates the platelets This changes their characteristics dramatically They extend many projections that enable them to contactone another and then they begin to liberate the contents of their granules This phase is called the platelet release reaction Liberated ADP and thromboxane A2 play a major role by acting on nearby platelets to activate them as well Serotonin and thromboxane A2 function as vasoconstrictors causing contraction of the vascular smooth muscle which decreases blood flow through the injured vessel
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