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By G. Gunock. Xavier University of Louisiana.

THE HEART AND HEART DISEASE 297 Abnormalities of Heart Rhythm Coronary artery disease or myocardial infarction often results in an abnor- mal rhythm of the heartbeat generic aristocort 15mg fast delivery, or arrhythmia (ah-RITH-me- ah). Extremely rapid but coordinated contractions, num- bering up to 300 per minute, are described as flutter. An episode of rapid, wild, and uncoordinated heart muscle contractions is called fibrillation (fih-brih-LA-shun), which may involve the atria only or both the atria and the ventricles. Ventricular fibrillation is a serious disorder be- cause there is no effective heartbeat. It must be corrected by a defibrillator, a device that generates a strong electri- cal current to discharge all the cardiac muscle cells at once, allowing a normal rhythm to resume. An interruption of electric impulses in the heart’s con- duction system is called heart block. The seriousness of Zone 1: Necrosis this condition depends on how completely the impulses Zone 2: Injury are blocked. It may result in independent beating of the Zone 3: Ischemia chambers if the ventricles respond to a second pacemaker. Treatment of Heart Attacks The death rate for Philadelphia: Lippincott Williams & Wilkins, 2004. Initial treatment involves cardiopulmonary resuscitation (CPR) and defibrillation at the scene when needed. The Ameri- Myocardial Infarction In the heart, thrombus forma- can Heart Association is adding training in the use of the tion results in a life-threatening condition known as coro- automated external defibrillator (AED) to the basic nary thrombosis. The AED detects fatal arrhythmia and au- closure, of a coronary vessel with complete obstruction of tomatically delivers the correct preprogrammed shock. Because 14 Work is underway to place machines in shopping centers, the area of tissue damaged in a heart attack is described sports venues, and other public settings. The oxy- itor the heart and give emergency drugs helps people to gen-deprived tissue will eventually undergo necrosis survive and reach a hospital.

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When glycogen synthase is covalently modified cheap 10 mg aristocort fast delivery, it is inactive, in the form of glycogen synthase b or glyco- gen synthase D (for dependent on a modifier for activity). REGULATION OF LIVER GLYCOGEN METABOLISM BY INSULIN AND GLUCAGON Insulin and glucagon regulate liver glycogen metabolism by changing the phosphory- lation state of glycogen phosphorylase in the degradative pathway and glycogen syn- thase in the biosynthetic pathway. An increase of glucagon and decrease of insulin during the fasting state initiates a cAMP-directed phosphorylation cascade, which results in the phosphorylation of glycogen phosphorylase to an active enzyme, and the A ATP P Glycogen phosphorylase b Glycogen phosphorylase a (inactive) (active) B ATP P Glycogen synthase I (or a) Glycogen synthase D (or b) (active) (inactive) Fig. The conversion of active and inactive forms of glycogen phosphorylase (A) and glycogen synthase (B). Note how the nomenclature changes depending on the phosphoryla- tion and activity state of the enzyme. CHAPTER 28 / FORMATION AND DEGRADATION OF GLYCOGEN 519 phosphorylation of glycogen synthase to an inactive enzyme (Fig. As a conse- With a deficiency of debrancher quence, glycogen degradation is stimulated, and glycogen synthesis is inhibited. GLUCAGON ACTIVATES A PHOSPHORYLATION CASCADE THAT degraded in vivo only to within 4 residues of CONVERTS GLYCOGEN PHOSPHORYLASE b TO GLYCOGEN the branchpoint. When the glycogen sam- PHOSPHORYLASE a ples were treated with the commercial preparation containing normal enzymes, Glucagon regulates glycogen metabolism through its intracellular second mes- one glucose residue was released for each senger cAMP and protein kinase A (see Chapter 26). However, in the patient’s cell membrane receptor, transmits a signal through G proteins that activates glycogen sample, with the short outer adenylate cyclase, causing cAMP levels to increase (see Fig. The catalytic subunits of protein kinase A are activated by the dissocia- -1,6 branch. Normal glycogen has 8-10 glu- tion and phosphorylate the enzyme phosphorylase kinase, activating it. Phospho- cosyl residues per branch, and thus gives a rylase kinase is the protein kinase that converts the inactive liver glycogen ratio of approximately 9 moles of glucose phosphorylase b conformer to the active glycogen phosphorylase a conformer 1-phosphate to 1 mole of glucose.

Thus buy aristocort 40mg cheap, the intact endothelium has the capa- bility of modifying thrombin action and inhibiting platelet aggregation. Fibrinolysis After successful formation of a hemostatic plug, further propagation of the clot must be prevented. This is accomplished in part by switching off blood coagulation and in part by turning on fibrinolysis. Fibrinolysis involves the degradation of fib- rin in a clot by plasmin, a serine protease that is formed from its zymogen, plas- minogen. Plasminogen is a circulating serum protein that has a high affinity for fib- rin, promoting the incorporation of plasminogen in the developing clot. The activity of plasminogen is mediated by proteins known as plasminogen activators. The con- version of plasminogen to plasmin by plasminogen activators can occur both in the liquid phase of the blood and at the clot surface; however, the latter process is by 838 SECTION EIGHT / TISSUE METABOLISM streptokinase far more efficient. Activated protein C (APC), in addition to turning off the blood Plasminogen coagulation cascade, also stimulates the release of plasminogen activator from tis- + sues (t-PA, tissue plasminogen activator) and simultaneously inactivates an inhibitor tPA streptokinase- of plasminogen activator, PAI-1. Clot-bound plasmin is not readily inactivated Plasmin by -antiplasmin. Thus, plasminogen binding to fibrin facilitates its activation to – plasmin, protects it from blood serpins, and localizes it on the fibrin substrate for α2-antiplasmin subsequent efficient proteolytic attack. This mechanism allows for dissolution of Fibrin Fibrin degradation products fibrin in pathologic thrombi or oversized hemostatic plugs, and at the same time prevents degradation of fibrinogen in the circulating blood. Plasminogen can be activated by either t-PA or Two endogenous plasminogen activators are most important; both are synthe- scu-PA ( ). Tissue plasminogen activator (t-PA) is chiefly produced Streptokinase binding to plasminogen allows by the vascular endothelial cells, has a high binding affinity for fibrin, and plays a autocatalysis to form plasmin.