Solve for C: H EC 825 .
Exam3Aid Figure 8.9: The vertebrate Circulatory Plan Vertebrates share a common circulatory plan in which the heart pumps blood to a larger artery, then diffuse to the tissues across the walls of the capillariesat leads to the capillary beds, where substances Figure 8.10: Variation in the structure of vertebrate blood vessels Representative portions of blood vessels from the systemic circuit of a mammalian circulatory system are shown in cross-section. Arteries and veins are composed of three layers (tunica externa, tunica media, and tunica intima) of carrying thickness, lined with an endothelium. Smaller vessels such as arterioles, capillaries and venules lack one or more of these layers. Figure 8.11: Variation Capillary Structure A: In a continuous capillary, the endothelial cells are connected via tight junctions B: In a fenestrated capillary, the endothelial cells have many oval pores (fenestrations) that allow the regulated movement of solutes C: In a sinusoidal capillary, the endothelial cells are loosely linked and large molecules can move between the cells Figure 8.20: Internal Anatomy of the Mammalian Heart Blood flows from the pulmonary veins into the left atrium and then the left ventricle. The left ventricle pumps blood to the aorta and the systemic circuit of the circulatory system. Blood from the tissues flows via the venae cavae to the right atrium and the right ventricle, which pumps blood to the pulmonary artery and the pulmonary circulation. One-way flow through the heart is ensured by two sets of valves. Figure 8.21: The Cardiac Cycle in Mammals Figure 8.22: Pressure Changes in the Heart and Arteries of Mammals Such as Humans The left side of the heart, which supplies the systemic circuit, develops substantially greater pressures than the right side of the heart, which supplies the pulmonary circuit. Figure 8.23: Pacemaker and Action Potentials In myogenic hearts, the pacemaker cells have an unstable resting membrane potential (the pacemaker potential). Nonselective caption (“funny”) channels open, increasing the permeability (P) of the membrane to Na+, which causes the membrane potential to increase gradually. As the membrane approaches threshold, T-type Ca2+ channels open, triggering an action potential. After about 200 msec these channels close and K+ channels open, repolarizing the cell and the cycle begins again. Figure 8.24: The Effects of Norepinephrine on Heart Rate Norepinephrine increases heart rate by binding to β adrenergic receptors, activating an adenylate cyclase (AC) signal transduction pathway that opens cation (funny) and T-type Ca2+ channels, increasing the rate of depolarization of the pacemaker potential. Figure 8.25: The Effects of Acetylcholine on Heart Rate Acetylcholine decreases heart rate by binding to muscarinic receptors, activating a signal transduction pathway that closes Ca2+ channels and opens K+ channels. This prevents Ca2+ ions from entering the cell and allows K+ ions to exit, causing a net hyperpolarization, which increases the time needed for the pacemaker potential to depolarize the cell to threshold. Figure 8.26: The Action Potential in Cardiomyocytes A: Phases of the action potential. Phase 0: the cell reaches threshold potential and voltage-gated Na+ channels open, increasing Na+ permeability (P Naand depolarizing the cell. Phase 1: the voltage-gated Na+ channels inactivate and K+ channels open, causing a transient outward K+ current, resulting in a slight repolarization. Phase 2: These inward rectifier K+ channels close and L-type voltage-gated Ca2+ channels open, causing the plateau phase of the action potential. Phase 3: L-type voltage-gated Ca2+ channels close and K+ channels open, causing repolarization. Phase 4: The cell returns to the resting membrane potential. B: Pacemaker and action potentials in various types of cardiomyocytes in the mammalian heart. The shapes of the pacemaker and action potentials differ across the parts of the heart as a result of the expression of different channel isoforms. Figure 8.28: EKG Tracings A: In the EKG of a normal cardiac rhythm, the P wave indicates atrial depolarization. The QRS complex indicates ventricular depolarization and atrial repolarization, the T wave indicates ventricular repolarization. B: During ventricular fibrillation, the EKG is disorganized and no consistent waves are observed. Figure 8.29: A summary of the electrical and mechanical events of the cardiac muscle Figure 8.30: Effects of Norepinephrine and Epinephrine on Cardiomyocyte Norepinephrine and epinephrine increase contractility by binding to beta receptors on the cardiomyocyte and activating an adenylate cyclase (AC) – mediated signal transduction pathway that activates protein kinases, which phosphorylate various proteins and cause an increase in the rate and strength of contraction. Figure 8.31: The Frank-Starling Effects A: Stroke volume increases as end-diastolic volume increases. When end-diastolic volume is low, cardiomyocytes are shorter than the optimal length needed for maximal contraction. Increasing end- diastolic volume stretches the muscle, increasing its length and increasing force generation. The greater the force generated, the greater the stroke volume. B: Changes sympathetic activity alter the position of the curve. An increase in sympathetic activity shifts the curve upward, whereas a decrease in activity shifts the curve downward. Figure 8.33 Pressure, velocity and total cross-sectional area across a vertebrate circulatory system Pressure is variable in the ventricle, high and more constant in the arteries, and drops greatly across the arterioles. Blood velocity is inversely proportional to total cross-sectional area of that part of the circulatory system. Figure 8.34: The Aorta as a Pressure Reservoir A: Blood flows rapidly into the aorta during the ejection phase of ventricular contraction, pushing out on the walls of the aorta and causing it to expand. B: As the heart relaxes, blood flow into the aorta ceases, but flow out into the arterioles continues, reducing the aortic pressure. Elastic recoil of the arterial walls helps to push blood through the vasculature, maintaining pressure and flow. Figure 8.35: Skeletal Muscle Pump A: When a skeletal muscle contracts, it puts pressure on the vein, pushing blood in both directions. The resulting pressure opens the proximal one-way valve and closes the distal one-way valve squeezing blood toward the heart and preventing backflow. B: When the skeletal muscle relaxes, the one-way valves are in the opposite configuration. The relaxation reduces pressure on the distal valve, which opens and allows blood to flow in. Back pressure from the blood in the proximal segment of the vein closes the proximal valve, preventing backflow. Figure 18.15 Autonomic innervation of the heart