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Adult Cardiac Surgery Ii MHBD054-CH19[335-356].qxd 09/05/2007 8:05 AM Page 335 PMAC-291 PMAC-291:Books:DAMS/ARCHIVE:MHBD054:Chapters:CH-19: TechBooks [PP PART II ADULT CARDIAC SURGERY MHBD054-CH19[335-356].qxd 09/05/2007 8:05 AM Page 336 PMAC-291 PMAC-291:Books:DAMS/ARCHIVE:MHBD054:Chapters:CH-19: TechBooks [PP MHBD054-CH19[335-356].qxd 09/05/2007 8:05 AM Page 337 PMAC-291 PMAC-291:Books:DAMS/ARCHIVE:MHBD054:Chapters:CH-19: TechBooks [PP CHAPTER CARDIOVASCULAR 19 FUNCTION AND PHYSIOLOGY Jeffrey M. Dodd-O BASIC MYOCYTE PHYSIOLOGY extracellular fluids differ because the cell’s surface mem- brane serves to maintain some compounds intracellularly Myocyte depolarization and exclude other compounds extracellularly. This segre- gating function is possible because water-insoluble com- Cardiac myocytes possess the capacity to contract because ponents of the membrane prevent free passage of water- they contain a series of protein filaments (myofibrils) ori- soluble components through the membrane. The initial ented along the longitudinal axis of the cell (see below). creation of a concentration gradient between extra- and For myocytes to shorten, these myofibrils must be stimu- intracellular ions is achieved by energy-dependent ion lated to slide. The impetus for the stimulation originates pumps located within the membrane. These pumps can on the myocyte’s surface membrane (sarcolemma) and is move ions across the membrane against a concentration transmitted to the intracellular myofibrils. Aspects of the gradient. Because of the uneven concentrations of charged composition of the sarcolemma allow it to assume this ions in the intra- and extracellular fluids separated by the function. The intra- and extracellular fluid is predomi- cell membrane, there is an electrical gradient across the nantly water. The ionic components within the intra- and membrane (i.e., a transmembrane potential). KEY CONCEPTS ● Membrane potentials are created by energy-dependent ● A ventricle exposed chronically to high afterload will ion pumps which segregate charged ions on either adapt by concentric hypertrophy because this reduces side of hydrophobic cell membrane. wall stress according to the law of Laplace. ● Cell depolarization possible because channels open ● Myocardium receiving insufficient energy supply will within the hydrophobic membrane to allow charged either die (infarction), become dysfunctional (ischemia), ions, driven by concentration gradients, to cross the or reduce its energy needs (hibernate). Reperfused tis- membrane. sue is termed “stunned” if it does not contract up to its ● Trigger for the opening of transmembrane ion channel potential in spite of adequate energy supply. is typically a change in the membrane potential. ● Diastole is more energy-demanding than systole, and Different channels are triggered to open at different diastolic dysfunction can be more difficult to treat membrane potentials. than systolic dysfunction ● The sarcomere is the contractile element of the ● Dysfunctional endothelium leads to vascular occlu- myocyte. Each sarcomere is composed of a series of sion by: (1) exposing underlying tissue factor to circu- parallel myofilaments. Coaxial movement of these lating factor VII, initiating thrombosis; (2) does not myofilaments, some of which are tethered to the ends allow for the interaction of thrombin with thrombo- of the sarcomere, result in sarcomere shortening. modulin and the subsequent activation of protein C to ● The strength of contraction is influenced by resting its anticoagulant form; (3) does not produce nitric length of the myocyte, sudden stretch of the myocyte, oxide, important to help decrease platelet activation, or rapidly repeated contraction of the myocyte. Speed decrease vasospasm, and decrease vascular of shortening is influenced by afterload. inflammation 337 MHBD054-CH19[335-356].qxd 09/05/2007 8:05 AM Page 338 PMAC-291 PMAC-291:Books:DAMS/ARCHIVE:MHBD054:Chapters:CH-19: TechBooks [PP 338 PART II ● ADULT CARDIAC SURGERY Physiology of the myocyte cell membrane transmembrane potentials, become exposed to the new transmembrane potential of the adjacent sarcolemma. The human body is composed predominantly of salts Exposure to this new transmembrane potential increases and water. This pool of salts and water is segregated into the open probability of these nearby channels. The pas- functional units (cells and their intracellular compo- sage of ions through these newly open channels changes nents) that locally alter the concentration of the salts the membrane potential surrounding the channel, they contain. Hydrophobic phospholipid membranes exposing an additional section of the cell membrane to a surrounding the cells (and intracellular compartments) different transmembrane potential. In this way, the new prevent the exit/entrance of water-soluble salts and allow transmembrane potential propagates along the surface of the cells to maintain this individualized environment.1 the myocytes. Invaginations in the cell membrane, called T Units within these phospholipid membranes allow contin- tubules, penetrate into the cell into close proximity to the ued adjustment of the ion content within the cell (or intra- myocyte contractile proteins. These T tubules act as exten- cellular compartment). For example, an energy-dependent sions off of the surface membrane and allow changes in the Naϩ,Kϩ pump extrudes Naϩ ions from the cell and takes cell surface to effect changes deep within the myocyte. Kϩ ions into the cell at an exchange of three Naϩ ions extruded per two Kϩ ions taken in. This allows cells to raise intracellular potassium concentrations and lower Physiology of the conduction system intracellular sodium. Another pump extrudes calcium in Relative to the extracellular fluid, the intracellular fluid in exchange for sodium, increasing intracellular calcium the resting state has higher concentrations of sodium, concentrations in relation to the extracellular fluid, ϩ ϩ lower concentrations of K and of Ca2 , and a relatively although it allows Naϩ (extruded by the Naϩ,Kϩ pump) to negative charge. When ion channels in the cell mem- reenter the cell. This pump is driven by the Na gradient ϩ ϩ brane are opened under these conditions, Na and Ca2 created by the energy-dependent Naϩ,Kϩ pump. Similarly, tend to enter the cell rapidly.2 They are driven both by intracellular compartments called the sarcoplasmic reticu- ion concentrations and electrical potential. By contrast, lum (SR) contain energy-dependent ion pumps in their ϩ K tends to leave the cell owing to its concentration gra- surrounding membranes that allow them to collect the dient, although the electrical potential gradient reduces majority of the intracellular calcium. Other channels its speed of exit. When the cell is depolarized so that the within the membrane act as passages that intermittently transmembrane gradient is less negative intracellularly, open to allow transit of a specific ion through the cell ϩ the rate of K exit is higher. membrane. Regulation of pump activation and channel When the transmembrane electrical potential, usually opening is vital for the proper functioning of the cell. Ϫ90 mV at rest, becomes less negative, sodium channels Moving ions against their concentration gradient to on the cell membrane are triggered to open (Fig. 19-1). create a relative intracellular deficit or abundance requires Also triggered in these channels by cell membrane depo- energy. In the cell, this energy is supplied in the form of larization is the closing of the channel, although this ATP. This segregation of ions, along with the imbalance of process is (of course) delayed until after the channel has ionic charge that is associated, creates a potential (energy) been opened. Other channels, like L-type calcium chan- gradient across the membrane, which drives the rapid flux of ions that occurs if and when a transmembrane ion chan- + 30 ms nel is opened. In the cell, the trigger to opening the ion +20 K + CI− K channels is often the potential or ionic concentration gra- C dient of the surrounding milieu. Thus, transmembrane 0 B channels are frequently described as being either voltage- gated (opening probability is increased if the transmem- K+ brane potential of the surrounding membrane is within Na+ mV certain parameters) or ion-gated (opening probability is A D increased if there is a sudden change in the concentration Na:K of an ion in the surrounding fluid). pump activated −90 T Tubules and sarcoplasmic reticulum Figure 19-1 Correlation between the changes in ion The cell-surface change initiating myofibril movement is conductance and the resultant changes in transmembrane a flux of charged ions across some point of the sar- potential during the various phases of the cardiac myocyte colemma.1 This ion flux disrupts the balance of charged action potential. A. depolarization; B. rapid repolarization; particles present in the baseline (resting) state, and a new C. plateau phase; D. late repolarization. (Modified from transmembrane electrical gradient develops at that point Rubart M, Zipes DP. Mechanisms of sudden cardiac death. on the sarcolemma. Ion channels traversing the adjacent J Clin Invest 2005;115(9):2305–2315. With permission.) sarcolemma, closed to the passage of ions under resting MHBD054-CH19[335-356].qxd 09/05/2007 8:05 AM Page 339 PMAC-291 PMAC-291:Books:DAMS/ARCHIVE:MHBD054:Chapters:CH-19: TechBooks [PP Chapter 19 ● Cardiovascular Function and Physiology 339 nels, also open when the cell membrane has begun to Closed depolarize. The initiation of ion passage through calcium Resting channels is delayed until after the Naϩ channels have begun to close. The opening of these Naϩ and Ca2ϩ chan- nels results in the entrance of cations into the cell, decreas- (Recovery) (Activation) ing the magnitude of the membrane potential. As the membrane potential reaches a nadir, Kϩ channels are trig- gered to open. Their opening increases the rate of exit of Closed Open ϩ K from the intracellular space into which it had been Inactive (Inactivation) concentrated. The loss of cations from the intracellular space helps return the transmembrane potential back to Figure 19-2 The three states of a voltage-gated ion channel.
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