Cardiac Cell membrane

In addition to modification of calcium influx/efflux, other mechanisms like inhibition of slow inward current [363] and nickel-calcium exchange [364] have been suggested to explain the positive inotropic effects of nickel. Moreover, these inotropic effects might be mediated by an action of nickel on the outside surface of the cardiac cell membrane, where nickel inhibits the ATP-dependent component of the calcium extrusion, thereby causing contraction-enhancement [364, 365],... 

Arrhythmias can be treated with the drugs discussed in this chapter and with nonpharmacologic therapies such as pacemakers, cardioversion, catheter ablation, and surgery. This chapter describes the pharmacology of drugs that suppress arrhythmias by a direct action on the cardiac cell membrane. Other modes of therapy are discussed briefly (see The Nonpharmacologic Therapy of Cardiac Arrhythmias). 

When the cardiac cell membrane becomes permeable to a specific ion (ie, when the channels selective for that ion are open), movement of that ion across the cell membrane is determined by Ohm s law current = voltage -f resistance, or current = voltage x conductance. Conductance is determined by the properties of the individual ion channel protein. The voltage term is the difference between the actual membrane potential and the reversal potential for that ion (the membrane potential at which no current would flow even if channels were... 

Local anesthetics have weak direct neuromuscular blocking effects that are of little clinical importance. However, their effects on cardiac cell membranes are of major clinical significance, and some local anesthetics are widely used as antiarrhythmic agents (eg, lidocaine) (see Chapter 14) at concentrations lower than those required to produce nerve block. Others of the same amide class (eg, bupivacaine, ropivacaine) can cause lethal arrhythmias if high plasma concentrations are inadvertently achieved. 

The sodium pump normally creates a small potential across cardiac cell membranes when digoxin blocks this pump, there is some depolarization of the cell. The heart then becomes more excitable and abnormal rhythms or ectopic beats may occur. Some patients also experience gastrointestinal disturbances, such as anorexia, nausea or vomiting. When blood concentration of digoxin is high, there may also be CNS effects, which can include confusion and visual disturbances. 

Our studies support the hypothesis that cardiac cell membrane lesion sealing with CSIL result in preservation of myocardial viability, as determined by function, histochemistry, and ultra-structural morphology. There is a time response to myocardial preservation with CSIL therapy. Early CSIL intervention after the onset of ischemia resulted in almost complete myocardial recovery (18). Even when the intervention was initiated at 20 min of global ischemia, myocardial preservation was still greater than that seen in hearts with IgG-L or placebo treatment. There is also a dose response to CSIL therapy. Sufficient concentration of CSIL is essential to achieve optimal cell membrane lesion sealing (I9).Therefore, CSIL therapy may find therapeutic applications in preservation of myocardial viability and efficient non-viral gene therapy. 

Answer B. Calcium channel antagonists decrease myocardial contractility by blocking the influx of Ca2+ ions through voltage-dependent L-type channels in the cardiac cell membrane. CCBs have no effects on Na+ channels, they do not change intracellular K+ levels, and they decrease not increase) conduction velocity. 

The precise mechanism and sight of action of most compounds categorized as calcium inhibitory compounds, therefore, remains obscure. Future refinements in experimental models and techniques will undoubtedly will lead to the classification of calcium inhibitory compounds based upon their primary mechanism of action and specific site(s) of action (extracellular vs. intracellar). Because of the uncertainty surrounding the precise mechanisms of action of calcium inhibitory compounds, I will describe their cardiac electrical and mechanical effects illuding when possible to those compounds that are believed to act l) competitively with Ca + for specific calcium channels (e.g., Co +, Mn +, La2+, etc.) 2) at the cardiac cell membrane and possibly by one of several intracellular mechanisms (e.g., verapamil, diltiazem, nifedipine) and 3) intracellularly (e.g., 2-n-propyl and 2-n-butyl MDI). 

The effects of calcium channel blocking drugs on the ionic currents of cardiac cell membranes can be studied by recording action potentials. In most cells, a large, fast inward Na+ current is responsible for the early spike component and... 

Martinez-Palomo a, Benitez D and Alanis J (1973) Selective deposition of lanthanum in mammalian cardiac cell membranes. Ultrastructural and electrophysiological evidence. J Cell Biol 58 1-10. 

This drug is capable of blocking potassium channels in cardiac cell membranes inhibition of its metabolism has led to cardiac arrhythmias. 

D. Calcium stabilizes cardiac cell membranes in hyperkalemic states. 

Quinidine, however, would appear to exhibit a certain degree of structural specificity with respect to its action on the heart [260, 861]. This action would seem to result from a binding to the cardiac cell membranes (possibly through interaction with histidine units [862, 863]) which inhibits the active transport of calcium ions into the cells [864] and so produces the characteristic reduction... 

Cardiac troponin complex consists of three parts. Troponin T facilitates contraction, troponin 1 (cTnl) inhibits actin-myosin interactions, and troponin C binds to calcium ions. Troponin I and T are specific to the heart, but cTnT is also expressed by injured skeletal muscle. In the course of cell damage, cardiac troponin is released from myocytes, facilitated by increased membrane permeability that allows smaller troponin fragments to traverse the membrane. Complicating the use of troponin levels is the fact that in cases where there is cardiac injury without cardiac cell membrane disruption, serum troponin level can increase. Also, altered ion homeostasis may not be reflected in troponin levels. 

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