Excitable tissue

Conductivity. Conductivity is an electrical property of excitable tissue which ensures that if one area of a membrane is excited to full activity, that area excites adjacent areas. Conduction of an impulse varies direcdy with the rate of development of phase 0 and the ampHtude of the action potential. Phase 0 is faster, and ampHtude of the action potential is greater, the more negative the transmembrane potential at the time of initiation of the impulse. Conduction velocity is faster when phase 0 is fast. 

Resting potential is a stable membrane potential in nonexcitable cells, or the most stable membrane potential between Action Potentials in excitable cells. In some excitable tissues it is impossible to define a resting potential because of continuous change in membrane potential. 

All the RyR channels are gated by cytoplasmic Ca2+, known as Ca2+-induced Ca2+ release (CICR). CICR functions as an amplifier of small Ca2+ signals in various excitable and non-excitable tissues and well documented in E-C coupling in the heart. In addition, RyRl can also mediate depolarization-induced Ca2+ release (DICR) , which is controlled by some protein-protein interactions. DICR is the principal Ca2+ release mode in E-C coupling in the skeletal muscle. 

Excitable tissue preparations were obtained fresh daily from live animals using the technique described by Dodd et al. (12). Protein was measured on each synapto-some preparation using the Coomassie Brilliant Blue dye technique described by Bradford (13) results were expressed as "toxin bound per mg synaptosome protein". 

This chapter summarizes recent work on the molecular basis of the toxic actions of ciguatoxin and brevetoxins. It is shown (i) that the molecular target for these toxins is the voltage-dependent Na channel of excitable tissues arid (ii) that ciguatoxin and brevetoxins share a common receptor site on the Na channel. 

Sykova, E., Hnik, P., Vyklicky, L. (eds.) Ion-Selective Microelectrodes and Their Use in Excitable Tissues, New York Plenum Press 1981... 

The discovery of galvanic electricity (i.e. electrical phenomena connected with the passage of electric current) by L. Galvani in 1786 occurred simultaneously with his study of a bioelectrochemical phenomenon which was the response of excitable tissue to an electric impulse. E. du Bois-Reymond found in 1849 that such electrical phenomena occur at the surface of the tissue, but it was not until almost half a century later that W. Ostwald demonstrated that the site of these processes are electrochemical semipermeable membranes. In the next decade, research on semipermeable membranes progressed in two directions—in the search for models of biological membranes and in the study of actual biological membranes. 

Brading There is a problem about this. You only established this in non-excitable tissues. In fact, in excitable tissues what is more important for the fast modulation of ion channels is Ca2+ coming in through the plasma membrane, rather than waves. A lot of people who are looking at waves are not measuring membrane potential and ignore spikes altogether. 

Ion-Selective Microelectrodes and Their Use in Excitable Tissues (ed. E. Sykovd,... 

Mechanism-specific adverse effects. Since local anesthetics block Na+ influx not only in sensory nerves but also in other excitable tissues, they are applied locally and measures are taken (p. 206) to impede their distribution into the body. Too rapid entry into the... 

In the case of digoxin we can visualize what is happening. The site of action and binding site of digoxin is to tissue Na+K+ATPase. This enzyme is distributed very widely in tissues, and particularly in excitable tissue, which depends on it to restore sodium/potassium balance to resting levels after excitation. Digoxin preferentially distributes therefore to these tissues, and a disproportionately small component is left in the plasma compartment from which we sample. 

Answer Bupivacaine use for local anesthesia of this type is very safe and commonly done. However, SOMETIMES inadvertent vascular injection results in a large amount of anesthetic in the systemic circulation. Because the heart is beating, the excitable tissue in the heart is being depolarized repetitively. Local anesthetics bind to rapidly depolarizing tissues more than tissues at rest (frequency-dependent block). Also, bupivacaine has a long duration of action because of its long residence time at receptors (sodium channel). Thus, this combination of factors contributed to the catastrophic outcome of this case. Had the same case involved lidocaine, the resuscitation would have likely been successful. 

G.R. Strichartz and J.M. Ritchie, The action of local anesthetics on ion channels of excitable tissues , in Local Anesthetics, G.R. Strichartz ed.. Handbook of Experimental Pharmacology, Volume 81, Springer-Verlag, Berlin, 1987, pp. 21-53. 

Schematic diagram of a reentry circuit that might occur in small bifurcating branches of the Purkinje system where they enter the ventricular wall. A Normally, electrical excitation branches around the circuit, is transmitted to the ventricular branches, and becomes extinguished at the other end of the circuit due to collision of impulses. B An area of unidirectional block develops in one of the branches, preventing anterograde impulse transmission at the site of block, but the retrograde impulse may be propagated through the site of block if the impulse finds excitable tissue that is, the refractory period is shorter than the conduction time. This impulse then reexcites tissue it had previously passed through, and a reentry arrhythmia is established.

Cardiac glycosides affect all excitable tissues, including smooth muscle and the central nervous system. The gastrointestinal tract is the most common site of digitalis toxicity outside the heart. The effects include anorexia, nausea, vomiting, and diarrhea. This toxicity is caused in part by direct effects on the gastrointestinal tract and in part by central nervous system actions. 

Electrokinetic membrane of excitable tissues. I. Experiments on oscillatory... 

A quantitatively important pathway of cysteine catabolism in animals is oxidation to cysteine sulfinate (Fig. 24-25, reaction z),450 a two-step hydroxyl-ation requiring 02, NADPH or NADH, and Fe2+. Cysteine sulfinic acid can be further oxidized to cyste-ic acid (cysteine sulfonate),454 which can be decarbox-ylated to taurine. The latter is a component of bile salts (Fig. 22-16) and is one of the most abundant free amino acids in human tissues 455-457 Its concentration is high in excitable tissues, and it may be a neurotransmitter (Chapter 30). Taurine may have a special function in retinal photoreceptor cells. It is an essential dietary amino acid for cats, who may die of heart failure in its absence,458 and under some conditions for humans.459 In many marine invertebrates, teleosts, and amphibians taurine serves as a regulator of osmotic pressure, its concentration decreasing in fresh water and increasing in salt water. A similar role has been suggested for taurine in mammalian hearts. A chronically low concentration of Na+ leads to increased taurine.460 Taurine can be reduced to isethionic acid... 

Milstein, C., Monoclonal antibodies. Sci. Am. 243(4) 66-74, 1980. An exciting, tissue-culture technique for obtaining pure antibodies specific for an antigen of choice. 

The action potential recorded from a cardiac Purkinje fiber is shown in Figure 23-1. At rest, the interior of the cell is negative relative to the cell s exterior. As in other excitable tissues (neurons, skeletal muscle), an action potential occurs when the cell interior suddenly becomes positive (depolarizes), primarily because of sodium ion influx. The cell interior then returns to a negative potential (repolarizes), primarily because of... 

Class I antiarrhythmic drugs are essentially sodium channel blockers.5,27,29 These drugs bind to membrane sodium channels in various excitable tissues, including myocardial cells. In cardiac tissues, class I drugs normalize the rate of sodium entry into cardiac tissues and thereby help control cardiac excitation and conduction.8,27 Certain class I agents (e.g., lidocaine) are also used as local anesthetics the way that these drugs bind to sodium channels is discussed in more detail in Chapter 12. 

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