![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
GR Li and GR Ferrier
Department of Pharmacology, Dalhousie University, Halifax, Nova Scotia, Canada.
Transmembrane electrical activity was recorded from endo- and epicardium of isolated segments of guinea pig right ventricles with standard microelectrode techniques. An ECG was also recorded by two electrodes placed at opposite ends of the tissue bath. Regular stimulation was delivered to the endocardium. Tissues were exposed to simulated ischemia for 15 min and then were reperfused with "normal" Tyrode's solution. Rapid sustained or nonsustained ventricular tachycardia, bigeminy or trigeminy with characteristics of transmural reentry occurred in early reperfusion in 14 of 20 hearts (70%). Arrhythmias were accompanied by prolongation of transmural conduction time and abbreviation of endocardial effective refractory period. With lidocaine, at 1, 5, 10 and 50 microM, reperfusion arrhythmias occurred in 53.3, 22.2, 20.8 and 14.3% of hearts, respectively. The decreased incidence of arrhythmias was statistically significant for 5 to 50 microM lidocaine (P less than .01). The antiarrhythmic effect did not correlate with changes in transmural conduction time, endocardial effective refractory period, or endocardial excitability. However, antiarrhythmic concentrations of lidocaine selectively depressed epicardial excitability and significantly increased endo- to epicardial conduction block during late ischemic and early reperfusion periods. Epicardial inexcitability extended to late diastole and conduction block was not restricted to premature beats. Thus, in transmural reentry in which the epicardium is an essential component of the circuit, lidocaine may interrupt the circuit by selectively rendering this component inexcitable.
This article has been cited by other articles:
|
|
 |
|
  S. Wang, J. Radhakrishnan, I. M. Ayoub, J. D. Kolarova, D. M. Taglieri, and R. J. Gazmuri Limiting sarcolemmal Na+ entry during resuscitation from ventricular fibrillation prevents excess mitochondrial Ca2+ accumulation and attenuates myocardial injury J Appl Physiol, July 1, 2007; 103(1): 55 - 65. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. J. Canyon and G. P. Dobson Pretreatment with an adenosine A1 receptor agonist and lidocaine: A possible alternative to myocardial ischemic preconditioning J. Thorac. Cardiovasc. Surg., August 1, 2005; 130(2): 371 - 377. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. J. Canyon and G. P. Dobson Protection against ventricular arrhythmias and cardiac death using adenosine and lidocaine during regional ischemia in the in vivo rat Am J Physiol Heart Circ Physiol, September 1, 2004; 287(3): H1286 - H1295. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. E. Billman, H. C. Englert, and B. A. Schölkens HMR 1883, a Novel Cardioselective Inhibitor of the ATP-Sensitive Potassium Channel. Part II: Effects on Susceptibility to Ventricular Fibrillation Induced by Myocardial Ischemia in Conscious Dogs J. Pharmacol. Exp. Ther., September 1, 1998; 286(3): 1465 - 1473. [Abstract] [Full Text]
|
|
|
|
 |
|
 A. Olschewski, M.E. Brau, H. Olschewski, G. Hempelmann, and W. Vogel ATP-Dependent Potassium Channel in Rat Cardiomyocytes Is Blocked by Lidocaine : Possible Impact on the Antiarrhythmic Action of Lidocaine Circulation, February 15, 1996; 93(4): 656 - 659. [Abstract] [Full Text]
|
|
 |
 |
 |
|
 |
 |
 |
