Effects of ischemia and hypoxia on the specialized conducting system of the canine heart

Bagdonas, Albin A.; Stuckey, Jackson H.; Piera, Juan; Amer, Norman S.; Hoffman, Brian F.

doi:10.1016/0002-8703(61)90577-4

Cited by 121 publications

(47 citation statements)

References 7 publications

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“…The following findings suggest that LSVF is maintained by activation spreading from the PF network to the WM: 1) the endocardium, the location of the PF-WM junctions, had the highest activation rate in our canine study, as opposed to previously reported findings that the activation rate during VF is high transmurally in porcine hearts (1,15), in which the PF-WM junctions are distributed intramurally almost to the epicardium (10, 11); 2) PF activation was coupled to and preceded WM activation during LSVF; 3) the activation sequences from the endocardium to the epicardium and the PF activation properties in LSVF were similar to sinus rhythm; and 4) the canine PF network is more resistant to the global ischemia caused by VF than is WM (2,8,9,13), so that during long-duration VF, it was possible for activation to initiate in the PF network and propagate through the PF-WM junctions and then spread in the WM. During LSVF, the WM activations have multiple initiation sites on the endocardium (Figs.…”

Section: Discussionmentioning

confidence: 99%

Activation becomes highly organized during long-duration ventricular fibrillation in canine hearts

Qi²,

Dosdall³

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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Ideker RE. Activation becomes highly organized during long-duration ventricular fibrillation in canine hearts. Am J Physiol Heart Circ Physiol 298: H2046 -H2053, 2010. First published April 9, 2010 doi:10.1152/ajpheart.01196.2009Little is known about the threedimensional (3-D) intramural activation sequences during long-duration ventricular fibrillation (VF), including the role of the subendocardium and its Purkinje fibers (PFs) in long-duration VF maintenance. Our aim was to explore the mechanism of long-duration VF maintenance with 3-D electrical mapping. We recorded 10 min of electrically induced VF in the left ventricular anterior free wall of six 10-kg, open-chest dogs using a 3-D transmural unipolar electrode matrix (9 ϫ 9 ϫ 6, 2-mm spacing) that allowed us to map intramural activation sequences. At 2.5 Ϯ 1.8 min of VF, although the body surface ECG continued to exhibit a disorganized VF pattern, intramurally a more organized, synchronous activation pattern was first observed [locally synchronized VF (LSVF)]. This pattern occurred one or more times in all dogs and was present 33.4 Ϯ 31.4% of the time during 5-10 min of VF. As opposed to the preceding changing complex activation sequences of VF, during LSVF, wavefronts were large and highly repeatable near the endocardium, first exciting the endocardium almost simultaneously and then rapidly spreading toward the epicardium with different levels of conduction block en route. During LSVF, PF activations always preceded working myocardium activations near the endocardium. In conclusion, long-duration VF in dogs frequently becomes highly organized in the subendocardium, with activation fronts arising in this region and passing intramurally toward the epicardium, even though the surface ECG continues to exhibit a disorganized pattern. PFs appear to play an important role during this stage of VF.intramural ventricular fibrillation; locally synchronized ventricular fibrillation; Purkinje fibers SUDDEN CARDIAC ARREST is a leading cause of death in the industrialized world (25). Many lethal cardiac arrests are caused by ventricular fibrillation (VF) (25). The mean time from collapse until defibrillation in the prehospital setting, where most cardiac arrests occur, ranges from 4 to 10 min (21,22). Yet, relatively few studies have dealt with activation sequences during VF lasting Ͼ1 min [long-duration VF (20)], and little is known about the mechanisms of long-duration VF maintenance.Some studies have suggested an important role of Purkinje fibers (PFs) during long-duration VF maintenance (1,4,20,23). As in humans, PFs in canines are primarily located in the subendocardium (19). In canines, an endocardial-epicardial gradient of the activation rate develops during long-duration VF (1, 4, 23), with discrete, regular, rapid deflections persisting in the subendocardium (23), possibly caused by PFs. After endocardial ablation with Lugol's solution to eliminate PF activations, subendocardial PF signals were no longer recorded, and the transmural activation rate gradient dis...

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Section: Discussionmentioning

confidence: 99%

Activation becomes highly organized during long-duration ventricular fibrillation in canine hearts

Qi²,

Dosdall³

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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“…The leading explanations for this observation are that PFs are more resistant than the myocardium to the effects of ischemia, as shown in several studies, and that the PFs are less ischemic because they receive oxygen by diffusion from the immobile blood in the ventricular cavities during VF. [11][12][13] Newton et al 32 used plunge needles in the left ventricular free wall of canines to show that after 2 minutes of VF, the endocardium is activating more rapidly, with conduction block occurring more commonly at the epicardium. On the basis of figures presented in that report, no apparent conducting wave fronts propagate from intramural regions toward the endocardium, consistent with activations arising from the PF system.…”

Section: Discussionmentioning

confidence: 99%

“…10 Even after extensive infarction of myocardial tissue, subendocardial PFs in canine models remain structurally and electrophysiologically intact and capable of rapid activation. [11][12][13] Using 3-dimensional modeling, Berenfeld and Jalife 14 have shown that focal activity may arise at the Purkinje muscle junctions, leading to initiation of VF. This model predicted that the PFs become irrelevant after intramyocardial reentry is established during the early stages of VF.…”

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confidence: 99%

“…14 However, global ischemia rapidly develops as VF progresses, and because PFs are more resistant to ischemia than is the working ventricular myocardium (WVM), PFs may play an important role during late VF. [11][12][13] The objectives of this study were to (1) record PF signals reliably from the endocardium of an isolated canine heart model, (2) quantitatively evaluate the activation patterns of PFs during VF, and (3) make inferences about the role of PFs in the maintenance of VF. We hypothesized that PFs are intimately involved in the maintenance of VF, either by acting as a substrate for reentry or as a spontaneously activating source of wave fronts.…”

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Activation Patterns of Purkinje Fibers During Long-Duration Ventricular Fibrillation in an Isolated Canine Heart Model

et al. 2007

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Background— The roles of Purkinje fibers (PFs) and focal wave fronts, if any, in the maintenance of ventricular fibrillation (VF) are unknown. If PFs are involved in VF maintenance, it should be possible to map wave fronts propagating from PFs into the working ventricular myocardium during VF. If wave fronts ever arise focally during VF, it should be possible to map them appearing de novo. Methods and Results— Six canine hearts were isolated, and the left main coronary artery was cannulated and perfused. The left ventricular cavity was exposed, which allowed direct endocardial mapping of the anterior papillary muscle insertion. Nonperfused VF was induced, and 6 segments of data, each 5 seconds long, were analyzed during 10 minutes of VF. During 36 segments of data that were analyzed, 1018 PF or focal wave fronts of activation were identified. In 534 wave fronts, activation was mapped propagating from working ventricular myocardium to PF. In 142 wave fronts, activation was mapped propagating from PF to working ventricular myocardium. In 342 wave fronts, activation was mapped arising focally. More than 1 of these 3 patterns could occur in the same wave front. Conclusions— PFs are highly active throughout the first 10 minutes of VF. In addition to retrograde propagation from the working ventricular myocardium to PFs, antegrade propagation occurs from PFs to working ventricular myocardium, which suggests PFs are important in VF maintenance. Prior plunge needle recordings in dogs indicate activation propagates from the endocardium toward the epicardium after 1 minute of VF, which suggests that focal sites on the endocardium may represent foci and not breakthrough. If so, in addition to reentry, abnormal automaticity or triggered activity may also occur during VF.

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“…Furthernore, ischemia and asphyxia also impair A-V node transmission (8)(9)(10) and enhance the atrial and ventricular cardiac cell production of adenosine (11,12). In addition, in isolated perfused guinea pig hearts, aminophylline, a competitive antagonist ofadenosine, significantly attenuates and reverses the A-V conduction delay and block caused by adenosine and/or hypoxia (3).…”

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confidence: 99%

Evidence for adenosine mediation of atrioventricular block in the ischemic canine myocardium.

Belardinelli¹,

Mattos²,

Berne³

1981

J. Clin. Invest.

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A B S T R A C T Adenosine levels in oxygen-deprived myocardium can rise to 10-100-,uM concentrations known to cause atrioventricular (AV) conduction delay and block. We reported that the AV conduction delay and block caused by hypoxia is markedly attenuated by 10 ,uM aminophylline, an adenosine competitive antagonist. The purpose of the present study was to investigate adenosine's role in ischemic AV conduction disturbances. Dogs were anesthetized and instrumented for His bundle and surface electrogram recordings. The total AV conduction time was subdivided into atrial-His bundle (AH) and His bundleventricle intervals. The atrioventricular node artery (AVNA) was cannulated for selective injection of drugs in the AV node region. Adenosine (10 to 100 ,ug), as a 2-ml bolus injection, rapidly produced a dose-dependent, transient increase in the AH interval; a 1,000-,ug dose caused second degree AV block. The duration of the increase in AH interval was also dose-dependent. Dipyridamole, an inhibitor of nucleoside transport, potentiated the negative dromotropic effects ofadenosine, whereas aminophylline attenuated them. In some dogs, after cannulation of the AVNA, first and second degree AV block occurred spontaneously or were induced by rapid atrial pacing. Injection of the aminophylline (5 mg/kg, i.v.) or theophylline (100-1,000 gg) into the AVNA rapidly reversed the AV blocks. Upon washout of the drugs the AV blocks recurred. We conclude that endogenously released adenosine may account for a major fraction of the AV conduction delay and block associated with impaired blood supply to the AV node, and that theophylline and aminophylline reverse the AV conduction defect by antagonizing the effects of adenosine. INTRODUCTION It has been demonstrated that adenosine and related compounds can produce heart block (1, 2). Recently we (3) reported that the atrioventricular (AV)' conduction delay and block caused by adenosine is due solely to a prolongation of the atria-to-His bundle (A-H) interval. Adenosine is also known to depress Ca2+-mediated action potentials in mammalian atria (4, 5) as well as inhibit the "slow" Ca2+-Na+-mediated action potential in the A-V node (6). This suggests that the A-V node conduction defect is restricted to the slow channel-dependent tissue of the A-V node.During hypoxia, the A-V node action potentials are depressed and, concomitantly, the A-H conduction time is markedly increased (7). Furthernore, ischemia and asphyxia also impair A-V node transmission (8)(9)(10) and enhance the atrial and ventricular cardiac cell production of adenosine (11,12). In addition, in isolated perfused guinea pig hearts, aminophylline, a competitive antagonist ofadenosine, significantly attenuates and reverses the A-V conduction delay and block caused by adenosine and/or hypoxia (3). These findings have led us to hypothesize a causal role for adenosine in the A-V conduction block seen during hypoxia. The objective of this study is to investigate the role of adenosine in the mediation of A-V conduction disturbances...

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Effects of ischemia and hypoxia on the specialized conducting system of the canine heart

Cited by 121 publications

References 7 publications

Activation becomes highly organized during long-duration ventricular fibrillation in canine hearts

Activation becomes highly organized during long-duration ventricular fibrillation in canine hearts

Activation Patterns of Purkinje Fibers During Long-Duration Ventricular Fibrillation in an Isolated Canine Heart Model

Evidence for adenosine mediation of atrioventricular block in the ischemic canine myocardium.

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