scholarly journals Role of the perinodal region in atrioventricular nodal reentry: Evidence in an isolated rabbit heart preparation

1983 ◽  
Vol 2 (3) ◽  
pp. 465-473 ◽  
Author(s):  
Hiroyuki Iinuma ◽  
Leonard S. Dreifus ◽  
Todor Mazgalev ◽  
Rohn Price ◽  
Eric L. Michelson
1990 ◽  
Vol 258 (5) ◽  
pp. H1388-H1394 ◽  
Author(s):  
J. F. Baron ◽  
E. Vicaut ◽  
X. Hou ◽  
M. Duvelleroy

The aim of this study of a blood-perfused isolated rabbit heart preparation was to differentiate the effects on coronary resistance of large changes in arterial O2 tension (arterial PO2 = 45-400 Torr) from the effects of variations in arterial O2 content or myocardial O2 delivery. Standard stored human blood was resuspended in Krebs-Henseleit buffer and was oxygenated to obtain normal PO2, high PO2, and low PO2. Hemoglobin concentrations were adjusted to obtain the same arterial O2 content (CaO2) for the three PO2s. In a first set of experiments, in which coronary blood flow (CBF) was free and adapted to a constant perfusion pressure, switching from control [138 +/- 17 (SE) Torr] to high PO2 blood (380 +/- 27 Torr) induced a significant decrease in CBF and myocardial O2 consumption (MVO2). Switching from control (125 +/- 3 Torr) to low PO2 blood (49 +/- 5 Torr) induced a significant increase in CBF and MVO2. In a second set of experiments, the switch from control (159 +/- 5 Torr) to high PO2 (389 +/- 32 Torr) was performed in a preparation in which CBF and consequently O2 delivery were constant. Under these conditions, the increase in perfusion pressure demonstrated that PO2 affected coronary resistance, even though the O2 delivery was constant. No significant change in myocardial performance was observed in any of these experimental procedures. These results show that arterial PO2 may affect coronary blood flow regulation independently of any mediation by the autonomic nervous system and of any associated changes in O2 content or O2 delivery.


2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Elena Tolkacheva ◽  
Jillian Wothe ◽  
Iryna Talkachova ◽  
Rebecca Smith ◽  
Ramjay Visweswaran

Alternans of action potential duration (APD) and intracellular calcium ([Ca 2+ ] i ) transients in the whole heart are thought to be markers of increased propensity to ventricular fibrillation during ischemia reperfusion injuries. During ischemia, ATP production is affected and the mitochondria become uncoupled. This uncoupling may play an important role in alternans formation in the heart. The aim of our study was to investigate the role of mitochondrial depolarization on the formation of APD and [Ca 2+ ] i alternans in the isolated rabbit heart. We performed dual voltage and [Ca 2+ ] i optical mapping of isolated rabbit hearts under control conditions, global no-flow ischemia (n=6), and after treatment with 50 nM of the mitochondrial uncoupler FCCP (n=6). We investigated the formation of alternans of APD, [Ca 2+ ] i amplitude (CaA), and [Ca 2+ ] i duration (CaD) in the heart, under different rates of pacing. We found that treatment with FCCP leads to the early occurrence of APD (192 ± 18 ms vs 136 ± 6 ms, p<0.05), CaD (182 ± 20 ms vs 133 ± 6 ms, p<0.05), and CaA (152 ± 5 ms vs 141 ± 3 ms, p<0.05) alternans, and an increase of intraventricular APD (0.44 ± 0.02 vs 0.2 ± 0.05, p<0.05) but not CaD (0.20 ± 0.03 vs 0.16 ± 0.03, p=N/S) heterogeneity, when compared to control. On the other hand, FCCP does not affect the conduction velocity in the heart (0.95 ± 0.06 m/s vs 1.05 ± 0.11 m/s, p=N/S). Furthermore, we demonstrated that FCCP and global ischemia have similar effects on the prolongation of [Ca 2+ ] i transients, whereas ischemia induces a significantly larger reduction of APD compared to FCCP treatment. Our results demonstrate that uncoupling of mitochondria leads to earlier occurrence of alternans in the heart. Thus, in conditions of mitochondrial stress, as seen during myocardial ischemia, uncoupled mitochondria may be responsible for the formation of both APD and [Ca 2+ ] i alternans in the heart, which in turn creates a substrate conducive to formation of ventricular arrhythmias.


1990 ◽  
Vol 212 (4) ◽  
pp. 387-394 ◽  
Author(s):  
THOMAS W. WAKEFIELD ◽  
LARRY E. BIES ◽  
SHIRLEY K. WROBLESKI ◽  
STEVEN F. BOLLING ◽  
JAMES C. STANLEY ◽  
...  

PLoS ONE ◽  
2018 ◽  
Vol 13 (12) ◽  
pp. e0209085
Author(s):  
Luis Such-Miquel ◽  
Laia Brines ◽  
Antonio M. Alberola ◽  
Manuel Zarzoso ◽  
Francisco J. Chorro ◽  
...  

2013 ◽  
Vol 305 (1) ◽  
pp. H9-H18 ◽  
Author(s):  
Rebecca M. Smith ◽  
Ramjay Visweswaran ◽  
Iryna Talkachova ◽  
Jillian K. Wothe ◽  
Elena G. Tolkacheva

Alternans of action potential duration (APD) and intracellular calcium ([Ca2+]i) transients in the whole heart are thought to be markers of increased propensity to ventricular fibrillation during ischemia-reperfusion injuries. During ischemia, ATP production is affected and the mitochondria become uncoupled, which may affect alternans formation in the heart. The aim of our study was to investigate the role of mitochondria on the formation of APD and [Ca2+]i alternans in the isolated rabbit heart. We performed dual voltage and [Ca2+]i optical mapping of isolated rabbit hearts under control conditions, global no-flow ischemia ( n = 6), and after treatment with 50 nM of the mitochondrial uncoupler FCCP ( n = 6). We investigated the formation of alternans of APD, [Ca2+]i amplitude (CaA), and [Ca2+]i duration (CaD) under different rates of pacing. We found that treatment with FCCP leads to the early occurrence of APD, CaD, and CaA alternans; an increase of intraventricular APD but not CaD heterogeneity; and significant reduction in conduction velocity compared with that of control. Furthermore, we demonstrated that FCCP and global ischemia have similar effects on the prolongation of [Ca2+]i transients, whereas ischemia induces a significantly larger reduction of APD compared with that in FCCP treatment. In conclusion, our results demonstrate that uncoupling of mitochondria leads to an earlier occurrence of alternans in the heart. Thus, in conditions of mitochondrial stress, as seen during myocardial ischemia, uncoupled mitochondria may be responsible for the formation of both APD and [Ca2+]i alternans in the heart, which in turn creates a substrate for ventricular arrhythmias.


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