Preconditioning reduces infarct size but accelerates time to ventricular fibrillation in ischemic pig heart

1995 ◽  
Vol 269 (1) ◽  
pp. H72-H79 ◽  
Author(s):  
M. Ovize ◽  
J. F. Aupetit ◽  
G. Rioufol ◽  
J. Loufoua ◽  
X. Andre-Fouet ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Action Potential ◽  
Infarct Size ◽  
Action Potential Duration ◽  
Ventricular Arrhythmias ◽  
Monophasic Action Potential ◽  
Control Group ◽  
Large Animal ◽  
Large Animal Models ◽  
Ventricular Fibrillation Threshold

Preconditioning protects the rat heart from ventricular arrhythmias. However, the mechanism of this beneficial effect and its existence in large animal models remain unknown. We submitted 49 pigs to 40 min of left anterior descending coronary occlusion and 2 h of reperfusion and assessed the incidence of ventricular fibrillation (VF) and time to VF. Monophasic action potential duration (MAPD) and ventricular fibrillation threshold (VFT) were measured throughout the experiment. Preconditioning significantly reduced infarct size but failed to reduce the incidence of VF either during the 40-min ischemic insult or the following reperfusion. Moreover, preconditioning accelerated the onset of VF during the prolonged ischemia; time to VF averaged 8 +/- 2 min in the preconditioned group vs. 18 +/- 2 min in the control group (P < 0.05). This premature peak of VF in preconditioned hearts was associated with a significant decrease of VFT and shortening of MAPD. This suggests that preconditioning does not limit the incidence of VF in the pig model. Rather, preconditioning decreases the time to VF in this species, likely through lowering of the VFT and shortening of the action potential duration.

scholarly journals 706-4 Preconditioning Shortens Action Potential Duration and Lowers Ventricular Fibrillation Threshold in Pig Hearts

1995 ◽  
Vol 25 (2) ◽  
pp. 43A
Author(s):  
Michel Ovize ◽  
Jean F Aupetit ◽  
Gilles Rioufol ◽  
Joseph Loufoua ◽  
Xavier André-Fouët ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Action Potential ◽  
Action Potential Duration ◽  
Ventricular Fibrillation Threshold

scholarly journals Blockade of NaV1.8 Increases the Susceptibility to Ventricular Arrhythmias During Acute Myocardial Infarction

2021 ◽  
Vol 8 ◽  
Author(s):  
Baozhen Qi ◽  
Shimo Dai ◽  
Yu Song ◽  
Dongli Shen ◽  
Fuhai Li ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Ventricular Fibrillation ◽  
Refractory Period ◽  
Ventricular Arrhythmias ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Effective Refractory Period ◽  
Control Group ◽  
Ventricular Fibrillation Threshold

SCN10A/NaV1.8 may be associated with a lower risk of ventricular fibrillation in the setting of acute myocardial infarction (AMI), but if and by which mechanism NaV1.8 impacts on ventricular electrophysiology is still a matter of debate. The purpose of this study was to elucidate the contribution of NaV1.8 in ganglionated plexi (GP) to ventricular arrhythmias in the AMI model. Twenty beagles were randomized to either the A-803467 group (n = 10) or the control group (n = 10). NaV1.8 blocker (A-803467, 1 μmol/0.5 mL per GP) or DMSO (0.5 mL per GP) was injected into four major GPs. Ventricular effective refractory period, APD90, ventricular fibrillation threshold, and the incidence of ventricular arrhythmias were measured 1 h after left anterior descending coronary artery occlusion. A-803467 significantly shortened ventricular effective refractory period, APD90, and ventricular fibrillation threshold compared to control. In the A-803467 group, the incidence of ventricular arrhythmias was significantly higher compared to control. A-803467 suppressed the slowing of heart rate response to high-frequency electrical stimulation of the anterior right GP, suggesting that A-803467 could inhibit GP activity. SCN10A/NaV1.8 was readily detected in GPs, but was not validated in ventricles by quantitative RT-PCR, western blot and immunohistochemistry. While SCN10A/NaV1.8 is detectible in canine GPs but not in ventricles, blockade of NaV1.8 in GP increases the incidence of ventricular arrhythmias in AMI hearts. Our study shows for the first time an influence of SCN10A/NaV1.8 on the regulation of ventricular arrhythmogenesis via modulating GP activity in the AMI model.

Expressed monophasic action potential alternans before the onset of ventricular arrhythmias induced by intracoronary bolus administration of endothelin-1 in dogs

2002 ◽  
Vol 103 (s2002) ◽  
pp. 219S-222S
Author(s):  
Béla MERKELY ◽  
Hajnalka VÁGÓ ◽  
Orsolya KISS ◽  
Endre ZIMA ◽  
Gábor SZÜCS ◽  
...  
Keyword(s):  
Blood Flow ◽  
Ventricular Tachycardia ◽  
Ventricular Fibrillation ◽  
Action Potential ◽  
Coronary Blood Flow ◽  
Ventricular Arrhythmias ◽  
Monophasic Action Potential ◽  
Bolus Administration ◽  
Endothelin 1 ◽  
Arrhythmogenic Effect

We showed previously a direct arrhythmogenic effect of the intracoronary infusion of endothelin-1 (ET-1). We aimed to examine the electrophysiological effects of intracoronary bolus administration of ET-1 using monophasic action potential (MAP) recordings. Eight mongrel dogs received boli of ET-1 (1 and 2nmol) into the left anterior descending coronary artery. These intracoronary ET-1 boli rapidly caused a marked decrease in coronary blood flow (1nmol, 78±7%; 2nmol, 89±7%). Ischaemic changes of MAP morphology, a decrease in upstroke velocity (baseline, 1.78±0.2V/s; 1nmol, 0.95±0.18V/s; 2nmol, 0.45±0.21V/s; P<0.01) and a decrease in MAP duration at 90% repolarization (MAPD90) [1nmol, from 191±3 to 176±5ms (P<0.05); 2nmol, from 212±4 to 180±8ms (P<0.05)] occurred after ET-1 bolus administration. However, at 7–10min after the 1nmol bolus, a significant increase in MAPD90 was observed (10min, in the left ventricular anterior epicardial region: from 191±3 to 206±6ms; P<0.05). The incidence of ventricular arrhythmias was as follows: after the 1nmol ET-1 bolus: ventricular tachycardia, 3/8 animals; ventricular fibrillation, 1/8; after the 2nmol ET-1 bolus: ventricular tachycardia, 5/7; ventricular fibrillation, 5/7. MAP alternans was present in each animal (1nmol, 18.2±5.8%; 2nmol, 10.8±2.5%). Thus electrophysiological and coronary blood flow changes indicate the predominance of an ischaemic arrhythmogenic effect of the bolus administration of ET-1 (shortening of action potential duration; appearance of MAP alternans), whereas the observed delayed prolongation of MAPD90 suggests a direct arrhythmogenic effect of ET-1. The expressed MAP alternans could have a pathogenic role in the onset of ventricular arrhythmias induced by an intracoronary bolus of ET-1.

Effect of Ado A1- and A2-receptor activation on ventricular fibrillation during hypoxia-reoxygenation

1994 ◽  
Vol 267 (4) ◽  
pp. H1447-H1454 ◽  
Author(s):  
L. Chi ◽  
G. S. Friedrichs ◽  
J. Y. Oh ◽  
A. L. Green ◽  
B. R. Lucchesi
Keyword(s):  
Ventricular Fibrillation ◽  
Action Potential ◽  
Action Potential Duration ◽  
Receptor Activation ◽  
Monophasic Action Potential ◽  
Perfused Heart ◽  
Receptor Stimulation ◽  
Myocardial Hypoxia ◽  
A1 Receptor ◽  
Hypoxia Reoxygenation

We examined the hypothesis that adenosine (Ado)-induced alterations in ventricular electrophysiology may contribute to arrhythmogenesis in a setting of myocardial hypoxia through activation of Ado A1 and A2 receptors in the rabbit isolated perfused heart. There was a 20% incidence of ventricular fibrillation (VF) in control hearts subjected to perfusion conditions of hypoxia and reoxygenation. The incidence of VF was increased to 50% in the presence of 1 microM Ado when hearts were exposed to hypoxia-reoxygenation. The incidence of VF was 20% when Ado was increased to 10 microM. Inhibition of the Ado A2 receptor with 3,7-dimethyl-l-propargylxanthine (DMPX; 10 microM) increased the incidence of VF to 100% when 10 microM Ado was added to the perfusion medium. The A1 antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 1 microM), attenuated (from 100% to 20%) VF induced by Ado + DMPX (10 microM each). The ventricular refractory period and monophasic action potential duration were determined in a separate group of hearts. Our findings indicate that 1) Ado A1-receptor stimulation facilitates VF by decreasing action potential duration and refractoriness in hearts subjected to hypoxia and reoxygenation and 2) the arrhythmogenic potential of Ado A1-receptor stimulation is modulated by simultaneous activation of the ventricular A2 Ado receptor.

P2564Levosimendan shortens action potential duration, decreases alternans threshold and prevents ventricular arrhythmia during therapeutic hypothermia in isolated rabbit hearts

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
Y C Hsieh ◽  
C H Li ◽  
Y C Liao ◽  
J C Lin ◽  
C J Weng ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Action Potential ◽  
Therapeutic Hypothermia ◽  
Action Potential Duration ◽  
Ventricular Arrhythmias ◽  
Cycle Length ◽  
Novel Approach ◽  
Mapping System ◽  
K Current ◽  
Calcium Sensitizer

Abstract Background Therapeutic hypothermia (TH) increases the susceptibility to ventricular arrhythmias (VA) by prolonging action potential duration (APD) and facilitating arrhythmogenic spatially discordant alternans (SDA). The calcium sensitizer levosimendan has been reported to shorten APD by enhancing ATP-sensitive K current. We hypothesize that levosimendan might shorten the already prolonged APD during TH, decreasing SDA threshold, and prevent the occurrence of VA. Methods Langendorff-perfused isolated rabbit hearts were subjected to 15-min TH (30°C) followed by 30-min treatment with levosimendan (0.5 μM, n=9) or vehicle (n=8). Using an optical mapping system, epicardial APD was evaluated by S1 pacing. SDA threshold was defined as the longest pacing cycle length (PCL) that induced SDA phenomenon. Ventricular fibrillation (VF) inducibility was evaluated by burst pacing for 30 s using the shortest PCL that achieved 1:1 ventricular capture. Results Levosimendan shortened the ventricular APD (at PCL 300 ms, from 229±9 ms to 211±18 ms, p=0.02) and decrease the SDA threshold (from 327±88 ms to 311±68 ms, p=0.001) during TH. The VF inducibility was decreased by levosimendan from 39±30% at 30°C to 14±12% after levosimendan infusion. In control hearts, the APD (p=0.75), SDA threshold (p=ns) and VF inducibility (p=0.12) were not changed by vehicle during TH. Conclusions Levosimendan protects the hearts against VA during TH by shortening APD and decreasing SDA threshold. Enhancing ATP-sensitive K current with levosimendan might be a novel approach to prevent VA during TH.

Protective mechanisms of resveratrol against ischemia-reperfusion-induced damage in hearts obtained from Zucker obese rats: the role of GLUT-4 and endothelin

2008 ◽  
Vol 294 (2) ◽  
pp. H859-H866 ◽  
Author(s):  
Istvan Lekli ◽  
Gergo Szabo ◽  
Bela Juhasz ◽  
Samarjit Das ◽  
Manika Das ◽  
...  
Keyword(s):  
Body Weight ◽  
Ventricular Fibrillation ◽  
Infarct Size ◽  
Ischemia Reperfusion ◽  
Serum Glucose ◽  
Control Group ◽  
Glut 4 ◽  
Reduced Body ◽  
Glucose Intake ◽  
Obese Rats

The resveratrol-induced cardiac protection was studied in Zucker obese rats. Rats were divided into five groups: group 1, lean control; group 2, obese control (OC); group 3, obese rats treated orally with 5 mg·kg−1·day−1 of resveratrol (OR) for 2 wk; group 4, obese rats received 10% glucose solution ad libitum for 3 wk (OG); and group 5, obese rats received 10% glucose for 3 wk and resveratrol (OGR) during the 2nd and 3rd wk. Body weight, serum glucose, and insulin were measured, and then hearts were isolated and subjected to 30 min of ischemia followed by 120 min of reperfusion. Heart rate, coronary flow, aortic flow, developed pressure, the incidence of reperfusion-induced ventricular fibrillation, and infarct size were measured. Resveratrol reduced body weight and serum glucose in the OR compared with the OC values (414 ± 10 g and 7.08 ± 0.41 mmol/l, respectively, to 378 ± 12 g and 6.11 ± 0.44 mmol/l), but insulin levels were unchanged. The same results were obtained for the OG vs. OGR group. Resveratrol improved postischemic cardiac function in the presence or absence of glucose intake compared with the resveratrol-free group. The incidence of ventricular fibrillation and infarct size was reduced by 83 and 20% in the OR group, and 67 and 16% in the OGR group, compared with the OC and OG groups, respectively. Resveratrol increased GLUT-4 expression and reduced endothelin expression and cardiac apoptosis in ischemic-reperfused hearts in the presence or absence of glucose intake. Thus the protective effect of resveratrol could be related to its direct effects on the heart.

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