ON THE MODE OF ACTION OF GLUCOSE IN THE MAINTENANCE OF VENTRICULAR FIBRILLATION

1963 ◽  
Vol 41 (7) ◽  
pp. 1519-1523 ◽  
Author(s):  
L. Tétreault ◽  
A. Beaulnes
Keyword(s):  
Ventricular Fibrillation ◽  
Action Potential ◽  
Adenosine Triphosphate ◽  
Sodium Pump ◽  
Sucrose Solution ◽  
Glucose Deprivation ◽  
Rabbit Heart ◽  
Second Phase ◽  
Available Energy ◽  
Sodium And Potassium

Glucose deprivation was previously shown to favor the induction of ventricular fibrillation in the isolated and perfused rabbit heart. On the other hand, glucose is required for the prolonged maintenance of the induced fibrillation.The mechanism of action of glucose in the maintenance of electrically induced fibrillation was studied in 54 hearts perfused with solutions containing either normal or decreased sources of available energy. Hearts perfused with a normal solution, a low-sucrose solution, or with a glucose-free solution containing lactate or adenosine-triphosphate develop long-lasting fibrillations.It is believed that glucose deprivation acts, initially, by inhibiting the active cardiac mechanism delaying repolarization and by reducing, therefore, the duration of the action potential and rendering the heart more vulnerable to fibrillatory factors. During a second phase, brought about by a decrease in the effectiveness of the sodium pump and by a shift in the sodium and potassium fluxes, glucose deprivation lengthens the duration of the action potential and refractory period and produces an antifibrillatory effect. Dinitrophenol is thought to act in a similar manner, but the fibrillatory action of adenosine triphosphate cannot be explained as satisfactorily.

ON THE MODE OF ACTION OF GLUCOSE IN THE MAINTENANCE OF VENTRICULAR FIBRILLATION

1963 ◽  
Vol 41 (1) ◽  
pp. 1519-1523
Author(s):  
L. Tétreault ◽  
A. Beaulnes
Keyword(s):  
Ventricular Fibrillation ◽  
Action Potential ◽  
Adenosine Triphosphate ◽  
Sodium Pump ◽  
Sucrose Solution ◽  
Glucose Deprivation ◽  
Rabbit Heart ◽  
Second Phase ◽  
Available Energy ◽  
Sodium And Potassium

Glucose deprivation was previously shown to favor the induction of ventricular fibrillation in the isolated and perfused rabbit heart. On the other hand, glucose is required for the prolonged maintenance of the induced fibrillation.The mechanism of action of glucose in the maintenance of electrically induced fibrillation was studied in 54 hearts perfused with solutions containing either normal or decreased sources of available energy. Hearts perfused with a normal solution, a low-sucrose solution, or with a glucose-free solution containing lactate or adenosine-triphosphate develop long-lasting fibrillations.It is believed that glucose deprivation acts, initially, by inhibiting the active cardiac mechanism delaying repolarization and by reducing, therefore, the duration of the action potential and rendering the heart more vulnerable to fibrillatory factors. During a second phase, brought about by a decrease in the effectiveness of the sodium pump and by a shift in the sodium and potassium fluxes, glucose deprivation lengthens the duration of the action potential and refractory period and produces an antifibrillatory effect. Dinitrophenol is thought to act in a similar manner, but the fibrillatory action of adenosine triphosphate cannot be explained as satisfactorily.

Effects of Synthetic Atrial Natriuretic Peptides on Sodium-Potassium Transport in Human Erythrocytes

1985 ◽  
Vol 69 (2) ◽  
pp. 223-226 ◽  
Author(s):  
G. A. Sagnella ◽  
D. A. Nolan ◽  
A. C. Shore ◽  
G. A. MacGregor
Keyword(s):  
Loop Diuretic ◽  
Sodium Pump ◽  
Human Erythrocytes ◽  
Atrial Natriuretic Peptides ◽  
Sodium Potassium ◽  
Potassium Ion Transport ◽  
Wide Range ◽  
Natriuretic Effect ◽  
Cotransport System ◽  
Sodium And Potassium

1. The effects of synthetic human and rat atrial peptides on sodium and potassium ion transport has been investigated in intact human erythrocytes. 2. The effects of these peptides have been tested on the active, sodium pump-dependent (ouabain-sensitive) and on the sodium-potassium cotransport system (bumetanide-sensitive) with 86Rb used as a tracer. 3. Human (α-ANP, 28 amino acids) or rat (atriopeptin III) atrial peptides, over a wide range of concentrations, did not influence the uptake of 86Rb in either the ouabain-sensitive or the bumetanide-sensitive transport system. 4. These results suggest that the natriuretic effect of the atrial peptides is not mediated through inhibition of the sodium pump or the loop-diuretic-sensitive Na-K cotransport.

Rate-dependent shortening of action potential duration increases ventricular vulnerability in failing rabbit heart

2011 ◽  
Vol 300 (2) ◽  
pp. H565-H573 ◽  
Author(s):  
Masahide Harada ◽  
Yukiomi Tsuji ◽  
Yuko S. Ishiguro ◽  
Hiroki Takanari ◽  
Yusuke Okuno ◽  
...  
Keyword(s):  
Action Potential ◽  
High Frequency ◽  
Rabbit Heart ◽  
Left Ventricular ◽  
High Frequency Stimulation ◽  
Electrophysiological Properties ◽  
Rate Dependent ◽  
Frequency Stimulation ◽  
And Control

Congestive heart failure (CHF) predisposes to ventricular fibrillation (VF) in association with electrical remodeling of the ventricle. However, much remains unknown about the rate-dependent electrophysiological properties in a failing heart. Action potential properties in the left ventricular subepicardial muscles during dynamic pacing were examined with optical mapping in pacing-induced CHF ( n = 18) and control ( n = 17) rabbit hearts perfused in vitro. Action potential durations (APDs) in CHF were significantly longer than those observed for controls at basic cycle lengths (BCLs) >1,000 ms but significantly shorter at BCLs <400 ms. Spatial APD dispersions were significantly increased in CHF versus control (by 17–81%), and conduction velocity was significantly decreased in CHF (by 6–20%). In both groups, high-frequency stimulation (BCLs <150 ms) always caused spatial APD alternans; spatially concordant alternans and spatially discordant alternans (SDA) were induced at 60% and 40% in control, respectively, whereas 18% and 82% in CHF. SDA in CHF caused wavebreaks followed by reentrant excitations, giving rise to VF. Incidence of ventricular tachycardia/VFs elicited by high-frequency dynamic pacing (BCLs <150 ms) was significantly higher in CHF versus control (93% vs. 20%). In CHF, left ventricular subepicardial muscles show significant APD shortenings at short BCLs favoring reentry formations following wavebreaks in association with SDA. High-frequency excitation itself may increase the vulnerability to VF in CHF.

scholarly journals Intramural optical mapping of Vm and Cai2+ during long-duration ventricular fibrillation in canine hearts

2012 ◽  
Vol 302 (6) ◽  
pp. H1294-H1305 ◽  
Author(s):  
Wei Kong ◽  
Raymond E. Ideker ◽  
Vladimir G. Fast
Keyword(s):  
Ventricular Fibrillation ◽  
Action Potential ◽  
Short Duration ◽  
Action Potential Duration ◽  
Cycle Length ◽  
The Other ◽  
Membrane Voltage ◽  
Long Duration ◽  
Intracellular Ca ◽  
Rapid Pacing

Intramural gradients of intracellular Ca2+ (Cai2+) Cai2+ handling, Cai2+ oscillations, and Cai2+ transient (CaT) alternans may be important in long-duration ventricular fibrillation (LDVF). However, previous studies of Cai2+ handling have been limited to recordings from the heart surface during short-duration ventricular fibrillation. To examine whether abnormalities of intramural Cai2+ handling contribute to LDVF, we measured membrane voltage ( Vm) and Cai2+ during pacing and LDVF in six perfused canine hearts using five eight-fiber optrodes. Measurements were grouped into epicardial, midwall, and endocardial layers. We found that during pacing at 350-ms cycle length, CaT duration was slightly longer (by ≃10%) in endocardial layers than in epicardial layers, whereas action potential duration (APD) exhibited no difference. Rapid pacing at 150-ms cycle length caused alternans in both APD (APD-ALT) and CaT amplitude (CaA-ALT) without significant transmural differences. For 93% of optrode recordings, CaA-ALT was transmurally concordant, whereas APD-ALT was either concordant (36%) or discordant (54%), suggesting that APD-ALT was not caused by CaA-ALT. During LDVF, Vm and Cai2+ progressively desynchronized when not every action potential was followed by a CaT. Such desynchronization developed faster in the epicardium than in the other layers. In addition, CaT duration strongly increased (by ∼240% at 5 min of LDVF), whereas APD shortened (by ∼17%). CaT rises always followed Vm upstrokes during pacing and LDVF. In conclusion, the fact that Vm upstrokes always preceded CaTs indicates that spontaneous Cai2+ oscillations in the working myocardium were not likely the reason for LDVF maintenance. Strong Vm-Cai2+ desynchronization and the occurrence of long CaTs during LDVF indicate severely impaired Cai2+ handling and may potentially contribute to LDVF maintenance.

scholarly journals Idiopathic Ventricular Fibrillation Characterized by Spatial Heterogeneity of Action Potential Duration and Its Restitution Kinetics

2008 ◽  
Vol 49 (6) ◽  
pp. 733-740 ◽  
Author(s):  
Sonoko Ashino ◽  
Ichiro Watanabe ◽  
Masayoshi Kofune ◽  
Kimie Ohkubo ◽  
Yasuo Okumura ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Action Potential ◽  
Spatial Heterogeneity ◽  
Action Potential Duration ◽  
Idiopathic Ventricular Fibrillation
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