The effect of heart rate on the termination of electrically induced ventricular fibrillation in the isolated perfused rat heart

1988 ◽  
Vol 83 (6) ◽  
pp. 678-686 ◽  
Author(s):  
M. Arad ◽  
S. Rogel ◽  
Y. Mahler ◽  
G. Uretzky
Keyword(s):  
Heart Rate ◽  
Ventricular Fibrillation ◽  
Rat Heart ◽  
Perfused Rat Heart ◽  
Isolated Perfused Rat Heart

Protective effects of an adenosine deaminase inhibitor on ischemia-reperfusion injury in isolated perfused rat heart

1990 ◽  
Vol 259 (3) ◽  
pp. H835-H838 ◽  
Author(s):  
Q. Y. Zhu ◽  
S. G. Chen ◽  
C. M. Zou
Keyword(s):  
Ventricular Fibrillation ◽  
Reperfusion Injury ◽  
Adenosine Deaminase ◽  
Rat Heart ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Treated Group ◽  
Perfused Rat Heart ◽  
Isolated Perfused Rat Heart ◽  
Resting Tension

We tested the effect of the adenosine deaminase inhibitor erythro-9-(2-hydroxy-3-nonyl)adenosine (EHNA) on ischemia-reperfusion injury in isolated perfused rat heart. In the ischemia-reperfusion group (n = 10), ventricular fibrillation occurred within 3 min of reperfusion after the 40-min ischemic period. The incidence of ventricular fibrillation was 90% with a mean duration of 3.15 +/- 0.97 (SE) min. Resting tension increased significantly. By contrast, the incidence of ventricular fibrillation after reperfusion in the EHNA-treated (5 microM) group (n = 10) was 20% (P less than 0.01), and the duration was 0.30 +/- 0.21 min (P less than 0.01). Resting tension was significantly lower and around the normal level in the EHNA-treated group (P less than 0.01). Contraction amplitude and heart rate recovered to nearly normal compared with the ischemia-reperfusion group (P less than 0.01). Coronary flow was greater in the EHNA-treated group (P less than 0.01). It is concluded that EHNA protects the heart, possibly by accumulation of adenosine that benefits the hearts and by blocking the xanthine oxidase pathway for free radical generation.

Protective action of amiodarone against ventricular fibrillation in the isolated perfused rat heart

1979 ◽  
Vol 43 (3) ◽  
pp. 533-540 ◽  
Author(s):  
W.F. Lubbe ◽  
M.L. McFadyen ◽  
C.A. Muller ◽  
M. Worthington ◽  
L.H. Opie
Keyword(s):  
Ventricular Fibrillation ◽  
Rat Heart ◽  
Protective Action ◽  
Perfused Rat Heart ◽  
Isolated Perfused Rat Heart

The effect of hexane on the ventricular fibrillation threshold of the isolated perfused rat heart

Toxicology ◽  
1992 ◽  
Vol 71 (1-2) ◽  
pp. 145-150 ◽  
Author(s):  
Shaun M. Khedun ◽  
Breminand Maharaj ◽  
William P. Leary ◽  
Cecil J. Lockett
Keyword(s):  
Ventricular Fibrillation ◽  
Rat Heart ◽  
Perfused Rat Heart ◽  
Isolated Perfused Rat Heart ◽  
Ventricular Fibrillation Threshold

Myocardial Contractility. II. Effect of Changes in Cardiac Function on the Subcellular Distribution of Calcium in the Isolated Perfused Rat Heart

1972 ◽  
Vol 50 (9) ◽  
pp. 853-859 ◽  
Author(s):  
Charles W. Tomlinson ◽  
Naranjan S. Dhalla
Keyword(s):  
Heart Rate ◽  
Subcellular Distribution ◽  
Rat Heart ◽  
Myocardial Contractility ◽  
Contractile Force ◽  
Tissue Homogenate ◽  
Perfusion Medium ◽  
Perfused Rat Heart ◽  
Isolated Perfused Rat Heart ◽  
Frequency Of Stimulation

The effects of changes in heart rate and contractile force due to electrical stimulation, alteration of the temperature of the perfusion medium, and varying degrees of stretch tension on the subcellular distribution of calcium in the isolated perfused rat heart were studied. Increasing the frequency of stimulation from 80 to 320 pulses/min decreased myocardial contractility without appreciable changes in the levels of calcium in the tissue homogenate and heavy microsomal (8000 – 40 000 × g) fraction. On the other hand, mitochondrial (800–8000 × g) calcium content was greater in hearts stimulated at 120 pulses/min than in hearts stimulated at 80 pulses/min; further increase in the frequency of stimulation resulted in a decrease in the level of mitochondrial calcium. Increasing the temperature of the perfusion medium from 25 to 37 °C increased the heart rate and decreased the contractile force without any changes in the levels of calcium in the homogenate or subcellular fractions. Increasing the stretch tension on the hearts from 0 to 5 g increased the developed contractile force and the level of heavy microsomal calcium without changing the heart rate or the levels of calcium in the homogenate and mitochondria. The results do not reveal any cause–effect relationship between changes in heart function and subcellular distribution of calcium.

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