Location of epicardial pacemaker electrodes and myocardial contractility

1969 ◽  
Vol 47 (3) ◽  
pp. 267-271 ◽  
Author(s):  
G. M. Tremblay ◽  
M. Nahas

Effects of pacing from different epicardial sites on cardiac contractility were studied in the isolated perfused rat heart. An indwelling balloon containing a known volume of saline was used to record intracavitary pressure (LVP), force, and maximum dp/dt during isovolumic paced contraction. Coronary flow was kept constant, and the adequacy of oxygenation was verified by lactate extraction. Forty male Sprague–Dawley rats weighing 250–300 g were divided into two groups, according to the rate of pacing, and stimulated. Pacing from four different epicardial sites failed to show any statistically significant difference in LVP, force, or maximum dp/dt at either different heart rate or calcium concentration. The present study suggests that myocardial contractility in the isolated perfused rat heart is not affected by the pacing site of the epicardial pacemaker.

2005 ◽  
Vol 289 (2) ◽  
pp. R424-R431 ◽  
Author(s):  
Adam J. Chicco ◽  
Carole M. Schneider ◽  
Reid Hayward

The clinical use of doxorubicin (DOX) is limited by a dose-dependent cardiotoxicity. The purpose of this study was to determine whether voluntary exercise training would confer protection against DOX cardiotoxicity in the isolated perfused rat heart. Female Sprague-Dawley rats were randomly assigned to standard holding cages or cages with running wheels for 8 wk. Twenty-four hours after the sedentary (SED) or voluntary exercise (VEX) running period, rats were anesthetized with pentobarbital sodium, and hearts were isolated and perfused with oxygenated Krebs-Henseleit (KH) buffer at a constant flow of 15 ml/min. After a 20-min stabilization period, hearts were paced at 300 beats per minute and perfused with KH buffer containing 10 μM DOX for 60 min. A set of control hearts from SED and VEX rats were perfused under identical conditions without DOX for the same period. DOX perfusion led to significant decreases in left ventricular developed pressure, +dP/d t, and −dP/d t, and significant increases in LV lipid peroxidation in sedentary rats compared with non-DOX controls ( P < 0.05). Prior voluntary exercise training attenuated these DOX-induced effects and was associated with a significant increase (78%, P < 0.05) in heat shock protein (HSP72), but not mitochondrial isoform of SOD (MnSOD) or CuZnSOD protein expression in the hearts of wheel-run animals. These data indicate that chronic physical activity may provide resistance against the cardiac dysfunction and oxidative damage associated with DOX exposure and provide novel evidence of HSP72 induction in the heart after voluntary exercise.


1991 ◽  
Vol 19 (2) ◽  
pp. 218-224 ◽  
Author(s):  
WANCHUN TANG ◽  
MAX HARRY WEIL ◽  
RAÜL J. GAZMURI ◽  
JOE BISERA ◽  
ERIC C. RACKOW

1974 ◽  
Vol 52 (3) ◽  
pp. 375-383 ◽  
Author(s):  
Beverley A. Young ◽  
John H. McNeill

Noradrenaline and tyramine increased contractility, phosphorylase a, and cyclic AMP in a dose-dependent manner in the isolated perfused rat heart. Time–response studies revealed that cyclic AMP was increased by both amines before the increase in contractility. Hearts from hyperthyroid rats responded to noradrenaline in a manner similar to control hearts when contractility or cyclic AMP was measured. The phosphorylase activating effect of noradrenaline was enhanced in the hyperthyroid hearts. It was concluded that a non-cyclic AMP mechanism was involved in the enhancement. The effects of tyramine on contractility and cyclic AMP were decreased in the hearts from hyperthyroid animals when compared with control hearts. Phosphorylase activation by tyramine was not enhanced by the hyperthyroid state and was in fact reduced at higher doses of tyramine.


1972 ◽  
Vol 50 (9) ◽  
pp. 853-859 ◽  
Author(s):  
Charles W. Tomlinson ◽  
Naranjan S. Dhalla

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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