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. 1968 Jun;47(6):1333–1342. doi: 10.1172/JCI105825

Left ventricular function in experimental aorto-caval fistula with circulatory congestion and fluid retention

Roger R Taylor 1, James W Covell 1, John Ross Jr 1
PMCID: PMC297289  PMID: 5653213

Abstract

The mechanical properties of left ventricular contraction were described in terms of tension, velocity, length, and time in closed-chest, sedated dogs in which a large aorto-caval fistula had resulted in circulatory congestion, and the results were compared with those in normal dogs. Instantaneous contractile element velocity was calculated from left ventricular pressure and its first derivative during isovolumic left ventricular contractions produced by sudden balloon occlusion of the ascending aorta during diastole. A range of ventricular end-diastolic volumes was induced and heart rate was controlled at 150 beats/min. Wall tension (stress) was derived from ventricular pressure and volume, the latter being obtained from the pressure-volume relation of the passive ventricle. Extrapolated velocity at zero tension, Vmax, averaged 3.0 circ/sec in the normal dogs and 2.9 circ/sec in the seven dogs with an aorto-caval fistula and fluid retention; in only one of these seven animals was Vmax below the lower limit of normal of 2.7 circ/sec. Isovolumic tension (Po) in dogs with aorto-caval fistulas tended to be slightly greater than normal at low ventricular filling pressures, and there was no difference in Po between the two groups of animals at high ventricular filling pressures. Time to peak pressure averaged 151 ± 6 (SE) msec (normal 139 ± 3). Left ventricular weight averaged 6.32 ± 0.23 g/kg of initial body weight (normal 5.25 ± 0.56 g/kg) (P < 0.001), which reflected moderate ventricular hypertrophy, and ventricular internal volume at a given filling pressure was increased proportionally. Therefore, the ventricular contractile state usually was normal in the dog with a large aorto-caval fistula, and it is proposed that mechanisms for fluid retention that results in circulatory congestion were activated because of the large hemodynamic burden despite normal myocardial contractile properties.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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