Why the study?
Does gradual aortic occlusion increase left ventricular myocardial contractility in anesthetized dogs?
Does gradual aortic occlusion increase left ventricular myocardial contractility in anesthetized dogs?
Gradual aortic occlusion acutely increases left ventricular myocardial contractility in dogs, suggesting an intrinsic homeometric autoregulation mechanism likely related to length-dependent calcium activation.
Supports homeometric autoregulation in canine LV; leaves open translation to human disease.
We evaluated the effects of pressure loading produced by gradual aortic occlusion on left ventricular (LV) myocardial contractility by assessing changes in the slope of the LV end-systolic force-diameter (Fes-Des) relation. Eleven adult mongrel dogs were prepared with ultrasonic crystals for measuring LV diameter and a micromanometer for measuring LV pressure. Preload was decreased by vena caval occlusion (VCO), and afterload was increased by aortic occlusion (AOO). The slopes (Ec) and extrapolated diameter intercepts (Do) of the LV Fes-Des relation were determined for each dog from the end-systolic data obtained during VCO and AOO. During VCO and also AOO, the heart rate showed little change (134 +/- 18 vs. 134 +/- 16 bpm in VCO, 135 +/- 16 vs. 132 +/- 17 bpm in AOO). The values of Ec and Do during VCO were 62.8 +/- 15.6 g/cm and 1.20 +/- 0.36 cm, respectively, while during AOO the respective values were 122.6 +/- 18.6 g/cm and 1.66 +/- 0.38 cm. Ec and Do were both significantly increased during AOO in comparison with VCO (p less than 0.001). These results suggest that gradual aortic occlusion increases LV myocardial contractility in anesthetized, open-chest dogs under autonomic blockade. This phenomenon might be related to length-dependent calcium activation.
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Kadota et al. (1991) studied this question.
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