Increased left ventricular contractility during cross-clamping of the descending thoracic aorta

To evaluate how left ventricular (LV) dimensions and contractility and proximal systemic hemodynamics respond during and after 30 minutes of cross-clamping of the descending thoracic aorta.

The study was prospective and controlled.

The study was performed in a university animal laboratory.

Ten pigs (bodyweight: 22 to 30 kg).

The pigs were anesthetized with fentanyl and ketamine, and the heart and aorta were exposed through a left thoracotomy. The aortic root pressure and flow and LV dimensions were monitored with a high-fidelity pressure catheter, a precalibrated ultrasonic transit-time flow probe, and by two-dimensional ultrasound imaging, respectively.

After 1 minute of cross-clamping, LV end-diastolic and end-systolic diameters were increased 17% and 32% above baseline (both p < 0.001), respectively, whereas LV fiber shortening was decreased by 35% (p < 0.05) corresponding to the 257% increase in wall stress (p < 0.001). After 5 minutes, LV dimensions, fiber shortening, and wall stress had returned to baseline levels. After 10 minutes, fiber shortening was increased 67% (p < 0.05), although wall stress was maintained at baseline levels. Simultaneously, the aortic mean blood pressure, heart rate, and cardiac output peaked 112% (p < 0.001), 81% (p < 0.001), and 125% (p < 0.01) above baseline, respectively.

Cross-clamping grossly increased systemic afterload grossly and was followed by moderate LV dilation, which resolved after 5 minutes owing to the combined effects of proximal vasodilation, increased myocardial contractility, and tachycardia. This hyperdynamic circulatory state was maintained during cross-clamping and decreased after declamping.