Direct effect of increased hemodynamic load on cardiac mass.

The hearts of rats were transplanted into the abdomens of recipients of the same inbred strain by attaching the stumps of aorta and pulmonary artery end to side to the abdominal aorta and inferior vena cava, respectively, of the recipient. The transplant functions as a denervated "nonworking" Langendorff heart; the recipient in situ heart serves as a normal control. One week after surgery, an onset of atrophy is observed in the transplanted heart, which stabilizes after 2 weeks; the in situ heart grows normally. Using this model, we increased the load of the left ventricle (LV) in the transplant by inserting a permanent polyethylene cannula into its aortic orifice during surgery to induce valvular incompetence and/or stenosis (TPE group). This resulted in significantly increased LV systolic pressure (115 +/- 5 versus 95 +/- 3 mm Hg) and a significantly increased rate-pressure product (34.7 +/- 1.7 versus 24.4 +/- 1.4 mm Hg.min-1 x 10(3) as compared with rats with control transplants (TC group). The LV mass in the TPE group decreased to only 85 +/- 4.8% of the mass of the corresponding in situ recipient heart as compared with 59 +/- 2.6% in the TC group (p less than 0.001). In three cases in the TPE group with highest overload, we observed about 20% larger LV mass in transplanted hearts as compared with the corresponding recipient in situ hearts. These results indicate that the increased load significantly attenuated the atrophy observed in LV of the isotransplants. This attenuation could be correlated with the increment of load as indicated by higher peak LV pressures and higher rate-pressure products.