[Ventricular function in animals undergoing renal mass ablation. Effect of blood pressure control]

The causes of left ventricular hypertrophy (LVH) in chronic renal failure are multifactorial. The tail arterial pressure, heart weight, maximum developed pressure and pressure-volume relationship in animals with 5/6 nephrectomy (CRF, n = 16) and CRF animals who received furosemide by oral gavage (CRF-F, n = 17) were studied. All CRF animals increased their blood pressure (Basal: 117.2 +/- 0.8; 6th week: 184.8 +/- 2.9, p < 0.001) but in those treated with furosemide the blood pressure stayed within normal levels (Basal: 118.23 +/- 1.3; 6th week = 118.8 +/- 1.6, p = 0.5734). SHAM animals served as control (SHAM, n = 15). All CRF and CRF-F animals increased their levels of serum creatinine (CRF = 1.81 +/- 0.05; CRF-F = 1.75 +/- 0.05; SHAM = 0.72 +/- 0.09 mg/dL p < 0.001). Cardiac weight was elevated in CRF and CRF-F when compared with SHAM rats. The operational maximum developed pressure was similar in the three groups (CRF = 221.2 +/- 7.04; CRF-F = 255.7 +/- 10.1; SHAM = 239.9 +/- 5.5 mmHg, n.s.). However, the end-diastolic volume was significantly increased in both CRF and CRF-F when compared with SHAM rats (CRF = 91.4 +/- 9.44; CRF-F = 70.9 +/- 6.22; SHAM = 28.75 +/- 3.12 microL. p < 0.001). These data demonstrate that LVH in chronic renal failure is not dependent of the arterial hypertension, that accompanies this condition. Moreover, the systolic work of LVH animals is similar to that of normal animals, but a greater utilization of Frank-Starling mechanism to maintain normal ventricular function is needed.