Saragoça M A, Cezaretti M L, Tavares A, Bessa A M, Almeida J B, Amorin M P, Ramos O L
Division of Nephrology, Paulista School of Medicine, São Paulo, Brazil.
Hypertension. 1988 Feb;11(2 Pt 2):I89-92. doi: 10.1161/01.hyp.11.2_pt_2.i89.
Reversal of cardiac hypertrophy has been obtained by treatment with some antihypertensive drugs but has not been achieved consistently with beta blockers. To investigate whether this difference might be explained by the distinct hemodynamic actions of the drugs, we studied the effects of propranolol and pindolol, beta blockers with distinct modes of action, on cardiac hypertrophy of hypertensive male Wistar rats, two-kidney, one clip (2K1C) Goldblatt model (n = 33) and sham-operated control rats (n = 34). We also assessed the effects of such therapies on the ventricular pumping ability during open-chest, transient aortic occlusion. Four weeks after surgery, propranolol (5 mg/kg/day p.o.) was given to hypertensive (n = 8) and control rats (n = 11); pindolol was also given orally (1 mg/kg/day) to similar groups (n = 7 and n = 5, respectively). Untreated animals served as controls for both groups. Cardiac hypertrophy developed with hypertension in the untreated rats of the propranolol (3.38 +/- 0.18 vs 2.60 +/- 0.08 mg/g; p less than 0.01) and pindolol groups (3.93 +/- 0.21 vs 2.40 +/- 0.03 mg/g; p less than 0.001). Treatment reversed cardiac hypertrophy in the pindolol-treated (3.01 +/- 0.19 vs 3.93 +/- 0.21 mg/g; p less than 0.001, NS) but not in the propranolol-treated rats (3.24 +/- 0.18 vs 3.38 +/- 0.21 mg/g, NS). The maximal pressure that developed during aortic occlusion in the propranolol group was similar to that observed in the pindolol group. These results indicate that cardiac hypertrophy is reversed by pindolol but not by propranolol, and that this reversal does not interfere with left ventricular pumping ability.
某些抗高血压药物治疗可使心脏肥大逆转，但β受体阻滞剂却未能始终实现这一效果。为研究这种差异是否可由药物不同的血流动力学作用来解释，我们研究了作用方式不同的β受体阻滞剂普萘洛尔和吲哚洛尔对雄性高血压Wistar大鼠（双肾单夹（2K1C）戈德布拉特模型，n = 33）及假手术对照大鼠（n = 34）心脏肥大的影响。我们还评估了此类治疗对开胸、短暂性主动脉阻断期间心室泵血能力的影响。术后四周，给高血压大鼠（n = 8）和对照大鼠（n = 11）口服普萘洛尔（5 mg/kg/天）；给类似组（分别为n = 7和n = 5）口服吲哚洛尔（1 mg/kg/天）。未治疗的动物作为两组的对照。在普萘洛尔组（3.38±0.18 vs 2.60±0.08 mg/g；p＜0.01）和吲哚洛尔组（3.93±0.21 vs 2.40±0.03 mg/g；p＜0.001）未治疗的大鼠中，心脏肥大随高血压而发展。吲哚洛尔治疗可使心脏肥大逆转（3.01±0.19 vs 3.93±0.21 mg/g；p＜0.001，无显著性差异），但普萘洛尔治疗的大鼠则未逆转（3.24±0.18 vs 3.38±0.21 mg/g，无显著性差异）。普萘洛尔组主动脉阻断期间产生的最大压力与吲哚洛尔组观察到的相似。这些结果表明，吲哚洛尔可使心脏肥大逆转，而普萘洛尔则不能，且这种逆转不影响左心室泵血能力。
