Mangieri E, Tanzilli G, Acri A, Mangiaracina F, Ferri F M, Mastroianni M A, Nardi M, Pignatelli A, Abbolito S, Missiroli B
II Cattedra di Cardiologia, Università degli Studi La Sapienza, Roma.
Cardiologia. 1994 Aug;39(8):577-83.
We studied the acute hemodynamic effects of nifedipine (N) on handgrip test (Hg) in 10 patients with aortic regurgitation in II NYHA functional class. In basal condition (B) we found a significant increase of mean aortic pressure (AoPmean) in all patients after Hg (101 +/- 9.72 versus 110.3 +/- 6.42 mmHg; p < 0.05). Hg did not induce significant changes of AoPmean after N. Hg increased left ventricular end-diastolic pressure (LVEDP) from 13.3 +/- 6.4 to 20.5 +/- 9.9 mmHg (p < 0.01) before N and from 9.7 +/- 3.2 to 12.8 +/- 5.5 mmHg after N (NS). LVEDP measured during Hg after N showed lower values than those measured before N (12.8 +/- 5.5 versus 20.5 +/- 9.9 mmHg; p < 0.01). Cardiac index (CI) increased by Hg in B (3.7 +/- 0.7 versus 4.0 +/- 1.1 L/min/m2; NS) and after N (4.5 +/- 0.7 versus 4.9 +/- 0.9 L/min/m2; NS). CI increased significantly after N at rest (3.7 +/- 0.7 versus 4.5 +/- 0.7 L/min/m2; p < 0.01) and during Hg (4.0 +/- 1.1 versus 4.9 +/- 0.9 L/min/m2; p < 0.01). The left ventricular stroke work index (LVSWI) decreased during Hg from 74.4 +/- 20.6 to 71.2 +/- 20.0 g.m/m2; NS. N caused an increase at rest to 81.4 +/- 22.5 g.m/m2; NS. LVSWI increased significantly during Hg to 83.5 +/- 26.2 g.m/m2; p < 0.05. Systemic arterial resistances (SAR) significantly decreased after N at rest (1,086.8 +/- 280.8 versus 843.5 +/- 133.1 dyne.s.cm-5; p < 0.01), but increased in B during Hg to 1,220.9 +/- 350.7 dyne.s.cm-5; p < 0.05. A significant reduction of SAR values was observed alter N during Hg (1,220.9 +/- 350.7 versus 838.9 +/- 139.9 dyne.s.cm-5; p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
我们研究了硝苯地平(N)对10例纽约心脏病协会(NYHA)心功能II级主动脉瓣反流患者握力试验(Hg)的急性血流动力学影响。在基础状态(B)下,我们发现所有患者在进行握力试验后平均主动脉压(AoPmean)显著升高(101±9.72对110.3±6.42 mmHg;p<0.05)。服用硝苯地平后,握力试验未引起平均主动脉压的显著变化。在服用硝苯地平前,握力试验使左心室舒张末期压力(LVEDP)从13.3±6.4升高至20.5±9.9 mmHg(p<0.01),服用硝苯地平后从9.7±3.2升高至12.8±5.5 mmHg(无统计学意义)。服用硝苯地平后握力试验期间测量的左心室舒张末期压力值低于服用硝苯地平前(12.8±5.5对20.5±9.9 mmHg;p<0.01)。在基础状态下,握力试验使心脏指数(CI)升高(3.7±0.7对4.0±1.1 L/min/m²;无统计学意义),服用硝苯地平后也升高(4.5±0.7对4.9±0.9 L/min/m²;无统计学意义)。服用硝苯地平后静息时心脏指数显著升高(3.7±0.7对4.5±0.7 L/min/m²;p<0.01),握力试验期间也显著升高(4.0±1.1对4.9±0.9 L/min/m²;p<0.01)。左心室每搏功指数(LVSWI)在握力试验期间从74.4±20.6降至71.2±20.0 g.m/m²;无统计学意义。硝苯地平使静息时升高至81.4±22.5 g.m/m²;无统计学意义。握力试验期间左心室每搏功指数显著升高至83.5±26.2 g.m/m²;p<0.05。服用硝苯地平后静息时全身动脉阻力(SAR)显著降低(1086.8±280.8对843.5±133.1 dyne.s.cm⁻⁵;p<0.01),但在基础状态下握力试验期间升高至1220.9±350.7 dyne.s.cm⁻⁵;p<0.05。服用硝苯地平后握力试验期间观察到全身动脉阻力值显著降低(1220.9±350.7对838.9±139.9 dyne.s.cm⁻⁵;p<0.01)。(摘要截短至250字)