Manohar M, Goetz T E
Department of Veterinary Biosciences, College of Veterinary Medicine, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801, USA.
J Appl Physiol (1985). 1998 Jun;84(6):1902-8. doi: 10.1152/jappl.1998.84.6.1902.
The present study was carried out to examine the effects of nitric oxide synthase inhibition with Nomega-nitro-L-arginine methyl ester (L-NAME) on the right atrial as well as on the pulmonary arterial, capillary, and venous blood pressures of horses during rest and exercise performed at maximal heart rate (HRmax). Experiments were carried out on seven healthy, sound, exercise-trained Thoroughbred horses. Using catheter-tip manometers, with signals referenced at the point of the shoulder, we determined phasic and mean right atrial and pulmonary vascular pressures in two sets of experiments [control (no medications) and L-NAME (20 mg/kg iv given 10 min before exercise studies)]. The studies were carried out in random order 7 days apart. Measurements were made at rest and during treadmill exercise performed on a 5% uphill grade at 6, 8, and 14.2 m/s. Exercise on a 5% uphill grade at 14.2 m/s elicited HRmax and could not be sustained for >90 s. In quietly standing horses, L-NAME administration caused a significant rise in right atrial, as well as pulmonary arterial, capillary, and venous pressures. This indicates that nitric oxide synthase inhibition modifies the basal pulmonary vasomotor tone. In both treatments, exercise caused progressive significant increments in right atrial and pulmonary vascular pressures, but the values recorded in the L-NAME study were not different from those in the control study. The extent of exercise-induced tachycardia was significantly decreased in the L-NAME study at 6 and 8 m/s but not at 14.2 m/s. Thus, L-NAME administration may not modify the equine pulmonary vascular tone during exercise at HRmax. However, as indicated by a significant reduction in heart rate, L-NAME seems to modify the sympathoneurohumoral response to submaximal exercise.
本研究旨在探讨用Nω-硝基-L-精氨酸甲酯(L-NAME)抑制一氧化氮合酶对马在静息和最大心率(HRmax)运动时右心房以及肺动脉、毛细血管和静脉血压的影响。实验在7匹健康、健全、经过运动训练的纯种马身上进行。使用导管尖端压力计,信号以肩部为参考点,我们在两组实验中[对照组(无药物)和L-NAME组(在运动研究前10分钟静脉注射20mg/kg)]测定了右心房和肺血管的相位和平均压力。研究以随机顺序进行,间隔7天。在静息状态以及在跑步机上以6、8和14.2m/s的速度在5%的上坡坡度上进行运动时进行测量。以14.2m/s的速度在5%的上坡坡度上运动可引发HRmax,且持续时间不能超过90秒。在安静站立的马中,给予L-NAME会导致右心房以及肺动脉、毛细血管和静脉压力显著升高。这表明一氧化氮合酶抑制会改变基础肺血管运动张力。在两种处理中,运动都会导致右心房和肺血管压力逐渐显著升高,但L-NAME研究中记录的值与对照研究中的值没有差异。在L-NAME研究中,6和8m/s时运动诱发的心动过速程度显著降低,但在14.2m/s时没有。因此,在HRmax运动期间给予L-NAME可能不会改变马的肺血管张力。然而,正如心率显著降低所表明的,L-NAME似乎会改变对次最大运动的交感神经体液反应。