Vogt M, Ott B, Rupp H, Jacob R
Basic Res Cardiol. 1986;81 Suppl 1:157-69. doi: 10.1007/978-3-662-11374-5_16.
In previous studies swimming training (ST) of spontaneously hypertensive rats (SHR) at 36 degrees water temperature (WT) led to a decrease in blood pressure (BP). A similar effect of ST has not been described in human hypertension. Our purpose was to investigate the influence of WT on this training effect, the influence of ST on LV hypertrophy and the involvement of adrenergic stimuli in the latter. Male SHR (20 weeks old) were divided randomly into 4 groups. 1) SHR sedentary 2) SHR ST 36 degrees 3) SHR ST 26 degrees 4) SHR ST 36 degrees + atenolol (50 mg/kg/die). ST was performed 2 X 90 min/day for 31 days and then reduced to 2 X 60 min/day. After 7 weeks of ST BP was lower in all ST groups compared with SHR sedentary (p less than 0.001). BP was higher in ST 26 degrees than in ST 36 degrees (p less than 0.05). No additional effect of atenolol on BP was observed. The increase in the degree of LV hypertrophy during ST (ST 36 degrees: +15%; ST 26 degrees: +26%) could be prevented by atenolol (ST 36 degrees + atenolol: -1.5%). ST 36 degrees led to improved ventricular and myocardial performance with decreased LV wall stress ("luxury hypertrophy"), while in ST 26 degrees ventricular dilatation occurred with increased systolic wall stress and elevated LVEDP. It was uncertain whether this should be interpreted as a state of LV pre-insufficiency in ST 26 degrees in spite of no indications of impaired myocardial contractile capability. Peripheral vascular resistance (PVR) was significantly reduced by ST. The reduction was more evident in ST 26 degrees, but was partially compensated for by an increased cardiac output. The weights of adrenal glands increased (p less than 0.001), most markedly for ST 26 degrees. The level of thyroid hormones (T3 and fT3) was increased in ST 26 degrees. In summary, ST proved to be effective in lowering BP of SHR. WT had great influence with respect to cardiovascular adaptation and mechanisms involved in ST of SHR. Cardioadrenergic drive was of great significance for the process of hypertrophy during ST in SHR.
在先前的研究中，将自发性高血压大鼠（SHR）在36摄氏度水温（WT）下进行游泳训练（ST）可导致血压（BP）下降。在人类高血压中尚未描述过ST的类似效果。我们的目的是研究WT对这种训练效果的影响、ST对左心室肥厚的影响以及肾上腺素能刺激在其中的作用。将20周龄的雄性SHR随机分为4组。1）SHR静息组 2）SHR 36摄氏度ST组 3）SHR 26摄氏度ST组 4）SHR 36摄氏度ST +阿替洛尔（50毫克/千克/天）组。ST每天进行2次，每次90分钟，共31天，然后减至每天2次，每次60分钟。ST 7周后，所有ST组的BP均低于SHR静息组（p < 0.001）。26摄氏度ST组的BP高于36摄氏度ST组（p < 0.05）。未观察到阿替洛尔对BP的额外影响。阿替洛尔可预防ST期间左心室肥厚程度的增加（36摄氏度ST组：+15%；26摄氏度ST组：+26%）（36摄氏度ST +阿替洛尔组：-1.5%）。36摄氏度ST可改善心室和心肌功能，降低左心室壁应力（“奢侈性肥厚”），而26摄氏度ST则出现心室扩张，收缩期壁应力增加，左心室舒张末期压力升高。尽管没有心肌收缩能力受损的迹象，但尚不确定这是否应被解释为26摄氏度ST时左心室预功能不全的状态。ST可显著降低外周血管阻力（PVR）。26摄氏度ST组的降低更为明显，但部分被心输出量增加所代偿。肾上腺重量增加（p < 0.001），26摄氏度ST组最为明显。26摄氏度ST组甲状腺激素（T3和游离T3）水平升高。总之，ST被证明对降低SHR的BP有效。WT对SHR的心血管适应及ST涉及的机制有很大影响。心脏肾上腺素能驱动对SHR在ST期间的肥厚过程具有重要意义。
