Bjurstedt H, Rosenhamer G, Tydén G
Acta Physiol Scand. 1977 Mar;99(3):353-60. doi: 10.1111/j.1748-1716.1977.tb10388.x.
Heart rate, arterial pressure and cardiac output were recorded in eight healthy male volunteers during exposure to 80 mmHg of lower body negative pressure (LBNP) in the supine position before and after beta-adrenergic and combined beta-adrenergic and parasympathetic blockade of the heart as induced by the i.v. administration of propranolol 0.25 mg/kg b.wt. and atropine 0.04 mg/kg b.wt. After propranolol, heart rate response to LBNP averaged 48% of that observed without blockade indicating that LBNP-induced cardioacceleration is of both sympathetic and parasympathetic origin. Tolerance to LBNP was reduced by beta-adrenergic blockade, since the decrease in mean arterial pressure during LBNP was exaggerated by such blockade. Although the addition of atropine markedly elevated mean arterial pressure and cardiac output in the control situation, tolerance to LBNP was not enhanced by this drug as judged from the arterial pressure response. Post-LBNP overshoot in mean arterial pressure was strikingly augmented by combined cardiac effector blockade and was in part due to a lingering elevation of total peripheral resistance, cardiac output remaining decreased for more than 110 s after release of LBNP.
在八名健康男性志愿者仰卧位接受80 mmHg下肢负压(LBNP)时,记录其心率、动脉压和心输出量,实验在静脉注射0.25 mg/kg体重的普萘洛尔和0.04 mg/kg体重的阿托品诱导心脏β-肾上腺素能以及联合β-肾上腺素能和副交感神经阻滞之前和之后进行。注射普萘洛尔后,对LBNP的心率反应平均为未阻滞时观察到的48%,这表明LBNP诱导的心动加速源于交感神经和副交感神经。β-肾上腺素能阻滞降低了对LBNP的耐受性,因为这种阻滞会夸大LBNP期间平均动脉压的下降。尽管在对照情况下添加阿托品会显著提高平均动脉压和心输出量,但从动脉压反应判断,该药物并未增强对LBNP的耐受性。联合心脏效应器阻滞显著增强了LBNP后平均动脉压的过冲,部分原因是总外周阻力持续升高,LBNP解除后心输出量持续下降超过110秒。