Martin C E, Shaver J A, Leon D F, Thompson M E, Reddy P S, Leonard J J
J Clin Invest. 1974 Jul;54(1):104-15. doi: 10.1172/JCI107731.
Selective autonomic blockade with intravenous propranolol, practolol, atropine, and combined atropine-propranolol was utilized to elucidate the role of the autonomic nervous system in the hemodynamic responses in young adult male volunteers to handgrip sustained at 30% of maximal voluntary contraction for 3 min. The initial 30 s of the tachycardia response was found to be mediated by withdrawal of vagal dominance, as evidenced by blockade of this response by prior atropinization. The mid and late portion of the heart rate response curve was demonstrated to be sympathetic in origin, since it was unaffected by atropine, but was suppressed by combined atropine-propranolol blockade. Sympathetic stimulation appears to be a secondary mechanism for increasing the heart rate, however, as it becomes operative only after the first mechanism of vagal withdrawal has been utilized. This was confirmed by the finding that beta adrenergic receptor blockade alone had little effect on the heart rate response curve. The pressor response to handgrip was accompanied by increased cardiac output and no change in calculated systemic vascular resistance. After propranolol, handgrip resulted in increased peripheral resistance and an equivalent rise in arterial pressure, but no increase in cardiac output. It was concluded that the increase in resistance was the result of sympathetically induced vasoconstriction. This response was shown to be independent of peripheral beta adrenergic receptor blockade by the use of practolol, a cardio-selective beta adrenergic receptor-blocking drug which caused identical hemodynamic responses to those observed after propranolol. Left ventricular ejection time (corrected for heart rate) was prolonged by handgrip. The increased afterload imposed on the left ventricle by sustained handgrip may explain the prolongation of ejection time index. Preejection period was prolonged by SHG after propranolol and shortened after atropine. In addition to confirming the previously defined role of the parasympathetic nervous system, this study delineates the role of the sympathetic nervous system in the heart rate and pressor responses to sustained handgrip.
采用静脉注射普萘洛尔、心得宁、阿托品以及阿托品 - 普萘洛尔联合用药进行选择性自主神经阻滞，以阐明自主神经系统在年轻成年男性志愿者对持续3分钟、强度为最大自主收缩30%的握力试验的血流动力学反应中的作用。心动过速反应的最初30秒被发现是由迷走神经优势的撤离介导的，预先使用阿托品阻断该反应就证明了这一点。心率反应曲线的中晚期被证明起源于交感神经，因为它不受阿托品影响，但被阿托品 - 普萘洛尔联合阻滞所抑制。然而，交感神经刺激似乎是增加心率的次要机制，因为它仅在迷走神经撤离的第一种机制被利用之后才起作用。单独使用β肾上腺素能受体阻滞剂对心率反应曲线几乎没有影响这一发现证实了这一点。对握力的升压反应伴随着心输出量增加，而计算出的全身血管阻力没有变化。使用普萘洛尔后，握力导致外周阻力增加和动脉压同等升高，但心输出量没有增加。得出的结论是，阻力增加是交感神经诱导的血管收缩的结果。使用心得宁（一种心脏选择性β肾上腺素能受体阻断药物，其引起的血流动力学反应与普萘洛尔后观察到的相同）表明，这种反应与外周β肾上腺素能受体阻断无关。握力使左心室射血时间（经心率校正）延长。持续握力对左心室施加的后负荷增加可能解释了射血时间指数的延长。使用普萘洛尔后，握力使射血前期延长，使用阿托品后缩短。除了证实先前确定的副交感神经系统的作用外，本研究还描述了交感神经系统在对持续握力的心率和升压反应中的作用。
