Mariano D J, Schomer S J, Rea R F
Department of Medicine, University of Iowa, Iowa City 52242.
J Am Coll Cardiol. 1992 Nov 15;20(6):1411-6. doi: 10.1016/0735-1097(92)90256-m.
The purpose of the present study was to test the hypothesis that intravenous quinidine, unlike procainamide, causes direct vasodilation and reflexly mediated increases in sympathetic nerve activity.
Intravenous quinidine can cause significant hypotension. Animal experiments have suggested that quinidine blocks alpha-receptors and also relaxes vascular smooth muscle by a nonadrenergic mechanism. In a recent study we showed that intravenous procainamide causes peripheral vasodilation, hypotension and inhibition of sympathetic nerve activity in humans. Intraarterial procainamide, however, did not cause vasodilation.
Postganglionic muscle sympathetic nerve traffic was recorded from the peroneal nerve at the fibular head with tungsten microelectrodes, and forearm blood flow was measured with venous occlusion plethysmography. Central venous pressure was measured directly. The direct effects of quinidine on vascular resistance were determined with brachial artery quinidine infusions and measurement of ipsilateral forearm blood flow.
In eight normal subjects intravenous quinidine (8 mg/kg body weight infused for 27 min) decreased mean arterial pressure from 87 +/- 3 (mean +/- SE) to 83 +/- 3 mm Hg, central venous pressure from 6.3 +/- 0.6 to 5.0 +/- 0.7 mm Hg and forearm vascular resistance from 32.2 +/- 5.5 to 25.3 +/- 4.7 U (all p < 0.05). Heart rate increased from 67 +/- 4 to 77 +/- 5 beats/min and muscle sympathetic nerve activity from 288 +/- 70 to 660 +/- 151 U/min (both p < 0.05). In five subjects intravenous nitroprusside that caused similar hemodynamic effects produced similar increases in sympathetic nerve activity. In eight subjects graded infusions of quinidine into the brachial artery (0.37, 0.74 and 1.48 mg/min) produced dose-dependent decreases in ipsilateral forearm vascular resistance and marked attenuation of forearm vasoconstriction caused by the cold pressor test.
These data show that quinidine, unlike procainamide, causes vasodilation directly and, when given intravenously, is associated with baroreflex-mediated increases in sympathetic nerve activity.
本研究的目的是验证以下假设，即静脉注射奎尼丁与普鲁卡因胺不同，会引起直接血管舒张以及反射介导的交感神经活动增加。
静脉注射奎尼丁可导致显著低血压。动物实验表明，奎尼丁可阻断α受体，并通过非肾上腺素能机制舒张血管平滑肌。在最近一项研究中，我们发现静脉注射普鲁卡因胺可导致人体外周血管舒张、低血压以及交感神经活动受到抑制。然而，动脉内注射普鲁卡因胺并不会引起血管舒张。
使用钨微电极在腓骨头处记录腓总神经节后肌肉交感神经冲动，并用静脉阻断体积描记法测量前臂血流量。直接测量中心静脉压。通过肱动脉输注奎尼丁并测量同侧前臂血流量来确定奎尼丁对血管阻力的直接影响。
在8名正常受试者中，静脉注射奎尼丁（按体重8mg/kg输注27分钟）使平均动脉压从87±3（平均值±标准误）降至83±3mmHg，中心静脉压从6.3±0.6降至5.0±0.7mmHg，前臂血管阻力从32.2±5.5降至25.3±4.7U（均p<0.05）。心率从67±4增加至77±5次/分钟，肌肉交感神经活动从288±70增加至660±151U/分钟（均p<0.05）。在5名受试者中，静脉注射产生类似血流动力学效应的硝普钠也使交感神经活动出现类似增加。在8名受试者中，向肱动脉分级输注奎尼丁（0.37、0.74和1.48mg/分钟）导致同侧前臂血管阻力呈剂量依赖性降低，并显著减弱冷加压试验引起的前臂血管收缩。
这些数据表明，与普鲁卡因胺不同，奎尼丁可直接引起血管舒张，静脉注射时会伴有压力感受器介导的交感神经活动增加。
