Manyari D E, Rose S, Tyberg J V, Sheldon R S
Cardiovascular Research Group, University of Calgary, Alberta, Canada.
J Am Coll Cardiol. 1996 Jun;27(7):1730-5. doi: 10.1016/0735-1097(96)00051-4.
We sought to compare the forearm reflex venous response to mental arithmetic stress in patients with neuromediated syncope and in normal subjects.
Patients with neuromediated syncope have a paradoxic arterial vasodilation in response to stressors that usually provoke vasoconstriction. Given the postulated role of diminished preload in provoking the reflex responses resulting in syncope, we hypothesized that mental stress might provoke paradoxic reflex venodilation in patients with neuromediated syncope.
Twelve normal subjects (mean age [+/-SD] 47 +/- 9 years) and 27 patients with neuromediated syncope (mean age 42 +/- 13 years) were studied before and during a mental arithmetic stress test. Forearm venous pressure-volume relations were determined by using radionuclide plethysmography.
During mental arithmetic stress, heart rate and systolic and diastolic blood pressure increased significantly and similarly both in normal subjects and in patients with neuromediated syncope. The heart rate and blood pressure changes were qualitatively similar in both groups. However, with mental arithmetic stress, forearm venoconstriction of 13 +/- 2% (mean +/- SEM) was noted in normal subjects (p < 0.001) but not in patients with neuromediated syncope (mean 2%, p = NS). This group response of patients with neuromediated syncope did not result from a lack of individual responses but occurred because these patients had a wide range of responses. The normal physiologic and methodologic variability of the method was +/- 4%. Thirteen of the 27 patients with neuromediated syncope had forearm venoconstriction of 14.5 +/- 6.8% during mental arithmetic stress, whereas 7 had paradoxic forearm venodilation of 14.6 +/- 8.8%, and 7 were considered nonresponders (-1.3 +/- 3.4%). Thus, 14 (52%) of the 27 patients with syncope did not have normal vasoconstriction in response to mental stress.
Patients with neuromediated syncope have an abnormal range of forearm venomotor responses to mental arithmetic stress. Reflex control of the veins may play an important role in the pathogenesis of neuromediated syncope.
我们试图比较神经介导性晕厥患者与正常受试者在进行心算应激时前臂反射性静脉反应。
神经介导性晕厥患者在面对通常会引起血管收缩的应激源时会出现反常的动脉血管扩张。鉴于预负荷降低在引发导致晕厥的反射反应中所假定的作用，我们假设精神应激可能会在神经介导性晕厥患者中引发反常的反射性静脉扩张。
对12名正常受试者（平均年龄[±标准差]47±9岁）和27名神经介导性晕厥患者（平均年龄42±13岁）在心算应激测试前及测试期间进行研究。使用放射性核素体积描记法测定前臂静脉压力-容积关系。
在心算应激期间，正常受试者和神经介导性晕厥患者的心率、收缩压和舒张压均显著且相似地升高。两组的心率和血压变化在性质上相似。然而，在心算应激时，正常受试者出现了13±2%（平均值±标准误）的前臂静脉收缩（p<0.001），而神经介导性晕厥患者未出现（平均值为2%，p=无显著性差异）。神经介导性晕厥患者的这种群体反应并非由于个体无反应，而是因为这些患者的反应范围广泛。该方法正常的生理和方法学变异性为±4%。27名神经介导性晕厥患者中有13名在心算应激期间出现了14.5±6.8%的前臂静脉收缩，7名出现了14.6±8.8%的反常前臂静脉扩张，7名被视为无反应者（-1.3±- 3.4%）。因此，27名晕厥患者中有14名（52%）在面对精神应激时未出现正常的血管收缩。
神经介导性晕厥患者在面对心算应激时前臂静脉运动反应范围异常。静脉的反射性控制可能在神经介导性晕厥的发病机制中起重要作用。
