Baujard C, Ponchon P, Elghozi J L
Laboratoire de Pharmacologie, CNRS URA 1482, Faculté de Médecine Necker-EM, Paris, France.
Fundam Clin Pharmacol. 1996;10(6):511-7. doi: 10.1111/j.1472-8206.1996.tb00608.x.
A controlled graded bleeding was performed in conscious rats with 15 min intervals between two withdrawals, in order to induce a 25% blood loss without hypotension. Heart rate (HR) was unaffected as well. The spectral profiles of systolic blood pressure (SBP) analyzed on 51.2 s segments exhibited increases in the high frequency (HR, respiratory) component. This increase paralleled the blood loss with a rise ranging from 20% for a 1 mL/kg hemorrhage to 90% for a 11 mL/kg removal. These changes were associated with increases in the mid-frequency (MF, Mayer waves) component of SBP variability. These latter rises were between 30 and 40% of the control value. Breathing frequency (BF) and blood gases were unaltered following hemorrhage. A shift of fluid occurred during the 3 h session as reflected by the significant hemodilution. Rats were also bled after pretreatment with prazosin (1 mg/kg) or with an association of prazosin (1 mg/kg) and losartan (10 mg/kg). These treatments increased HR. A marked fall in SBP occurred with the double blockade. Hemorrhage determined a relative bradycardia together with the SBP decrease (reversible shock) after prazosin and losartan treatment. Prazosin determined opposite changes in MF (-33%) and HF (+58%) SBP components. A further decrease in the MF SBP component was observed following the double blockade. Spectral profiles following hemorrhage were unchanged compared to the prehemorrhage blocked levels. Therefore graded nonhypotensive, ie, normotensive hemorrhage in rats, was associated with progressive increases in the respiratory SBP variations, estimated from the SBP spectrum. This sensitive index could reflect the low preload state due to hypovolemia. The hemorrhage-induced MF SBP component increase could reflect an increased sympathetic vasomotor drive, prevented with prazosin, as a reflex adjustment to hypovolemia. Renin activation could also contribute to the genesis of MF waves and its role in maintaining BP following hemorrhage was exemplified with alpha 1-adrenoceptor blockade.
对清醒大鼠进行控制性分级放血，两次放血间隔15分钟，以诱导25%的失血且不出现低血压。心率（HR）也未受影响。对51.2秒时间段分析的收缩压（SBP）频谱图显示高频（HR、呼吸）成分增加。这种增加与失血量平行，从1 mL/kg出血时的20%上升到11 mL/kg放血时的90%。这些变化与SBP变异性的中频（MF，迈尔波）成分增加有关。后者的上升幅度为对照值的30%至40%。出血后呼吸频率（BF）和血气未改变。在3小时的实验过程中发生了液体转移，表现为明显的血液稀释。大鼠在预先用哌唑嗪（1 mg/kg）或哌唑嗪（1 mg/kg）与氯沙坦（10 mg/kg）联合预处理后也进行了放血。这些处理使HR增加。双重阻断时SBP显著下降。出血导致哌唑嗪和氯沙坦治疗后出现相对心动过缓以及SBP下降（可逆性休克）。哌唑嗪使MF（-33%）和HF（+58%）SBP成分发生相反变化。双重阻断后观察到MF SBP成分进一步下降。出血后的频谱图与出血前阻断水平相比无变化。因此，大鼠分级非低血压性，即正常血压性出血，与根据SBP频谱估计的呼吸性SBP变化逐渐增加有关。这个敏感指标可以反映由于血容量不足导致的低前负荷状态。出血诱导的MF SBP成分增加可能反映了交感血管运动驱动增加，哌唑嗪可预防这种增加，这是对血容量不足的一种反射性调节。肾素激活也可能促成MF波的产生，α1肾上腺素能受体阻断证明了其在出血后维持血压中的作用。
