Vajda Z, Pedersen M, Dóczi T, Sulyok E, Stødkilde-Jørgensen H, Frøkiaer J, Nielsen S
The Water and Salt Research Center, Institute of Anatomy, University of Aarhus, Denmark.
Neurosurgery. 2001 Sep;49(3):697-704; discussion 704-5. doi: 10.1097/00006123-200109000-00031.
Centrally released arginine vasopressin (AVP) and atrial natriuretic peptide (ANP) have been shown to participate in brain volume regulation. The aim of the present study was to evaluate the effects of centrally administered AVP and ANP on the time course of development of brain edema in vivo in hyponatremic rats, using diffusion-weighted magnetic resonance imaging.
We performed intracerebroventricular (ICV) administration of 120 microg AVP, 20 microg ANP, or physiological saline into the right lateral ventricle in 18 rats. Twenty-five minutes after the treatment, we induced systemic hyponatremia by the intraperitoneal administration of 140 mmol/L dextrose solution. Serial diffusion-weighted imaging scans were obtained up to 96 minutes after the start of the hyponatremia. Changes in the brain extra-to intracellular volume fraction ratio were estimated as changes in the apparent diffusion coefficient (ADC).
No change in the ADC was observed after the ICV injection of saline or AVP. The onset of hyponatremia induced a rapid and marked ADC reduction in both groups, indicating an increased intracellular space. However, the ADC decrease became significantly more pronounced in the ICV AVP group (83.3+/-4.7% of baseline level, mean +/- standard deviation) than in the saline group (93.7+/-3.3% of baseline, P < 0.001) after 78 minutes of hyponatremia. The ICV injection of ANP induced a prompt ADC increase to 111.5+/-10.0% (P < 0.05) of the baseline level, indicating a rapid reduction in the intracellular compartment. In the initial phase of hyponatremia, the ADC values in the ANP group were consistently higher than those in the saline group, decreasing finally to 86.9+/-9.6% after 96 minutes of hyponatremia.
Our findings demonstrate the opposite effects of AVP and ANP on the intracellular volume fraction of the brain during the development of cellular brain edema, with an immediate effect on ANP and a delayed effect on AVP. The results emphasize the direct effects of these hormones on the cellular volume regulatory mechanisms in the brain during the development of cerebral edema.
中枢释放的精氨酸血管加压素(AVP)和心房利钠肽(ANP)已被证明参与脑容量调节。本研究的目的是使用扩散加权磁共振成像评估中枢给予AVP和ANP对低钠血症大鼠体内脑水肿发展时间进程的影响。
我们对18只大鼠的右侧脑室进行脑室内(ICV)注射120微克AVP、20微克ANP或生理盐水。治疗25分钟后,通过腹腔注射140毫摩尔/升葡萄糖溶液诱导全身性低钠血症。在低钠血症开始后长达96分钟内进行系列扩散加权成像扫描。脑细胞外与细胞内体积分数比的变化通过表观扩散系数(ADC)的变化来估计。
ICV注射生理盐水或AVP后,未观察到ADC有变化。低钠血症的发生导致两组的ADC迅速且显著降低,表明细胞内空间增加。然而,在低钠血症78分钟后,ICV注射AVP组的ADC降低比生理盐水组(基线水平的93.7±3.3%)更明显(基线水平的83.3±4.7%,平均值±标准差,P<0.001)。ICV注射ANP导致ADC迅速增加至基线水平的111.5±10.0%(P<0.05),表明细胞内区室迅速减少。在低钠血症的初始阶段,ANP组的ADC值始终高于生理盐水组,在低钠血症96分钟后最终降至86.9±9.6%。
我们的研究结果表明,在细胞性脑水肿发展过程中,AVP和ANP对脑内细胞内体积分数有相反的影响,ANP有即时作用,AVP有延迟作用。结果强调了这些激素在脑水肿发展过程中对脑细胞体积调节机制的直接作用。