Levine D N
Department of Neurology, NYU Medical Center, 400 E. 34th St., New York, New York, 10016, USA.
Microvasc Res. 1998 Nov;56(3):154-65. doi: 10.1006/mvre.1998.2098.
The classical theory of spontaneous pulsation of the retinal veins is that during systole intraocular pressure exceeds venous pressure, causing the veins to collapse. We show that this theory is internally inconsistent and not in accord with experimental data. It is inconsistent in assuming both (a) that oscillations of intraocular pressure (IOP) occur because the veins cannot immediately discharge the systolic arterial inflow and (b) that retinal venous pressure (RVP) can fluctuate independently of IOP during the cardiac cycle. It is not in accord with experimental data, which shows that RVP always exceeds IOP and that fluctuations in the latter are instantly transmitted to the former. We present an alternative theory that does not have these problems. We assume the following. (1) Inflow to the retinal venous tree from the capillaries is constant, the pulsatile arterial flow having been completely damped by the arterioles and capillaries. (2) Outflow from the central retinal vein (CRV) varies during the cardiac cycle because oscillations of IOP, transmitted to the intraocular CRV, are of greater amplitude than oscillations in cerebrospinal fluid pressure, transmitted to the extraocular CRV. By showing that the radial blood flow distending the veins obeys a diffusion equation and by employing an "equivalent cylinder" analysis of the branched venous tree to simplify the boundary conditions, we demonstrate that, with the above assumptions and the additional assumption of low amplitude of radial flow, the CRV will pulsate, and the pulsations will remain confined to a small segment near the exit point. The proposed theory can explain disappearance of pulsation with intracranial hypertension, intensification of pulsation in glaucoma, and variability in the linear extent and amplitude of pulsation among normal individuals. The theory may also be applied to other venous pulsations, such as the respiratory pulsation of the terminal portions of large veins entering the thorax or the cardiac cycle pulsation of the superior vena cava.
视网膜静脉自发性搏动的经典理论认为，在心脏收缩期，眼内压超过静脉压，导致静脉塌陷。我们发现该理论内部存在矛盾，且与实验数据不符。其矛盾之处在于，它同时假设：（a）眼内压（IOP）的波动是因为静脉无法立即排出心脏收缩期的动脉流入血量；（b）在心动周期中，视网膜静脉压（RVP）可独立于IOP波动。它也与实验数据不符，实验数据表明RVP总是超过IOP，且IOP的波动会立即传递给RVP。我们提出了一种不存在这些问题的替代理论。我们做如下假设：（1）从毛细血管流入视网膜静脉树的血流量是恒定的，搏动性动脉血流已被小动脉和毛细血管完全缓冲。（2）视网膜中央静脉（CRV）的流出量在心动周期中会发生变化，因为传递到眼内CRV的IOP波动幅度大于传递到眼外CRV的脑脊液压力波动幅度。通过证明使静脉扩张的径向血流服从扩散方程，并采用对分支静脉树的“等效圆柱体”分析来简化边界条件，我们证明，基于上述假设以及径向血流低幅度的额外假设，CRV会发生搏动，且搏动将局限于出口点附近的一小段区域。所提出的理论可以解释颅内高压时搏动消失、青光眼时搏动增强以及正常个体之间搏动的线性范围和幅度变化。该理论也可应用于其他静脉搏动，如进入胸腔的大静脉末端部分的呼吸搏动或上腔静脉的心动周期搏动。
