Pries Axel R, Reglin Bettina, Secomb Timothy W
Dept. of Physiology and CCR, Charité, Berlin.
Int J Dev Biol. 2011;55(4-5):399-405. doi: 10.1387/ijdb.103218ap.
Vascular beds are generated by vasculogenesis and sprouting angiogenesis, and these processes have strong stochastic components. As a result, vascular patterns exhibit significant heterogeneity with respect to the topological arrangement of the individual vessel segments and the characteristics (length, number of segments) of different arterio-venous pathways. This structural heterogeneity tends to cause heterogeneous distributions of flow and oxygen availability in tissue. However, these quantities must be maintained within tolerable ranges to allow normal tissue function. This is achieved largely through adjustment of vascular flow resistance by control of vessel diameters. While short-term diameter control by changes in vascular tone in arterioles and small arteries plays an important role, in the long term an even more important role is played by structural adaptation (angioadaptation), occurring in response to metabolic and hemodynamic signals. The effectiveness, stability and robustness of this angioadaptation depend sensitively on the nature and strength of the vascular responses involved and their interactions with the network structure. Mathematical models are helpful in understanding these complex interactions, and can be used to simulate the consequences of failures in sensing or signal transmission mechanisms. For the tumor microcirculation, this strategy of combining experimental observations with theoretical models, has led to the hypothesis that dysfunctional information transport via vascular connexins is a major cause of the observed vascular pathology and increased heterogeneity in oxygen distribution.
血管床由血管生成和芽生血管生成产生,并且这些过程具有很强的随机成分。因此,血管模式在各个血管段的拓扑排列以及不同动静脉通路的特征(长度、段数)方面表现出显著的异质性。这种结构异质性往往会导致组织中血流和氧供应的异质性分布。然而,这些量必须维持在可容忍的范围内,以保证正常的组织功能。这在很大程度上是通过控制血管直径来调节血管流动阻力来实现的。虽然小动脉和小动脉中血管张力变化引起的短期直径控制起着重要作用,但从长期来看,对代谢和血流动力学信号作出反应的结构适应性变化(血管适应性变化)起着更重要的作用。这种血管适应性变化的有效性、稳定性和稳健性敏感地取决于所涉及的血管反应的性质和强度及其与网络结构的相互作用。数学模型有助于理解这些复杂的相互作用,并可用于模拟传感或信号传输机制故障的后果。对于肿瘤微循环,这种将实验观察与理论模型相结合的策略,导致了这样一种假说,即通过血管连接蛋白的功能失调的信息传递是观察到的血管病理和氧分布异质性增加的主要原因。