ABSTRACT
Since the laticiferous system of Hevea brasiliensis is anastomosed, the opening of a number of laticiferous tubes by tapping could trigger latex flow lasting a relatively indefinite period of time if latex did not possess its own "antihemorrhagic" mechanism. The same kind of reasoning led Hanower to investigate the role of oxygen in the stopping of latex flow precisely at the open ends of latex tubes only. The phenomenon was thought First to promote latex flow and then to impeded flow when the latex vessels collapse under the turgor pressure of parenchyma cells. The breakdown of lutoids during or after tapping may liberate some hydrolytic enzymes able to attack the phospholipoprotein films which protect the stability of rubber particles. The fragility of lutoid membranes may be one of the prime factors in the destabilization of rubber particles when they are subjected to substantial mechanical stress. However, most research has been on the coagulation mechanisms of latex in vitro.
