Acute Lymphangitis of Plethora in Horse. 541 



especially of the lower part which is permanently swollen, are 

 enormously increased in calibre (lymphangiectasia), and have 

 their walls correspondingly thickened. The connective tissue is 

 the seat of extensive fibrous hyperplasia, and its interstices are 

 greatly enlarged. 



Causes. Nature. This disease has not been sufficiently studied 

 to ascertain what toxic agents are produced in the plethoric con- 

 dition, under the torpid processes of nutrition and sanguification 

 entailed by absolute compulsory rest. A consideration, however, 

 of the relations of the lymph and lymph vessels and glands to 

 other parts will in part explain the pathology of the maladyv 

 The lymphatics take their origin in the nuclear spaces of the 

 various tissues, the anastomosing canals of such pericellular 

 spaces together with the latter forming the actual radicles of this 

 set of vessels. They receive, therefore, the surplus plasma 

 which is not used up by the tissue cells in performing their 

 trophic, secretory and other functions. This lymph carried on 

 by the vis a tergo, muscular compression and other movements, 

 is delayed in the adenoid tissue known as lymph nodes, and espec- 

 ially in the lymph glands, in which the proliferation of Ivmph 

 cells is mainly carried on. Thus the lymph cells are very scarce 

 in the lymph radicles of the connective and other tissues, and are 

 found in greater numbers after passing through the lymph nodes, 

 and in still greater after passing through the lymph glands. But 

 the increase of cells is also in inverse ratio with the rapidity of 

 the circulation of the lymph. When this is rapid the cells are 

 hurried on and there is little time for their reproduction. When 

 slow, on the other hand, there is time for cell growth and division 

 in the glandular detention cavities, and the ratio of cells to the 

 plasma is materially increased. Consider next that the multi- 

 plicity of cells determines an increase of the fibrine factors, so 

 that the more cells the lymph contains the more material there is 

 for fibrine (I,andois), and we have one good reason why under 

 enforced rest the overcharged and congested gland may become 

 the seat of fibrinous coagula or lymphatic embolism. Any over- 

 distension, toxic element or other cause of disturbance, which 

 deranges the functions of the cell or causes its rapid multiplica- 

 tion by division — as in inflammation — at once sets free the fibrine 

 ferment and determines the coagulation. In the disease before 



