1046 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



found that linoleic acid-1-C 14 incorporated in dietary 

 triglycerides, or fed as free acid, becomes esterified 

 with the same classes of lipids in human thoracic 

 duct lymph as oleic and palmitic acid. Evidently, 

 digestion and absorption of these fatty acids are com- 

 parable, as well as their transfer into intestinal 

 mucosa and resynthesis in lymph lipids. This is in 

 confirmation of work on animals by the same group. 

 They also confirmed earlier findings on animals that 

 stearic acid-1-C 14 was found in a higher percentage 

 incorporated in lymph phospholipids than was 

 found for linoleic acid and for palmitic and oleic 

 acids. After isolation of lymph lecithins, there was a 

 difference in the position of the label in lecithins of 

 lymph according to the fatty acid used. After feeding 

 linoleic acid-i-C 14 , approximately 75 per cent of the 

 label in lymph lecithins was localized in the alpha- 

 position. With stearic acid-i-C 14 , however, about 80 

 per cent of the label was found in the beta-positions. 

 Their evidence indicates that there is a distinct 

 manner in which stearic acid-i-C 14 and linoleic 

 acid- 1 -C 14 are incorporated into thoracic duct lymph 

 lecithins, reflecting probable differences in their 

 metabolism. 



Rampone (178) recently reported experiments in 

 which he measured phospholipids of lymph in rela- 

 tion to the total lipid in 16 dogs with chronic thoracic 

 duct fistula during the postabsorptive state and fol- 

 lowing the administration of various lipid types 

 (triolein, soya lecithin, oleic acid, etc.) in the diet. 

 He found that phospholipid transport related linearly 

 to total lipid transport under all conditions studied, 

 including the postabsorptive state. The percentage 

 of lymph lipid transported as phospholipid ranged 

 from 3 to 18 per cent and was independent of the 

 type of lipid led. Depriving the animals of phospho- 

 lipid precursors in the diet for as long as 90 days 

 previously failed to alter this relationship or the total 

 quantity of lipid transported. Since the phospholipids 

 increased linearly with the total lipid under all condi- 

 tions studied, Rampone believes it likely that the 

 phospholipids associate with the absorbed lipid in 

 some manner which relates to lipid transport, possibly 

 serving in the capacity of chylomicron emulsion 

 stabilizers during the transport phase. He points 

 out that while the plasma may be the source of the 

 phospholipids, the rate of filtration from plasma to 

 lymph would be somehow dependent on the lipid 

 concentration in lymph, since the phospholipids of 

 lymph increased in proportion to the total lymph. 

 Previous work by Bollman et al. (26) suggests that 

 the mucosa of the small intestine mav normally be 



the source of phospholipids for plasma during fat 

 absorption. 



An interesting application of the study of lymph 

 and its possible role in the pathogenesis of athero- 

 sclerosis was reported by Kellnor (1 1 1). He collected 

 leg lymph from rabbits rendered hyperlipemic by 

 cholesterol feeding, by the injection of the surface- 

 active agent Triton A-20, and by the injection of 

 alloxan. He found (as have others) that leg lymph 

 contained protein in a concentration equal to one- 

 third to one-half that of the blood serum. Electro- 

 phoretic analyses showed a pattern similar to that 

 of serum. The total lipid concentration was also about 

 one-third to one-half that of blood serum and the 

 major lipid fractions, cholesterol and phospholipid, 

 were present in lymph in about the same relation- 

 ship. In the cholesterol-fed rabbits, the leg lymph 

 showed a striking increase in lipids as did the serum. 

 On the basis of his results he concluded that: "It 

 seems likely that under normal conditions there is a 

 constant flow of fluid containing various serum lipids 

 and proteins across the endothelium into the walls 

 of blood vessels; this material normally passes through 

 the wall and is completely removed by way of vasa 

 vasorum and lymphatics. In certain conditions, how- 

 ever, where there are increased amounts of lipid in 

 the blood, or where there are excessive quantities of 

 certain types of lipids (beta-lipoproteins of the Sf 12- 

 20 molecules of Gofman), the removal of these 

 particles from the wall of the vessel is incomplete and 

 some remain behind to initiate the process of athero- 

 sclerosis. In hypertension, the increased hydrostatic 

 pressure appears to cause an increase in the quantity 

 of serum lipoprotein that diffuses across the vessel 

 wall, thereby increasing the possibility for incomplete 

 removal and hence for deposition of lipids. In those 

 areas of the vascular tree where the removal mech- 

 anism has been altered, as for example in syphilitic 

 aortitis or in experimentally produced trauma to the 

 vessel wall, the free transport of lipid and other 

 particles across the vessel wall is impeded, and in 

 these areas the lipid is therefore more apt to pre- 

 cipitate and to give rise to atherosclerosis. In this 

 theoretical formulation of the pathogenesis of athero- 

 sclerosis, the artery wall is regarded as an organ which 

 is constantly bathed by a serum transudate containing, 

 among other things, various serum lipoproteins, most 

 of which pass on through, some of which doubtless 

 are metabolized locally, and a few of which remain 

 behind to cause mischief. Atherosclerosis, broadly 

 considered, may thus result either from qualitative 

 or quantitative changes in the serum lipoproteins 



