1268 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



stances where arteriovenous connections develop in 

 newly formed circulations, as in the rabbit ear 

 chamber (36). It is of interest that such arteriovenous 

 shunts are normally present in the rabbit's ear (34). 



Some Effects of Collateral Circulation 



Blood supply arriving of necessity by way of col- 

 lateral routes is usually not so efficient as the original 

 in maintaining full function. Rarely it may exceed 

 the needs of the tissue, as in association with large 

 peripheral arteriovenous fistulas, and in the lungs, as 

 has been described. In the latter, however, it never- 

 theless falls short of normal pulmonary perfusion 

 that is carried on in the service of the body as a 

 whole. 



Certain special effects of collateral circulation 

 occur under pathological circumstances, but these 

 can only be mentioned in passing. Thus, in the lung, 

 the seat of severe fibrosing disease such as bronchi- 

 ectasis, where large precapillary anastomoses are 

 formed between bronchial and pulmonary arteries, 

 the higher pressure in the former tends to shunt the 

 pulmonary arterial blood into normal tissue where 

 oxygenation can occur. Consequently, there may be 

 no peripheral arterial desaturation. When suffi- 

 ciently numerous, these connections may contribute 

 to an increased resistance to the output of the right 

 ventricle. Reverse flow in pulmonary arteries from 

 the periphery via these anastomoses has also been 

 demonstrated, by analysis of gases in blood drawn 

 from catheters placed within such arteries, and by 

 angiography (103), and most convincingly by 

 aortography (3). In the last mentioned a radiopaque 

 substance introduced above the origins of the bron- 

 chial vessels has been shown to fill the pulmonary 

 arteries retrogradely. 



The hepatic circulation bears certain analogies to 

 the pulmonary. Enlargement of the hepatic arteries 

 has been demonstrated in cirrhosis, and the suggestion 

 has been made that they may contribute to portal 

 hypertension as a consequence of more direct connec- 

 tions with the portal veins (68). 



Bronchial veins so enlarged that their valves become 

 incompetent have been demonstrated in pulmonary 

 emphysema, and the possibility of reverse flow of 

 blood, i.e., from the azygos system into the pul- 

 monary veins has been inferred (100, 114). Such 

 shunting has also been considered as an explanation 

 of the cyanosis sometimes encountered in fibrosis of 

 the liver (27). Enlargement of bronchial veins, 

 probably as a result of high pressure in the azygos 



system which may carry a large volume of blood 

 bypassing the liver, has been demonstrated by injec- 

 tion. 



Structure of Collateral Vessels 



It is now well established that vessels reflect in their 

 structure the mechanical conditions to which they 

 are subjected. As early as 1883 von Recklinghausen 

 (142) stated in his textbook that as collaterals carry 

 more blood, they become thicker and more tortuous. 

 That there is both hypertrophy and hyperplasia of 

 smooth muscle in the larger collaterals was described 

 and illustrated by Nothnagel (fig. 9). Fischer & 

 Schmieden (51) provided an experimental demon- 

 stration of adaptive changes in larger vessels sub- 

 jected to altered circumstances of pressure and flow. 

 When a segment of external jugular vein was in- 

 serted into the course of the carotid artery of a dog, 

 it became reduced in caliber, firmer, and as much as 

 two or three times thicker. Histologically, the media 

 was shown to contain much more muscle and con- 

 nective tissue (fig. 13). The medial elastic fibers were 

 thought to be reduced, but this was not convincingly 

 demonstrated. The adventitia also was seen to con- 

 tain denser connective tissue. The intima generally 

 remained unchanged. The trunk of the pulmonary 

 artery, when subjected to a sufficiently increased 

 pressure, becomes markedly thickened with an 

 increase both in elastic tissue and smooth muscle 

 (105, 145). 



With the enlargement of small arteries as they 

 become able to carry more blood there often appear 

 remarkable aggregates of longitudinal smooth muscle 

 fibers that dissect or even replace the internal elastic 

 lamina, and that may lead to the subtotal or even 

 complete obliteration of the lumen. Such vessels 

 have been most extensively studied in the lung and 

 in manv tvpes of chronic pulmonary disease where 

 bronchial collateral circulation is characteristically 

 increased (109, 187). Some have called these "Sperr- 

 arterien" (72-74, 93) and have thought them to 

 possess a regulatory function in relation to their 

 anastomoses with pulmonary arteries. In more 

 general terms it may be said that longitudinal muscle 

 tends to increase in other small muscular arteries with 

 an augmentation in the blood that they carry, as in 

 the bases of the cardiac valves in rheumatic fever, in 

 the vasa vasorum of the aorta in syphilis, and in 

 the intercostal vessels as they traverse adhesions to 

 enter the lung. Probably the hypertrophy and hyper- 

 plasia of muscle is in fact a response to increased 



