CHANGES IN VASCULAR PATTERNS 



1265 



that substances transported through the lumen of a 

 vessel serve to nourish it, or that after the flow be- 

 comes greater both nourishment and growth increase. 



Compelling evidence does exist that chemical 

 factors affect the growth of vessels in general, and the 

 development of collateral circulation in particular. 

 This becomes especially clear in organs with a 

 double blood supply such as the lung. For example, 

 there is general agreement that the actively metaboliz- 

 ing cells of primary malignant pulmonary neoplasms 

 receive their blood supply from systemic vessels (39, 

 99, 194, 195). This would indicate the effect of 

 chemical rather than mechanical factors, since the 

 vast majority of the pulmonary capillaries represent 

 a bed supplied by the pulmonary artery. In fact, 

 with the growth of tumors the pulmonary arteries and 

 veins tend to be obstructed or peripherally displaced. 

 This may have some practical importance, since at- 

 tempts have been made to subject pulmonary neo- 

 plasms to high concentrations of cytotoxic agents by 

 injecting them into the pulmonary arteries leading to 

 the involved segments. There is disagreement on the 

 blood supply of metastatic tumors, since some (99) 

 have found them likewise to be vascularized from 

 the aorta, while others (39) concluded that the 

 bronchial arteries did not nourish the metastatic 

 tumors. Possibly the disagreement indicates variation 

 in the blood supply. In the case of the liver, according 

 to Hales (personal communication), both primary 

 and metastatic tumors are supplied by the hepatic 

 arteries. 



Other newly formed tissues in the lung also are 

 nourished by systemic arteries. Again this implies 

 that chemical factors must be at work. Thus, in or- 

 ganizing pulmonary disease, as in bronchiectasis, the 

 granulation tissue is derived at least in large part 

 from the bronchial arteries (104, 194). Ultimately 

 precapillary anastomoses are formed with branches 

 of the pulmonary arteries. That this is not necessarily 

 the outcome of enlargement of existing precapillary 

 anastomoses, is indicated by the observation that 

 vessels penetrating into the lung from intercostal 

 arteries via adhesions anastomose with pulmonary- 

 arteries in similar fashion (102). 



The peculiar "tropism" exhibited by newly formed 

 collaterals in the lung must also have a chemical 

 explanation. It is well established that ligature of the 

 pulmonary artery induces expansion only of arterial 

 collaterals (102). After interruption of the pulmonary 

 veins, only the venous collaterals expand (86). Pro- 

 liferating branches of intercostal vessels that enter the 



lung through the pleura are of the same type, arterial 

 or venous, depending on the stimulus, and the ar- 

 teries form precapillary connections only with ar- 

 teries, and the veins only with veins. When both 

 major limbs of the pulmonary circulation are inter- 

 rupted, the expansion of both collateral systems is 

 induced, and both types of collaterals penetrate in- 

 ward through pleural adhesions (183). These col- 

 laterals must be newly formed, from capillaries in 

 granulation tissue which did not exist previously but 

 which comes to obliterate the pleural space after the 

 operative manipulation. Remarkably, again the 

 transpleural branches of the intercostal arteries 

 establish precapillary connections only with the pul- 

 monary arteries, and the intercostal veins connect 

 likewise only with pulmonary veins. If these were 

 mechanically induced there should be "short cir- 

 cuits'' between the intercostal arteries and veins, 

 since they share a common capillary bed in the granu- 

 lation tissue as it is first formed, and the greatest 

 pressure gradient under the circumstances is obvi- 

 ously from intercostal arteries to intercostal veins. 

 Yet such short circuits have rarely if ever been ob- 

 served. Rather, the blood pursues the longest course, 

 from the intercostal arteries through precapillary 

 anastomoses into the pulmonary arteries, to the pul- 

 monary capillaries, to pulmonary veins, and finally 

 through precapillary connections into the collateral 

 veins. The chemical factors that must be responsible 

 for this are still unknown. 



There is some suggestive, but as yet imperfect, 

 evidence that hormones can exert an influence on the 

 development of collateral circulation. The collateral 

 circulation that develops within a few months after 

 ligature of a pulmonary artery in puppies less than 

 48 hours old seems immensely greater by gross in- 

 spection than that appearing after a comparable 

 interval of time in adult animals after the same pro- 

 cedure (105). The results of a study of the effect of 

 hormones on collateral circulation after interruption 

 of the iliac artery in rats were, however, equivocal 

 (147). Cortisone seemed to inhibit the collateral circu- 

 lation, just as it did the connective tissue proliferation 

 in the region of the lower abdominal incision where, 

 as a result, hernias appeared. The weight increase of 

 these animals, however, stopped when cortisone was 

 administered. It might be expected at the end of the 

 experiment that the smaller animals would have 

 smaller vessels. This problem, however, should be 

 reinvestigated. 



Studies of the earliest phases of development of the 



