CHANGES IN VASCULAR PATTERNS 



1267 



fig. 12. The calculated regression lines for rates of increase 

 of collateral blood flow are plotted when both pulmonary 

 arteries and veins are ligated (solid line) and when the pulmon- 

 ary artery alone is interrupted (broken line). These are re- 

 markably congruent; this indicates that the collateral veins can 

 expand at least as rapidly as the arteries. The data for "artery 

 alone" have been recalculated in ml/kg/min from a paper by 

 Bloomer el al. (20). An adjustment for nitrogen shift in the 

 bronchospirometry has also been made and this has made pos- 

 sible the construction of the graph, using also data previously 

 published by Vidone & Liebow (183). 



In certain other situations progressive increase in 

 expansion of collateral beds can take place for at least 

 1 year and possibly longer. As discussed previously, 

 this has been observed in the arterial collateral circu- 

 lation related to an arteriovenous fistula. 



Regression of Collaterals 



That preformed collaterals can open rapidly and 

 disappear as quickly when the stimulus to their 

 formation is abrogated has been shown angiographi- 

 cally by Winblad et al. (192) and John & Warren (90). 



As a collateral bed develops, certain of its com- 

 ponents tend to enlarge and to persist as major 

 channels, while others regress. This was noted in 

 successive angiograms after ligating the femoral 

 artery in the rabbit (108). North & Sanders (127) 

 found in the ear of the mouse that when continuity 

 of an interrupted vascular channel was regained cer- 

 tain minor collaterals regressed. 



Even collaterals of long standing remain only so 

 long as the stimuli that led to their expansion are 

 maintained. Bosher et al. (22) observed regression of 

 collateral circulation associated with a peripheral 

 arteriovenous fistula by comparing angiograms im- 



mediately and again 6 weeks after fistulectomy; some 

 regression was apparent as early as the fourth or fifth 

 day. Anatomically the collaterals in regression were 

 described as showing marked subendothelial pro- 

 liferation. The results after fistulectomy were similar 

 to those after ligature of the major participating ves- 

 sels in the fistula, and this was considered further 

 evidence against the "tissue need" theory. Winblad 

 et al. (192) Schoop (156) and Hasse & Schoop (70) 

 noted the regression of collaterals after adequate 

 thrombo-intimectomy or bypass grafting in major 

 systemic arteries. Similar phenomena were described 

 by Jacobson & McAllister (89). 



Arterial Versus Venous Collaterals 



"Nature has been more prodigal in the provision of 

 alternative venous and lymphatic routes than she 

 has been in arranging for arterial collaterals" [Lear- 

 month (96)]. 



In the lung the stimuli to the development of 

 arterial and of venous collaterals are independent. 

 This is true not only where mechanical forces seem 

 dominant as in the expansion of pre-existing col- 

 laterals, but also where chemical influences appear to 

 be pre-eminent as in the case of newly formed trans- 

 pleural vessels. 



When both arteries and veins are compromised 

 under appropriate conditions, both arterial and 

 venous limbs of the collateral circulation will expand. 

 This has already been discussed for the lung. In seg- 

 ments of small intestine transplanted to the sub- 

 cutaneous tissue by the Florey- Harding method 

 (128) both arterial and venous collaterals appeared 

 when the original mesenteric vascular pedicle was 

 severed. 



It is of interest that in these experiments the venous 

 collaterals seemed to develop to a larger size more 

 quickly than the arterial. Similar observations had 

 been reported by North & Sanders (127) in the ear 

 of the mouse. The veins seemed to expand within 24 

 hours, while it took 4 to 5 days for visible expansion 

 of arteries to take place. Quantitative data are avail- 

 able for the lung. When both the pulmonary arteries 

 and veins are interrupted, the collateral blood flow is 

 approximately the same as when arteries alone are 

 ligated (fig. 12). This means that expansion of the 

 venous collateral can at least keep pace with that 

 of the arterial. 



In these experiments arteries became joined to 

 arteries, and veins to veins, but there are circum- 



