PERIPHERAL VASCULAR DISEASES 



I237 



vascular responses in young dogs are of interest (56). 

 After acute arterial occlusion the artery developed 

 severe spasm whereas the vein exhibited a mild 

 degree of spasm. On release of the occlusion there 

 was a period of residual spasm in artery and vein. 

 Sympathectomy abolished both the arterial and 

 venous spasm during occlusion as well as after re- 

 lease. Papaverine administered during the arterial 

 occlusion had no effect on the arterial spasm, but 

 after release of the occlusion the residual spasm was 

 abolished. 



Recent studies, however, have cast considerable 

 doubt on the significance of diffusely distributed 

 vasospastic phenomena in response to acute arterial 

 occlusion in man. Compensatory mechanisms in 

 response to sudden arterial occlusion have been the 

 subject of a recent report on clinical, pathologic, 

 and experimental observations by Wessler et al. (102). 

 They noted that three major important compensa- 

 tory phenomena follow sudden arterial occlusion, 

 namely, clot fragmentation, clot lysis, and function 

 of preformed inter-arterial collateral anastomoses. 

 The authors considered that clot fragmentation and 

 clot lysis, although not disproving the role of "spasm," 

 provide an alternative to the concept of release of 

 spasm as an explanation for the occasionally witnessed 

 sudden relief of arterial insufficiency in some pa- 

 tients. The gradual enlargement of anastomotic 

 channels, bypassing complete obstructions, accounts 

 for the delayed and gradual improvement (even 

 with return of distal pulsatile flow) observed in some 

 patients weeks to months after the initial occlusion. 

 The authors further stated that unlike embolectomy, 

 blockage of autonomic nervous supply for the relief 

 of ischemia, secondary to arterial occlusion, has 

 neither a sound physiologic rationale nor satisfactory 

 clinical documentation of its efficacy (102). Based 

 on their own (102) and other studies (76) they found 

 little evidence that vessels in the ischemic zone are 

 in spasm in organic arterial insufficiency. 



More recent observations by Hardy & Tibbs (33) 

 have further minimized the role of diffuse ''spasm" in 

 acute arterial thrombosis. These authors emphasized 

 that a healthy artery is normally in a state of con- 

 siderable elastic distention and that when occluded 

 the vessels distal to the occlusion become narrow from 

 "elastic recoil." Apparently this recoil has been the 

 basis for the erroneous diagnosis of diffuse arterial 

 "spasm." Patients are described (33) in whom the 

 distal arteries remained contracted and pulseless after 

 embolectomy, and in whom a residual "consecutive" 

 clot was found. When this residual clot was removed 



completely by retrograde irrigation, the "spasm" 

 disappeared and pulsation returned. 



Regardless of the above and other arguments, it 

 is impossible to state dogmatically whether or not 

 arterial "spasm" is significant in the pathophysiology 

 of the circulation in acute arterial occlusion. The 

 suggestion that a powerful vasoconstrictor substance 

 (possibly serotonin) is released from a fresh thrombus 

 and that it causes spasm of the affected vessel and 

 adjacent collaterals (25, 83, 101) needs further 

 study. 



Vasoconstrictor mechanisms in chronic arterial occlusion. 

 This topic has caused considerable discussion, espe- 

 cially among surgeons who advocate sympathectomy 

 in the treatment of chronic arterial occlusive disease. 

 One major basis for this suggestion has been the 

 thesis that even if superimposed arterial spasm is not 

 of pathogenic importance, sympathectomy is of 

 benefit because it reduces normal arterial "tone" 

 causing arterial dilatation and fostering collateral 

 circulation. Particularly with respect to muscle 

 circulation, neither experimental nor clinical evidence 

 in man justifies pursuing this topic further. 



Vasoconstrictor mechanisms in collagen diseases and 

 diseases of the fine blood vessels. These diseases and dis- 

 eases of "immune" mechanisms arc on the forefront 

 of medicine today. Much progress has been made in 

 understanding these conditions. In general, the 

 "collagen diseases" include lupus erythematosus, 

 scleroderma, dermatomyositis, periarteritis nodosa, 

 rheumatic fever, and rheumatoid arthritis. Also in- 

 cluded among these diseases are thrombotic thrombo- 

 cytopenic purpura, multiple forms of "vasculitis" 

 (see Appendix) and several other disease states. The 

 present day concept of the collagen diseases is that 

 they represent diseases which primarily involve con- 

 nective tissue structures. Since connective tissue is 

 ubiquitous the manifestations of these diseases are 

 protean. Regardless of terminology, there is no 

 reason to assume that the collagen fiber is the only 

 structure involved in these processes, but rather that 

 the disease is generalized including all connective 

 tissue constituents such as reticulum fibers, elastic 

 fibers, ground substance, and all related cells such 

 as fibroblasts, histiocytes, lymphoid elements, plasma 

 cells, and mast cells. 



Even to attempt to discuss briefly the generalities 

 of this group of diseases would be beyond the scope 

 of this presentation. Numerous sources are available 

 in the literature. A brief review with particular 

 emphasis on cardiovascular manifestations has been 

 published (97). The blood vessels certainly are the 



