[Q 36 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



tion, section of the posterior roots or sympathectomy. 

 It has been assumed that these patients represent 

 examples of "thalamic dysfunction." 



Other theories involving higher centers are of 

 interest, but will not be expanded. For example, it 

 has been suggested that an irritative focus in the 

 extremity produces afferent impulses over sensory- 

 nerves to the spinal cord which results in continual 

 impulse discharges and nervous disturbance in this 

 zone. This results in stimulation of the elements of 

 the lateral and anterior horns, which then produce 

 the characteristic peripheral signs (53). A theory- 

 proposed by Leriche (44) involved reflex overactivity 

 of the central vasomotor center. 



Some theories of note have suggested involvement 

 of afferent sympathetic nerve fibers. Of interest in 

 this regard are studies by Kuntz (42) demonstrating 

 afferent spinal nerve fibers which traverse the sym- 

 pathetic trunk and communicating rami. Stimulation 

 of appropriate nerves results in conduction of pain 

 impulses by these afferent fibers which appear to be 

 distributed chiefly in relation to blood vessels rather 

 than to the skin and muscles of the extremity. Whether 

 or not these phenomena function in the causalgia 

 svndromes is unknown, but relief of pain by sym- 

 pathectomy might be explained by such mecha- 



miscellaneous states. Spasm of major arteries. Spasm 

 of a large artery is initiated by some type of trauma 

 in or near the artery. The initiating trauma is usually 

 a severe penetrating injury such as a gunshot wound, 

 but it may be provoked by contusing or crushing 

 injuries even though the artery itself is not directly- 

 involved in the injury. The spasm may be sufficient 

 to occlude the lumen completely. The spasm may be 

 limited to a small isolated discrete segment of the 

 artery or it may involve a long segmental length 

 including the orifices of many collateral arteries (3). 

 The exact mechanism of this type of spasm is not 

 clear but the ''myogenic" factor or the inherent 

 property of smooth muscle to contract when directly 

 traumatized appears to be paramount. It has been 

 shown experimentally that local segmental spasm 

 in large arteries can be produced by mechanical 

 trauma irrespective of the presence of the adventitia 

 or nerve supply (38). These facts are in accordance 

 with observations that this type of spasm usually 

 cannot be released with periarterial injections of 

 local anesthetics, sympathetic nerve interruption, 

 periarterial nerve stripping, or even by amputation 

 of the involved extremity above the site of the arterial 



spasm (3, 13, 26). It has been shown, however, both 

 experimentally and clinically, that direct applica- 

 tion of a 2.5 per cent solution of papaverine to an 

 artery will relieve traumatic spasm in the majority 

 of instances (39). The mechanism of this response is 

 unknown. 



Vasoconstrictor mechanisms in acute arterial occlusion. 

 The changes which occur after acute circulatory 

 arrest have been presented in a preceding section. It 

 is not the purpose of this discussion to present the 

 clinical signs and symptoms nor the pathogenesis of 

 events leading to acute circulatory arrest, which 

 include occlusive arterial disease, thrombosis, and 

 embolism. Arteriosclerosis, intravascular clotting, 

 and embolism are discussed in other chapters of this 

 Handbook. The purpose of the present discussion is to 

 indicate, briefly, concepts concerning possible vaso- 

 constrictor mechanisms which operate in acute 

 arterial occlusion. 



The obvious factor in acute arterial occlusion is 

 acute impairment of blood flow through the arterial 

 lumen. Studies suggest, however, that this is not 

 necessarily the major cause of the resulting profound 

 ischemia associated with acute arterial occlusion, 

 since only mild to moderate degrees of ischemia may- 

 be produced when a comparable peripheral artery is 

 ligated. The implication then is that a superimposed 

 functional disturbance must be operative in patho- 

 logic occlusion. 



It has been considered that reflex vasospasm of the 

 distal portion of the artery and the collateral arteries 

 is mediated in the efferent arc through the sym- 

 pathetic nervous system (3, 87). This has been the 

 basis for recommendation of prompt sympathetic 

 interruption in patients with acute arterial occlusion 

 (87). Experimental work has shown, however, that 

 the superimposed diminution in blood supply af- 

 fected by spasm and inadequate dilatation of col- 

 lateral arteries is temporary and spontaneously 

 disappears in a few hours (31, 64). Several investi- 

 gators (3) have postulated that the spasm in col- 

 lateral arteries, if prolonged, produces degenerative 

 changes in the intima of distal arteries and veins 

 which in turn provokes widespread vascular thrombo- 

 sis with the resultant organic obstruction to flow even 

 after the spasm disappears. This would account for 

 progression to complete irreversible circulatory arrest 

 in some patients. However, when spasm has not 

 been severe or prolonged, a satisfactory collateral 

 circulation may be established permitting the limb 

 to survive (3). 



Some experimental studies on the mesenteric 



