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HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



(229), this level of backflow has not been made to 

 increase for 8 to 1 o hours by drugs or by any known 

 physiological means, such as increased heart rate, 

 increased flow in the other coronary arteries, in- 

 duction of hypoxia or hypoxemia in the other coronary 

 arteries (204). Why the collateral flow remains fixed, 

 why the anastomoses function as a set of inert tubes, 

 and why they do not exhibit vasomotion or participate 

 in the vasodilatory response of the normal coronary 

 bed are not known. This situation contrasts with the 

 rapid development of collaterals in other vascular 

 beds such as the femoral and carotid arteries (153). 



This retrograde flow can, however, be greatly 

 reduced by excessive stretch of the myocardium and 

 reactive hyperemia in the other nonoccluded coro- 

 nary artery branches. The improvement that occurs 

 with drugs such as neosynephrine and norepinephrine 

 in the human heart in the presence of coronary 

 insufficiency and infarction could result from an 

 increase in the oxygen supply to regionally ischemic 

 muscle (337), and from augmentation of the col- 

 lateral flow through increase of the coronary per- 

 fusion pressure and a smaller heart size. Spasm of the 

 coronary arteries with diminished blood flow is also 

 frequently invoked to explain the onset of episodes of 

 angina pectoris and of reduction in collateral flow. 

 However, no firm conclusion can yet be drawn as to 

 whether flow in one coronary artery can be in- 

 fluenced reflexly and adversely by impulses arising 

 from an intra- or extracardiac source (see the section 

 on Reflexes). 



Lysis of coronary thrombi induced experimentally 

 can be observed to follow fibrinolytic therapy. 

 Whether this will change the evolution of early 

 myocardial infarction and result in salvage of ischemic 

 tissue without collateral development has not yet 

 been determined (276). 



collateral stresses to which the hearts have been 

 previously exposed. 



Evidence, largely from the classical work of Zoll 

 et al. (411), indicates that the incidence of injectable 

 coronary artery collaterals is quite small in normal 

 human hearts, but is greatly increased in the presence 

 of coronary artery constriction or occlusion. There is 

 also evidence in different species that nature adopts 

 prophylactic measures to protect some hearts against 

 subsequent coronary artery occlusion. The coronary 

 vessels appear to be capable of setting up or enlarging 

 anastomoses between themselves without the stimulus 

 of coronary occlusion or insufficiency. Presumably, 

 this is due to some form of antecedent stress. In these 

 hearts, stresses, some known but mostly unknown, 

 prophylactically enhance the potential collateral 

 circulation without the stimulus of coronary occlusion 

 or constriction. These are exemplified in man by the 

 increase in the incidence of the injectable coronary 

 arterial collateral bed in the presence of hypertrophy, 

 valvular disease, cor pulmonale, anemia, and prob- 

 ably high altitude (38, 412; also Rotta, personal 

 communication). This is exemplified in the pig by an 

 increase in the injectable collaterals in the presence of 

 anemia (39, 412), and in the dog by an increase in 

 both the injectable and functional collaterals in the 

 presence of high altitude (Rotta, unpublished ob- 

 servations), and transfused anemia (97). No good 

 experimental evidence exists, however, to indicate 

 that physical exercise per se augments prophylacti- 

 cally the collateral flow as measured in a normal 

 coronary artery immediately after its occlusion. 

 The injectable coronary collateral bed, however, is 

 stated to increase in exercised rats (360). Individuals 

 who escape serious consequences from coronary 

 occlusion may well be those whose collaterals have 

 been previously expanded by such means. 



RESPONSE OF THE CORONARY COLLATERAL CIRCULATION 

 TO NATURALLY OCCURRING PROPHYLACTIC STIMULI. 



As indicated earlier, the intercoronary arterial com- 

 munications are generally small in normal man, 

 fewer than 10 per cent having anastomoses with 

 diameters of 40 p. or more (39). However, others using 

 corrosion and injection techniques found anastomoses 

 of greater size and with greater frequency (18, 226, 

 371). The coronary arterial tree of the pig is strikingly 

 similar to that of man (96, 289), while in the dog the 

 anastomoses are larger and more frequent. These 

 differences in collateral function might be explained 

 on a technical basis or as fundamental species varia- 

 tions; however, they could be related to the types of 



MEDICAL, PHYSIOLOGICAL, AND SURGICAL ATTEMPTS TO 

 IMPROVE THE CORONARY ARTERY COLLATERAL CIRCU- 

 LATION prophylactically. Either before or after 

 establishment of coronary insufficiency, it should be 

 possible to improve the state of the heart of dog or 

 man by augmentation of the coronary artery col- 

 lateral circulation which naturally functions, by 

 retrograde perfusion of the ischemic coronary bed 

 with arterial blood, or by elevation of the ventricular 

 fibrillation threshold. In man, in addition, positive 

 and subjective benefit could arise through psychogenic 

 effects which are not necessarily related to the heart. 

 Chronic experiments have produced no good 

 evidence to indicate that any drug promotes collateral 



