Native collaterals in the development of collateral circulation after chronic coronary stenosis in mongrel dogs

The response of native collateral circulation to chronic stenosis of the left circumflex coronary artery (LCx) was studied in 17 mongrel dogs. Stenosis restricted reactive hyperemia of the LCx without affecting resting flow. Regional myocardial blood flow was measured by the tracer microsphere technique. Coronary collateral blood flow to the LCx was determined during maximal reactive hyperemia of the left anterior descending branch before and 5 weeks after implantation of a fixed LCx stenosis in the open-chest preparation. The protective effect of collaterals was tested by LCx ligation 5 weeks after implantation of stenosis. Presence of acute myocardial infarction was determined by nitroblue tetrazolium staining. Eleven dogs had a myocardial infarction (group A), but six dogs showed no evidence of infarction at autopsy (group B). In group A, collateral flow and minimal coronary resistance of the LCx bed changed little after LCx stenosis, from 12 to 15 ml/min/100 g and from 10.5 to 10.0 mm Hg/ml/min/100 g, respectively (both p less than 0.05). In contrast, collateral flow in group B increased from 22 to 102 ml/min/100 g (p less than 0.05), and minimal coronary resistance of the LCx bed decreased from 4.8 to 1.4 mm Hg/ml/min/100 g (p less than 0.01). Group A had lower native collateral flow (p less than 0.05) and higher native minimal coronary resistance of the LCx bed than group B (p less than 0.05). Postobstructive LCx pressure correlated well with blood flow data. The LCx risk region was of comparable size in groups A and B, 36.4% vs 39.0% of total left ventricle (p greater than 0.05). Two responses of collateral circulation to chronic stenosis were documented: lack of collateral growth in group A, but significant collateral growth in group B. The natural variation of collateral circulation was the major determinant of the different responses that were important with stenosis of a major coronary artery.