In the first instance, survival of the myocardium is well correlated with collateral blood flow, independent of the size of risk zone. Infarct size is also determined by oxygen consumption of the myocardium, being greater if oxygen consumption is elevated by tachycardia. In pigs, collateral circula tion was initially absent, leading to a defined infarct area with higher blood flow in the lateral border zone. Six to eight weeks later, mechanical cardiac func tion was normal even though collateral flow was only partially restored, and mitochondrial respiration was still reduced in the collateralized region. Collateral flow reached of maximal flow between and wk and did not improve further. Whereas in dogsflow was in existing collaterals after acute coronary artery occlusion, DNA synthesis was demonstrable days later by thymidine labeling in vascular smooth muscle and endothelial cells of arteries, and labeled nu clei were observed in veins, venules, arterioles, and capil laries in nonischemic areas, with the highest labeling in vessels of smallest caliber days after constriction. This suggests development of collat eral circulation involves the whole vascular tree.Gradual coronary artery Granisetron hydrochloride occlusion in dogs produced similar growth of all vessels outside but not within the area of Naftifine hydrochloride potential ischemia. In pigs, all classes and sizes of arterial and venous vessels showed proliferation in terms of number and size. Tritiated thymidine labeling was also pres ent within the area at risk in contrast to dogs. In human hearts, the response is similar to that in pigs.The first vessels appearing were veinlike, having thin walls with the muscular layers de veloping wk after complete occlusion.It has been established that repeated brief coronary occlusions are also capable of promoting collateral devel opment occlusions every min with long occlusions every min in dogs.The latter regime was more efficient in promoting collateral growth than the former, implicating a sufficient dura tion of ischemia as a requirement for vascular growth.Also it was found that the number of occlusions needed to induce sufficient collateralization to preserve systolic segment shortening was reduced in dogs treated with heparin. Whether hepa rin can act under these circumstances by interaction with FGF has so far not been established.Hypoxia produced by anemia has long been known to enhance coronary collateral growth in humans. The latter investigators cite their results as evidence for collateral growth in the absence of a pressure difference across the collateral circulation, thus stressing the role of hypoxia as a stimulus.Chronic chemical sympathectomy did not lead to collat eral development after coronary ischemia in either rats. Schaper and coworkers have discussed a multitude of possible mechanisms for collateral growth.Physical factors such as pressure gradients and increased wall stresses were discounted, since DNA syn thesis was seen in capillaries in which flow velocity would have been decreased by arterial occlusion.Thus flow re sumed with a time course inversely related to the extent of collateralization: within sin the rat cremaster mus cle after iliac artery occlusion, albeit at a lower rate. The restitution offlow clearly depends on the extent of its initial deprivation, which relates to the degree of existing collateralization and the speed with which either existent collateral vessels develop andor new vessels grow.