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  • Title: Early changes in collateral blood flow to ischemic myocardium and their influence on bimodal vulnerability during the first 30 min of acute coronary artery occlusion in dogs.
    Author: von Mutius S, Neumann M, Meesmann W.
    Journal: Basic Res Cardiol; 1988; 83(1):94-106. PubMed ID: 3377745.
    Abstract:
    Coronary collateral blood flow and its changes during the first 30 min of acute coronary artery occlusion were studied in 34 anesthetized dogs to clarify its influence on the vulnerability of the heart in this first arrhythmic phase. Collateral flow was determined with 9-micron tracer microspheres (TM) injected at 1, 10 and 30 min after acute proximal occlusion of the left circumflex (LCX, n = 30) or left anterior descending (LAD, n = 4) coronary artery. The post-mortem selective retrograde coronary angiography was used to evaluate the functional extent of preexisting coronary collaterals. After acute LCX occlusions collateral flow increased significantly (p less than 0.05) from 17.8 +/- 2.7 ml.(min.100 g)-1 (mean +/- SE; n = 13) at 1 min to 29.3 +/- 5.1 ml . (min . 100 g)-1 at 30 min of occlusion in animals with well-formed preexisting coronary collaterals (group 1), whereas it was very low (4.7 +/- 0.6 ml . (min . 100 g)-1; n = 13) and changed only slightly in dogs with poor collaterals (group 2). Most of these animals died by ventricular fibrillation (VF) before a second measurement could be carried out. In four dogs with poor collaterals but an unusually small LCX area (group 3), flow remained almost constant (11.0 +/- 4.7 versus 11.0 +/- 4.4 ml . (min . 100 g)-1) during this period. Similar results were obtained in animals with acute LAD occlusion (group 4). Ventricular extrasystoles (VES) mainly developed in animals with poor collaterals and respective low and almost unchanging collateral flow (group 2,3,4) while none or only a few VES occurred in dogs in which flow initially was clearly higher and increased significantly (group 1). The animals of group 1, 3 and 4 all survived the first arrhythmic phase, whereas all the animals of group 2 died by VF, either in the arrhythmic subphase Ia (n = 7) or Ib (n = 6). The results of the present study show that only the initial magnitude of flow is decisive for the development of VES and VF during the first arrhythmic phase, whereas the subsequent increase in flow is of no importance to the bimodal vulnerability in the first arrhythmic phase (subphases Ia and Ib). The in vivo measured critical minimal collateral flow of about 5 ml . (min . 100 g)-1 corresponds well with the survival limit (border between collateral state III and IV) previously determined by post-mortem retrograde coronary angiography.
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