Introduction 75 97 87 2 99 54 55 108 94 95 2 43 70 43 1 Fig. 1 MI  Characteristics of LV remodelling and dysfunction after MI in swine 82 96 t max t max 43 98 t max 2 Fig. 2 L S P L P 43  83 98 3 t max 43 100 Fig. 3 L L L L 2 2 P  L † P <  43  2 88 85 90 2 2 90 49 89 2 102 55 54 108 2 4 54 55 108 P =  43 43 97 2 2 4 2  43 70 2 Fig. 4 2 Epi OM IM Endo 2 2 2 2 2 2 P  L † P <  43  Vasomotor control of the coronary microcirculation in remodelled myocardium Neurohumoral control 56 56 Sympathetic control 11 36 56 8 32 101 35 34 23 43 43 98 100 27 39 2 5 Fig. 5 2 2 2 2 P  † P  23  2 2 39 51 27 2 5 23 Parasympathetic control 12 33 6 12 30 76 23 t max 23 1 23 109 27 5 23 Angiotensin II 1 2 14 4 107 34 43 1 62 98 2 6 1 68 1 44 2 84 2 103 68 1 78 63 84 Fig. 6 1 2 2 2 2 P  † P  68  Local metabolic control Adenosine 5 3 28 67 93 2 2 3 28 67 93 2 61 2 43 70 108 71 2 7 65 Fig. 7 8PT ATP 2  2 2 2 2 P † P 2 2 ‡ P 2 71  2 16 17 10 13 15 13 10 41 ATP ATP ATP 24 25 31 ATP 106 ATP ATP 106 ATP 65 ATP 2 65 2 2 7 71 ATP ATP ATP ATP 65 ATP ATP 106 ATP 29 81 ATP 67 ATP ATP Ca v 9 46 48 ATP Ca v ATP ATP 71 ATP 65 Endothelial control 2 26 59 80 105 Nitric oxide 92 45 57 19 52 57 64 22 64 105 26 80 105 2 8 45 58 64 60 20 42 21 79 21 86 37 50 7 44 Fig. 8 2 2 P  44  91 74 18 Endothelin 9 69 70 A B 104 70 72 73 Fig. 9 A  P  † P  70  40 77 Conclusions and physiological relevance 2 ATP 53 27 66 69 2 ATP 71 ATP 70 68 10 11 Fig. 10 2 2 open circles open triangles solid diamonds solid squares ATP solid triangles graph  Fig. 11 Alterations in vasomotor balance in the coronary resistance vessels within remodelled myocardium in swine with a 2–3-week-old myocardial infarction  ATP 97 38