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The functional morphology of the coronary microcirculation in the dog

Microvascular Research
Publication Date
DOI: 10.1016/0026-2862(74)90061-2
  • Agricultural Science
  • Biology


Abstract Dog hearts were perfused in a Langendorff preparation with whole blood. When beating was established a silicone rubber injectate (Microfil) was added to the perfusion and allowed to flow until it appeared on the venous side of the system. Perfusion was stopped, Microfil allowed to harden, and the specimen cleared. The basic anatomy comprised subepicardial networks of anastomosing vessels maximum dimension between 70 and 120 μm from which arose superficial precapillary networks and many perforating vessels of varying length which supplied the subendocardial networks, the muscle mass of the ventricle and the papillary muscles. The venous drainage was by short venules leading through a system of short branches to the main veins. In general the larger veins were distributed in close association with the arteries. Evidence is presented to show the existence of routes of flow through the microcirculation of continuously fluctuating resistance. The evidence is compatible with “physiological shunting” taking place through low resistance channels and against the separate existence of arteriovenous anastomoses in the dog myocardium. Following acute ligation of the anterior descending coronary artery, arterioles and precapillaries up to 20 μm in diameter remained patent distal to the ligature and filled retrogradely from arteries unaffected by the ligature. However, Microfil entering these vessels retrogradely did not enter capillaries. Veins in the ischaemic area remained filled with blood and engorged. Injections of Trypan Blue, having a lower viscosity than Microfil, also demonstrated a patchy failure of capillaries to fill. The evidence indicates a large increase in resistance to blood flow at the level of precapillaries, which is, however, irregular so that in the infarct there are areas of normal irrigation and areas in which no capillary filling at all can be demonstrated. A possible active component in the infarction process is suggested.

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