The validity of using blood sampled from the anterior interventricular vein (AIV), anatomically located within the myocardium perfused by the left anterior descending (LAD) coronary artery, to represent venous drainage originating from the LAD vascular territory was studied in eight anaesthetised, open chest dogs. The LAD was cannulated and perfused from a blood reservoir isolated from the systemic circulation. To determine the presence of blood from non-LAD sources that appears in the AIV sample, 51Cr-labelled red blood cells were injected into the left atrium and distributed in the systemic circulation while the LAD was perfused by non-radioactive blood. The percentage spillover of red blood cells from non-LAD sources into the AIV drainage was determined under control, reduced LAD flow, ischaemia, and reperfusion conditions as 100 X (AIV chromium content/arterial chromium content). Spillover of red blood cells into AIV blood samples averaged only 1.5(1.3)% under control conditions and increased insignificantly to 8.6(3.5)% during reduced LAD flow. During ischaemia red blood cells in AIV blood increased insignificantly to 98.3(5.0)% but decreased to 1.9(1.3)% after reperfusion. Studies in five dogs with microspheres showed that a portion of this admixture from non-LAD sources originated from precapillary nutritional collateral or overlapping blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

This study evaluated changes in coronary blood flow (CBF), myocardial oxygen consumption (MVo2), and myocardial segmental shortening (SS) during intracoronary administrations of enflurane in in situ canine hearts. The left anterior descending coronary artery (LAD) of 11 anesthetized and mechanically ventilated dogs was perfused at constant perfusion pressure (80 mm Hg) with enflurane-free blood or with blood equilibrated in an extracorporeal oxygenator with enflurane (1.1%, 2.2%, 4.4%). CBF (measured with a Doppler flow transducer) was multiplied by the local arteriovenous (A-V) O2 difference to calculate MVo2. SS was measured with ultrasonic crystals. Myocardial lactate uptake was assessed. Peak CBF responses during enflurane were compared with those during maximum coronary vasodilation with adenosine. Enflurane caused concentration-dependent increases in CBF, and decreases in MVo2 and SS. The greatest increase in CBF during enflurane (4.4%) was similar to that achievable with adenosine. Myocardial lactate uptake was not affected by enflurane. In conclusion, enflurane has a direct coronary vasodilating effect. The potency of this effect is underscored by the ability of enflurane to cause marked increases in CBF, while appreciably reducing myocardial O2 demand. Since the enflurane-induced reduction in myocardial contractility was not due to ischemia, it likely reflected a direct negative inotropic effect. When the direct effects of enflurane are compared with those of equianesthetic concentrations of halothane and isoflurane previously shown in the same model, enflurane has a coronary vasodilating effect similar to that of halothane but less than that of isoflurane, and it has a negative inotropic effect greater than that of both isoflurane and halothane.

No abstract