A technique is presented for the 3D visualisation of the coronary arterial tree using an imaging cryomicrotome. After the coronary circulation of the excised heart was filled with a fluorescent plastic, the heart was frozen and mounted in the cryomicrotome. The heart was then sliced serially, with a slice thickness of 40 microm, and digital images were taken from each cutting plane of the remaining bulk material using appropriate excitation and emission filters. Using maximum intensity projections over a series of images in the cutting plane and perpendicular plane, the structural organisation of intramural vessels was visualised in the present study. The branching end in the smallest visible vessels, which define tissue areas that are well delineated from each other by 1-2 mm wide bands populated only by vessels less than 40 microm in diameter. The technique presented here allows further quantification in the future of the 3D structure of the coronary arterial tree by image analysis techniques.

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Diastolic time fraction (DTF) has been recognized as an important determinant for subendocardial perfusion, but microsphere studies in which DTF was the independent variable are practically absent. In 21 anesthetized goats, the left coronary main stem was artificially perfused at controlled pressure. DTF was varied by pacing the heart, vagus stimulation, or administration of dobutamine. Regional coronary flow was measured with fluorescent microspheres under full adenosine dilation. Perfusion pressure (P(c)) was defined as mean coronary arterial pressure minus minimal left ventricular pressure. Regional flow conductances (flow/P(c)) were as follows: for the subendocardium, C(endo) = -0.103 + 0.197 DTF + 0.00074 P(c) (P < 0.001); for the midmyocardium, conductance = -0.048 + 0.126 DTF + 0.00049 P(c) (P < 0.001); and for the subepicardium, C(epi) was not significant. C(endo)-DTF relations demonstrated a finite value for DTF at which flow is zero, implying that, at physiological pressures, systolic subendocardial flow limitation extends into diastole. The DTF corresponding to an equal conductance in subendocardium and subepicardium (DTF1) was inversely related to P(c): DTF1 = 0.78 - 0.003 P(c) (P < 0.01). When heart rate and P(c) were held constant and dobutamine was administered (5 goats), contractility doubled and DTF increased by 39%, resulting in an increase of C(endo) of 40%. It is concluded that 1) DTF is a determinant of subendocardial perfusion, 2) systolic compression exerts a flow-limiting effect into diastole, and 3) corresponding to clinical findings on inducible ischemia we predict that, under hyperemic conditions, C(endo) < C(epi) if P(c) is lower than approximately 75% of a normal aortic pressure and heart rate >80 beats/min.

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. Hyaluronidase treatment of coronary glycocalyx increases reactive hyperemia but not adenosine hyperemia in dog hearts. Am J Physiol Heart Circ Physiol 289: H2508 -H2513, 2005. First published July 22, 2005; doi:10.1152/ajpheart.00446.2005.-Because adenosine is commonly used for inducing maximal coronary hyperemia in the clinic, it is imperative that adenosine-induced hyperemia (AH) resembles coronary hyperemia that can be attained by endogenous stimuli. In the present study we hypothesized that coronary reactive hyperemia (RH) is limited compared with AH due to the presence of the glycocalyx and that the AH response is therefore unable to detect glycocalyx modifications. In anesthetized open-chest dogs, blood flow and pressure were measured in the left circumflex artery. RH after 15-s occlusion was compared with an intracoronary infusion of adenosine (650 g; AH) during control conditions and after intracoronary treatment of the glycocalyx with hyaluronidase (20.000 U, 2 ϫ 20 min; n ϭ 6) or heat-inactivated hyaluronidase (n ϭ 5). During control, coronary conductance during RH was 1.49 Ϯ 0.15 ml ⅐ mmHg Ϫ1 ⅐ min Ϫ1 and 76 Ϯ 7% of coronary conductance during AH (P Ͻ 0.05). After hyaluronidase, RH conductance increased (P Ͻ 0.01) by 43 Ϯ 13% and became 93 Ϯ 4% of AH conductance (P ϭ NS). Heatinactivated hyaluronidase had no effect on RH and AH conductance. Our results demonstrate that adenosine-induced coronary hyperemia profoundly exceeds RH and that the difference is virtually abolished on selective removal of the glycocalyx. It is concluded that, compared with RH, adenosine-induced coronary hyperemia is not affected by modification of the glycocalyx. This glycocalyx insensitivity should be taken into account when using adenosine-induced coronary hyperemia as a marker for vasodilating capacity to an ischemic stimulus. coronary circulation; hyaluronidase; dogs TO ASSESS the functional severity of coronary stenoses in the clinic, use of adenosine for inducing maximal coronary hyperemia in patients has been well established (8,10,17,34). Clinical decision-making to intervene is based on intracoronary parameters that are derived during hyperemia, and it is therefore critical that the adenosine-induced hyperemia accurately reflects the coronary hyperemia that can be attained by endogenous stimuli (7). Intravital microscopic studies of cremaster tissue have suggested that adenosine affects capillary perfusion by limiting the effect of the glycocalyx on vascular resistance (3,12,21). The glycocalyx is the carbohydrate-rich matrix that lines the luminal surface of blood vessels and forms the true interface between the endothelium and flowing blood (6,24,26,30). Normally, flowing red blood cells and large dextrans are excluded from the glycocalyx in cremaster capillaries (6, 30, 31). However, it was shown that adenosine superfusion impaired glycocalyx exclusion properties (21). Because an intact glycocalyx strongly reduces the volume available for flow of plasma and red blood cells in capillaries (3,22,30), an impaired g...