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1 Medical Physics, Cardiovascular Research Institute Amsterdam, Academic Medical Center, Amsterdam, The Netherlands
* To whom correspondence should be addressed. E-mail: j.w.vanteeffelen{at}amc.uva.nl.
Since 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 to 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 to an intracoronary infusion of adenosine (650 µg; AH) during control conditions and after intracoronary treatment of the glycocalyx with hyaluronidase (20.000 U, 2 x 20 min; n=6) or heat-inactivated hyaluronidase (n=5). During control, coronary conductance during RH was 1.49 ± 0.15 ml/mmHg.min, and 76 ± 7% of coronary conductance during AH (P<0.05). After hyaluronidase, RH conductance increased (P<0.01) with 43 ± 13% and became 93 ± 4% of AH conductance (P=NS). Heat-inactivated hyaluronidase had no effect on RH and AH conductance. Our results demonstrate that adenosine-induced coronary hyperemia profoundly exceeds reactive hyperemia and that the difference is virtually abolished upon selective removal of the glycocalyx. It is concluded that, compared to reactive hyperemia, 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 marker for vasodilating capacity to an ischemic stimulus.
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