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Am J Physiol Heart Circ Physiol 289: H2508-H2513, 2005. First published July 22, 2005; doi:10.1152/ajpheart.00446.2005
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Hyaluronidase treatment of coronary glycocalyx increases reactive hyperemia but not adenosine hyperemia in dog hearts

Jurgen W. G. E. VanTeeffelen, Simone Dekker, Dirk S. Fokkema, Maria Siebes, Hans Vink, and Jos A. E. Spaan

Department of Medical Physics, Cardiovascular Research Institute Amsterdam, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

Submitted 3 May 2005 ; accepted in final form 1 July 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 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–1·min–1 and 76 ± 7% of coronary conductance during AH (P < 0.05). After hyaluronidase, RH conductance increased (P < 0.01) by 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 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



Address for reprint requests and other correspondence: J. VanTeeffelen, Dept. of Medical Physics, Academic Medical Center, Univ. of Amsterdam, Meibergdreef 15, 1100 AZ Amsterdam, The Netherlands (e-mail: j.w.vanteeffelen{at}amc.uva.nl)




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