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J Thorac Cardiovasc Surg 2000;120:707-711
© 2000 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology

Exogenous hyaluronidase induces release of nitric oxide from the coronary endothelium

Paulo R. B. Evora, MD, PhD, Paul J. Pearson, MD, PhD, Yeow Leng Chua, MD, Berent Discigil, MD, Hartzell V. Schaff, MD

From the Section of Cardiovascular Surgery, Mayo Clinic and Mayo Foundation, Rochester, Minn.

Supported in part by The FAPESP-Fundacao de Amparo a Pesquisa do Estado de São Paulo and the Mayo Foundation.

Address for reprints: Paulo R. B. Evora, MD, PhD, Rua Rui Barbosa, 367, 14015-120 Ribeirao Preto, São Paulo, Brazil (E-mail: prbevora{at}keynet.com.br).

Objective: Hyaluronidase, an endogenous enzyme that hydrolyzes mucopolysaccharides, has been shown to enhance myocardial protection when added to preservation solutions. In addition, hyaluronidase infusion reduces injury to ischemic myocardium. Endothelium-derived nitric oxide is an endogenous vasodilator that prevents leukocyte adhesion to the intima and inhibits platelet adhesion and aggregation in the coronary artery. Experiments were undertaken to determine whether the protective action of hyaluronidase could be mediated by the endogenous release of nitric oxide.
Methods: Segments of coronary artery, with and without endothelium, were placed in organ chambers (25 mL) to measure isometric force. Blood vessel segments were contracted with prostaglandin F2{alpha} (2 x 10–6 mol/L) and exposed to hyaluronidase (3-15 units).
Results: Hyaluronidase induced vasodilation of arteries with intact endothelium but not of arteries without endothelium (n = 6, P < .05). Endothelium-dependent vasodilation to hyaluronidase was blocked by NG-monomethyl-L-arginine (10–5 mol/L), an inhibitor of nitric oxide synthesis from L-arginine (n = 6, P < .05). Inhibition of vasodilation by NG-monomethyl-L-arginine was reversed by L-arginine (10–4 mol/L) but not D-arginine (10–4 mol/L; n = 6, each group). Vasodilation to hyaluronidase also was inhibited by hemoglobin (2 x 10–6 mol/L), a scavenger of the nitric oxide radical (n = 6, P < .05).
Conclusions: Hyaluronidase induces the release of nitric oxide from the coronary endothelium. Because nitric oxide, an endogenous vasodilator, inhibits leukocyte adhesion to the intima in addition to inhibiting platelet adhesion and aggregation, stimulated production of endothelium-derived nitric oxide by exogenous hyaluronidase could be the mechanism of the protective action of hyaluronidase infusion.






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