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J Thorac Cardiovasc Surg 2009;137:492-498
© 2009 The American Association for Thoracic Surgery


Evolving Technology

Cellular electrophysiologic and mechanical evidence of superior vascular protection in pulmonary microcirculation by Perfadex compared with Celsior

Min Wu, MDa,b, Qin Yang, MD, PhDa, Anthony P.C. Yim, MDa, Malcolm J. Underwood, MDa, Guo-Wei He, MD, PhD, DSca,c,d,*

a Department of Surgery, The Chinese University of Hong Kong, Hong Kong
b Guangdong Provincial People's Hospital, Guangzhou, China
c Medical College, Nankai University and TEDA International Cardiovascular Hospital, Tianjin, China
d Providence Heart and Vascular Institute, Albert Starr Academic Center, Department of Surgery, Oregon Health and Science University, Portland, Oregon

Received for publication December 28, 2007; revisions received May 29, 2008; accepted for publication August 28, 2008.

* Address for reprints: Guo-Wei He, MD, PhD, DSc, Department of Surgery, The Chinese University of Hong Kong, 5A, Block B, Prince of Wales Hospital, Shatin, N.T., Hong Kong SAR, China. (Email: gwhe{at}cuhk.edu.hk).

Objective: Pulmonary endothelial function is critical in posttransplant lung performance. Hyperkalemic organ preservation solutions alter vascular endothelial function through the non-nitric oxide and non-prostacyclin pathway, but the most frequently used lung preservation solutions, Perfadex (Vitrolife Sweden, Kungsbacka, Sweden) (K+ 6 mmol/L) and Celsior (IMTIX SangStat Company, Lyon, France) (K+ 15 mmol/L), have not been evaluated on pulmonary endothelial protection. We compared the non-nitric oxide and non-prostacyclin–mediated endothelial function in porcine pulmonary microarteries of lung preserved by Perfadex or Celsior solution at 4°C for 4 hours.

Methods: The non-nitric oxide and non-prostacyclin–mediated endothelial function was determined by measuring the membrane potential in a single pulmonary smooth muscle cell (group II, n = 6) and bradykinin-induced relaxation (group I, n = 8) in pulmonary microarteries preserved in Krebs (a, control), Perfadex (b), or Celsior (c), with inhibitors of nitric oxide and prostacyclin.

Results: Membrane potential hyperpolarization decreased in IIc (4.5 ± 0.2 mV, P < .05) but was preserved (P > .05) in IIa (6.6 ± 0.1 mV) and IIb (6.3 ± 0.3 mV). Resting membrane potential was depolarized in IIc (–42.8 ± 1.3 mV) compared with IIa (–58.7 ± 0.6 mV) and IIb (–56.7 ± 0.9 mV) (P < .05). Hyperpolarization-associated relaxation (37.3% ± 7.2% vs 59.7% ± 7.7%) and sensitivity (EC50) (–7.29 ± 0.13 vs –7.75 ± 0.06 log M) to bradykinin significantly (P < .05) decreased in Ic but not in Ia and Ib.

Conclusion: This in vitro study simulating clinical conditions demonstrates that Perfadex preserves endothelium-dependent smooth muscle relaxation and hyperpolarization better than Celsior solution in regard to the electrophysiologic and mechanical properties observed at cellular and vascular levels. This study provides a new method at the level of basic science to evaluate the solutions for heart/lung preservation.



Abbreviations and Acronyms BK = bradykinin; CI = confidence interval; EC = Euro-Collins; EDHF = endothelium-derived hyperpolarizing factor; HbO = oxyhemoglobin; Indo = indomethacin; L-NNA = N-nitro-L-arginine; NNONPG = non-nitric oxide and non-prostacyclin; NO = nitric oxide; PGI2 = prostacyclin; UW = University of Wisconsin








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