COLD-STORAGE OF RABBIT THORACIC AORTA IN UNIVERSITY-OF-WISCONSIN SOLUTION REDUCES ENDOTHELIUM-INDEPENDENT VASODILATION

Citation
Jvd. Gryflowczowski et al., COLD-STORAGE OF RABBIT THORACIC AORTA IN UNIVERSITY-OF-WISCONSIN SOLUTION REDUCES ENDOTHELIUM-INDEPENDENT VASODILATION, Journal of Pharmacy and Pharmacology, 49(11), 1997, pp. 1096-1101
Citations number
26
ISSN journal
00223573
Volume
49
Issue
11
Year of publication
1997
Pages
1096 - 1101
Database
ISI
SICI code
0022-3573(1997)49:11<1096:CORTAI>2.0.ZU;2-6
Abstract
Optimum preservation conditions for storage of donor livers and blood vessels are essential for successful transplantation. The blood vessel s are used as vascular conduits to facilitate anastomosis of the liver to the recipient's systemic vasculature. Failure of some transplants has been ascribed to thrombosis of these vascular conduits possibly be cause of alterations in vascular reactivity owing to inadequate storag e techniques. To restrict data variability previously associated with studies using a heterogeneous sample of vessels from man, this study i nvestigated changes in vascular reactivity in segments of rabbit thora cic aorta from male, age-matched, New Zealand White rabbits stored at 4 degrees C in either University of Wisconsin solution (UW; Du Pont Ph armaceuticals, UK) or Krebs-Bulbring buffer (KB). Percent vasodilation to acetylcholine remained significantly greater in UW than in KB at - log (M) concentrations of 7.0 (UW = 47.05 +/- 4.26 compared with KB = 13.20 +/- 7.20%; P < 0.001), 6.5 (UW = 66.82 +/- 4.83 compared with KB = 26.60 +/- 9.48%; P < 0.01), and 6.0 (UW = 83.68 +/- 5.26 compared w ith KB = 31.20 +/- 9.83%; P < 0.001). This was not significantly diffe rent to relaxation in unstored arteries and suggested improved endothe lial function and structure, confirmed by electron microscopy. Percent vasodilation to sodium nitroprusside was significantly lower in UW th an in unstored (D-0) arteries at -log (M) concentrations of 7.5 (D-0 = 28.27 +/- 4.02 compared with UW = 15.21 +/- 1.82%; P < 0.01), 7.3 (D- 0 = 52.58 +/- 5.05 compared with UW = 29.23 +/- 1.94%; P < 0.01), 7.0 (D-0 = 69.70 +/- 4.85 compared with UW = 49.72 +/- 2.49%; P < 0.05), a nd 6.4 (D-0 = 93.16 +/- 2.93 compared with UW = 71.29 +/- 5.20%; P < 0 .05). Percent vasodilation was also lower in UW-compared with KB-store d arteries at -log (M) sodium nitroprusside concentrations of 7.0 (UW = 49.72 +/- 2.49 compared with KB = 64.11 +/- 5.03%; P < 0.05) and 6.4 (UW = 71.29 +/- 5.20 compared with KB = 96.91 +/- 5.96; P < 0.05). El ectron microscopy confirmed that this was not a result of degradation of smooth muscle structure. The nitric oxide synthase inhibitor L-N-G- nitro-L-arginine methyl ester (100 mu M) did not significantly modulat e sodium nitroprusside-induced vasodilation in unstored arteries, when endothelial function was maximum, or in UW-stored arteries, suggestin g that the reduced responses in UW-stored arteries were not because of increased synthesis of nitric oxide. This reduced relaxation to sodiu m nitroprusside was therefore nitric oxide-independent and not a resul t of competition between sodium nitroprusside and endothelial 'nitric oxide donation' for cGMP. In summary, cold-storage preservation with U W reduced endothelium-independent vascular relaxation by mechanisms ot her than competition with NO; this requires further evaluation.