Question: 

Cold storage is used to preserve tissue for later transplantation. We tested if vessel derived adiponectin may be protective for vessels subjected to cold storage.

Methodology: 

Following two days of cold storage at 4°C isometric force measurements were performed at 37 °C in a Mulvany myograph to determine vascular tone development and vessel relaxation. Adiponectin expression and secretion from fat-free mouse aorta were measured by quantitative PCR, Western blot and ELISA.

Result: 

Adiponectin mRNA in fat free mouse aorta was 21-fold higher compared to mouse heart tissue. Western blot analysis under non-heat denaturating, non-reducing conditions showed multiple bands including trimeric, hexameric and high order adiponectin multimers. ELISA measurements revealed an accumulation of adiponectin in cold storage supernatant over two days compared to one hour storage indicating release of adiponectin from fat-free aortic tissue. After two days storage receptor-independent vessel tone development and acetylcholine-induced, endothelium-dependent relaxation were impaired. Especially the share of maximum acetylcholine relaxation persisting glibenclamide stimulation is lowered via various contributing pathways including nitric oxide-dependent and -independent ones. Addition of full length adiponectin containing 55–75 % high molecular weight fraction re-established this vessel response. Addition of adiponectin unable to form high order multimers failed to improve vessel function.

Conclusion: 

Adiponectin is expressed and secreted from fat-free vascular tissue during cold storage. High molecular weight adiponectin can protect mouse aorta from cold storage induced failure of endothelium-dependent relaxation. The mechanism of protection remains to be clarified.