Effect of sodium nitroprusside and L-arginine methyl ester on rat hearts stored at 4 °C for 24 h

Abstract

1. This study examined the effects of altering nitric oxide levels with sodium nitroprusside or L-arginine in rat hearts stored hypothermically.2. Hearts were microperfused at 4 degrees C for 24 h with a modified Krebs-Henseleit buffer (KHB) that contained either sodium nitroprusside, L-arginine, L-arginine methyl ester or dexamethasone.3. After hypothermic storage, hearts were rewarmed to 37 degrees C with KHB alone or KHB containing sodium nitroprusside or L-arginine. Cardiac function was then assessed in either Langendorff mode or working heart mode.4. Compared with values from fresh unstored hearts, hypothermic stored hearts showed a significant decrease in coronary flow and left ventricular developed pressure when the stored hearts were perfused in Langendorff mode. These hearts also produced less aortic flow and cardiac output when perfused in the working mode.5. Hearts hypothermically microperfused with buffer containing either L-arginine or sodium nitroprusside and then reperfused in the Langendorff mode with untreated KHB buffer had the highest left ventricular developed pressure and coronary flow values. Aortic flow and cardiac output were also higher in these hearts.6. In all groups of stored hearts, the concentrations of both ATP and creatine phosphate were significantly low, when compared with values from freshly isolated hearts. Addition of dexamethasone to the buffer either during storage or during reperfusion had no beneficial effect on high-energy phosphate loss or cardiac performance of stored hearts.7. This study showed that the addition of nitric oxide donors to storage buffer significantly improves cardiac function on normothermic reperfusion. The improved functional recovery is unrelated to the high-energy phosphate content of these hearts.

ROS scavenging before 27°C ischemia protects hearts and reduces mitochondrial ROS, Ca2+ overload, and changes in redox state

“…Other studies showed that L-NAME, N G -monomethyl-L-arginine and oxyhemoglobin, all NO ⅐ scavengers, provide protection against I/R injury (50). However, Fagbemi and Northover (20) showed that the presence of NO ⅐ donors and not inhibitors in the cold buffer improved coronary flow during subsequent warm reperfusion. In any case, these studies demonstrate a significant role of NO ⅐ in the pathogenesis of cold-induced I/R injury.…”

“…Portions of this work were presented in abstract form at the 48th Annual Meeting of the Biophysical Society, Baltimore, MD, February 14 -18, 2004, and at the Experimental Biology Conference, Washington, DC, April [17][18][19][20][21] 2004.…”