Extracellular HTK Perfusion and Intracellular Acidification in Ischemic Dog Kidneys: A sup 31 P NMR Spectroscopic Study

Abstract

Bretschneider's histidine-tryptophan-ketoglutarate solution (HTK) for organ preservation is in wide clinical use. Its high buffering capacity is its major protective principle. It is assumed that renal ischemic tolerance benefits from this principle. The study was undertaken to determine the degree to which extracellular buffering influences intracellular acid load. Canine kidneys were investigated for intracellular and extracellular pH changes during a clinically relevant period of ischemia after preperfusion with either HTK or Ringer solution (Ringer) at different temperatures. Extracellular pH (pHe) was measured with ion-sensitive electrodes. Intracellular pH (pHi) was determined with 31P NMRS. Morphologic and functional parameters were assessed in reperfusion experiments. After perfusion with HTK, pHe values of 7.35, 7.25, and 7.30 were determined for 5C, 20C and, normothermia, respectively. The pHe values after 150 minutes were 7.37, 6.84, and 6.76 at the temperatures indicated. The corresponding pHi values 150 minutes after HTK perfusion were 7.20, 6.79 and 6.54. After Ringer perfusion and 150 minutes at 20C and normothermia, pHi values of 6.29 and 5.92 were measured. Reperfusion experiments showed better results in the HTK group. Preperfusion with HTK considerably decreases ischemic acidification of extracellular and intracellular compartments at 20C and 37C, compared with Ringer. In kidneys preperfused with HTK and kept at 5C, a nearly physiologic pH was maintained during the observation period of 150 minutes and longer, HTK leads to better functional and morphologic preservation compared to Ringer.