Contribution of amino acids in protective solutions to postischemic functional recovery of canine kidneys

Abstract

Amino acids are known to increase glomerular filtration rate (GFR). There is also an early resumption of filtration following 2-h renal ischemic stress under protection by histidine-buffered histidine-tryptophan-ketoglutarate solution (HTK), possibly due in part to an amino acid effect. Hence, we have examined the possibility of further enhancing the postischemic GFR by adding 32 (ASP I; 4 mM Mg2+) or 36 (ASP II; 6 mM Mg2+) mM L-aspartate (asp) or 32 mM DL-aspartate (ASP III) to the HTK solution in place of chloride. After infusion of 500 ml 5% glucose, canine kidneys were protected by an 8-min perfusion with HTK (n = 5), ASP I (n = 4), ASP II (n = 5) or ASP III-solution (n = 3). The subsequent ischemia lasted for 2 h at 27-31 degrees C. During reperfusion, both GFR and filtration fraction (FF) were higher in kidneys protected by L-aspartate-containing solutions. ASP III showed no improvement against HTK. An additional preischemic intra-aortal application of HTK or ASP I solution just above the exit of the renal arteries prior to the intrinsic protective perfusion further raised the postischemic GFR. The present results suggest that L-aspartate but also histidine may have favorable amino acid effects in renal protective solutions in addition to known positive effects of histidine.

Postischaemic interrelations between energy metabolism and functional recovery of protected canine kidneys

“…It has been shown that the exchange of the Na+-, K+-and M$+-chloride in the HTK-solution by the corresponding salts of L-aspartic acid leads to a distinctly higher GFR and higher transport rates in the early phase of postischaemic recovery after 2 h of ischaemia. With an extra 2 mM Mg2+ in addition to a solution modification with Laspartate, an even higher GFR was reached [3]. However, contrary to the HTK groups with different ischaemia times, this higher GFR with aspartate solutions did not increase, in the case of 6 mM Mg2+ (Asp 11) it even slightly decreased the renal ATP content compared to HTK kidneys with a comparable ischaemic stress (Fig.…”

“…Since aspartate especially after ischaemia is a good renal substrate, aspartate metabolism could have mediated the effects [3]. However, a relevant SAN elevation by an enhanced synthesis of purine nucleotides by aspartate was not detectable (Fig.…”

“…Canine kidneys were protected by perfusion with one of the protective solutions before they were rendered ischaemic. A detailed description of the experimental procedure up to the onset of ischaemia including anaesthesia, premedications and perfusion technique is given elsewhere [3]. As a rule one kidney was treated and subjected to ischaemia while the other kidney was retained as a control (n = 19).…”

“…In six further experiments, prior to the selective renal protective perfusion 500 ml of either HTK-solution (n = 2), HTK-aspartate-solution (Asp I: n = 2) or Tutofusina (n = 2) had been pumped into the aorta next to the origins of the renal arteries ('preperfusion'). (For details see [3].) With HTK or Tutofusin@ preperfusion HTK was then used as the solution for renal protection.…”

“…On the other hand, although the renal heterogeneity complicates the interpretation, the apparently higher transport activity in the L-aspartate group could also have been the consequence of glomerulo-tubular balance at higher filtration rates [37]. In this case the GFR could have been increased primarily as a result of vascular events, mediated perhaps by the renin-angiotensin system or by renal eicosanoids [3]. In addition, the Ca2+ complexing properties of aspartate may have been involved [3].…”