Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to examine glucose metabolism in liver grafts during cold preservation (24 and 48 hr), warm ischemia (60 and 120 min), a combination of the two and reperfusion, the amount of protein and mRNA of glucose transporter 2 and the activities of enzymes in glycolysis (glucokinase, phosphofructokinase, pyruvatekinase), gluconeogenesis (glucose 6-phosphatase, fructose 1,6-bisphosphatase), and the pentose phosphate pathway (glucose 6-phosphate dehydrogenase) were measured. It appeared that glucose transport, the pentose phosphate pathway, and gluconeogenesis were maintained during cold preservation and warm ischemia. The activity of glucokinase significantly decreased from the control value of 1.33 +/- 0.23 IU/g protein to 0.70 +/- 0.17 (24 hr, P<0.05) and 0.57 +/- 0.12 (48 hr, P<0.01) only during cold preservation. However, the activity of phosphofructokinase significantly decreased from the control value of 4.37 +/- 0.06 IU/g protein to 2.67 +/- 0.15 (60 min, P<0.0001) and 1.53 +/- 0.06 (120 min, P<0.0001) only during warm ischemia. This indicates that glycolysis deteriorates during both cold preservation and warm ischemia and demonstrates further that the balance between glycolysis and gluconeogenesis shifts to gluconeogenesis. Even when cold preservation was combined with warm ischemia, the activity of glucokinase decreased only during cold preservation and the activity of phosphofructokinase decreased only during warm ischemia. Furthermore, these changes were time-dependent. It is suggested that they can be used as a clock to measure the durations of cold preservation and warm ischemia separately and that the magnitude of an ischemic injury to a liver and a liver graft's viability can be indirectly estimated before transplantation.
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PMID:Changes in glucose transporter 2 and carbohydrate-metabolizing enzymes in the liver during cold preservation and warm ischemia. 862 51

This study was undertaken to test the hypothesis that ischemia prior to transplantation causes tubular damage without clinical evidence of graft dysfunction. The urinary excretion of fructose-1,6-bisphosphatase (EC 3.1.3.11, FBPase), a cytosolic enzyme located exclusively in the proximal tubules, and the lysosomal enzyme N-acetyl-beta-D-glucosaminidase (EC 3.2.1.30) were measured daily between postoperative days 1 and 4 in 25 renal cadaveric graft recipients who enjoyed an entirely uncomplicated first postoperative month. During the first 4 posttransplant days urinary FBPase excretion was 0.9 +/- 0.5 U/g (0.1 +/- 0.06 U/mmol) urinary creatinine [+/-SD; range 0.2-2.1 U/g (0.02-0.24 U/mmol)]. Cold ischemia time was 20.6 +/- 8.4 h (median 22 h, range: 3-32 h). Multiple regression revealed a significant correlation between cold ischemia time and posttransplant urinary FBPase excretion (multiple R = 0.65, p < 0.001). There were no confounding effects of recipient's age and gender, number of previous transplants, cyclosporin A levels, warm ischemia time, anastomosis time, donor age and gender. Urinary FBPase excretion was significantly lower in grafts stored for a shorter time than the median cold ischemia time of 22 hours (0.69 +/- 0.42 U/g, n = 13) as compared to those stored for a longer period of time (1.13 +/- 0.56 U/g; n = 12; p = 0.035). These results indicate that graft injuries occur even in the absence of graft dysfunction and that the duration of cold ischemia itself correlates with a degree of tubular cell damage as defined by urinary FBPase excretion.
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PMID:Graft ischemia correlates with urinary excretion of the proximal marker enzyme fructose-1,6-bisphosphatase in human kidney transplantation. 938 Feb 40