Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated the use of urinary lactic dehydrogenase (LDH) in predicting renal injury in a convenience sample of 36 blunt trauma patients with hematuria. The mean +/- SEM urinary LDH for the five patients with renal injuries was 129.4 +/- 35 U/L, which was not significantly different from the mean urinary LDH levels in either the 22 patients without demonstrable genitourinary or retroperitoneal injuries (92.9 +/- 20.7 U/L) or the nine patients with nonrenal genitourinary or retroperitoneal injuries (165 +/- 46 U/L). Urinary LDH at a threshold of 135 U/L was more specific (75% vs 53%, P less than .01) and more accurate (74% vs 57%, P less than .01) than hematuria at a threshold of 50 red blood cells per high-power field in predicting lacerations of the kidney or ureter; urinary LDH was less sensitive than hematuria at these thresholds (67% vs 100%), but not significantly. We conclude that urinary LDH is a nonspecific marker of cellular disruption anywhere along the genitourinary tract in otherwise healthy blunt trauma patients.
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PMID:Urinary lactic dehydrogenase as a marker of renal injury in blunt trauma patients with hematuria. 339 82

Distension of the perfused guinea pig ureter at pressures from 20 to 700 cmH(2)O increased the amount of ATP released from the epithelium in a pressure-dependent manner. During basal perfusion (40 microl/min), the perfusate contained 10 pmol/ml ATP; this increased 10- to 50-fold at various distending pressures. ATP was released from epithelial cells during distension as mechanical removal of the urothelium blocked release. No lactate dehydrogenase was detected in the perfusate, and scanning electron microscopy confirmed an intact urothelium after distension. ATP was not released due to the activation of stretch-activated channels, as gadolinium (10 microM) failed to affect ATP release. Glibenclamide (10 microM), known to inhibit two members of the ATP-binding cassette (ABC) protein family, did not affect ATP release after distension; nor did verapamil (10 microM). In contrast, both monensin (100 microM) and brefeldin A (10 microM), which interfere with vesicular formation or trafficking, inhibited distension-evoked ATP release, which was Ca(2+)-dependent. This suggests that ATP release from the ureter epithelium might be mediated by vesicular exocytosis. The role of ATP released by distension of hollow visceral organs is discussed in relation to the concept of purinergic mechanosensory transductions, with special reference to nociception and the activation of P2X(3) receptors on the subepithelial sensory nerves.
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PMID:ATP is released from guinea pig ureter epithelium on distension. 1178 42