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)

The purpose of this study was to investigate the possibility of improving the organ preservation properties of the University of Wisconsin (UW) solution by adding the calcium entry blocker lidoflazine. We also investigated the possibility of decreasing the cold ischemia and reperfusion damage by pretreatment with lidoflazine of the donor and/or recipient. The protective effects of lidoflazine treatment were estimated by measuring the amount of trapped erythrocytes in the rat renal medulla after 48 h of cold storage, subsequent transplantation, and 20 min of reperfusion. Lidoflazine (20 mg/liter) added to the UW solution decreased the amount of erythrocyte trapping from 14.8 +/- 3.1% in controls to 8.6 +/- 1.7% (P less than 0.01). The flow rate of the flush-out solution during the harvesting procedure was also significantly (P less than 0.01) increased when lidoflazine was included in the UW solution (1.10 +/- 0.21 ml/min vs 0.75 +/- 0.22 ml/min). Administration of lidoflazine (0.28 mg/kg body wt) to the donor and/or the recipient did not further reduce the postischemia/reperfusion damage as estimated by the degree of erythrocyte trapping. In conclusion, the results indicate that the preservation properties of the UW solution can be significantly improved by adding lidoflazine to the solution.
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PMID:Improvement of renal preservation by adding lidoflazine to University of Wisconsin solution. An experimental study in the rat. 149 15

Lidoflazine, a calcium channel blocker, was administered to dogs following twelve minutes of cerebral ischemia, induced by aortic cross-clamping. The effects of lidoflazine (1 mg/kg i.v.) on cerebral blood flow following ischemia was studied in 15 anesthetized, mechanically ventilated dogs. Cerebral blood flow was measured with the radiolabelled microsphere technique before and 10, 30, 60, 90 and 150 minutes following ischemia. Cerebral blood flow increased in all brain regions following ischemia, but by 60 minutes had decreased to control values. Lidoflazine had no effect on this reperfusion phenomenon, or on the distribution of blood flow within the brain. Regional cerebral blood flow was also not altered by lidoflazine therapy. Our data demonstrate that this dose of lidoflazine has no effect on regional or total cerebral blood flow following 12 minutes of cerebral ischemia in dogs. These data do not support perfusion preservation as a mechanism of amelioration of neurologic injury after ischemia by this calcium channel blocker.
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PMID:Effect of lidoflazine on cerebral blood flow following twelve minutes total cerebral ischemia. 642 83