Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.11.8 (FAST)
 758 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because end-organ injury can occur with reperfusion following hemorrhage or ischemia, we hypothesized that aggressive intravenous fluid resuscitation would aggravate tissue injury in a fixed-volume model of hemorrhagic shock. Unanesthetized chronically prepared male rats were hemorrhaged 33-36 mL/kg for 2.5 h. Then Lactated Ringers Solution (3x hemorrhage volume) was infused over 5 min (FAST), 20 min (MEDIUM), 180 min (SLOW), or not at all (NO RESUS). Plasma ornithine carbamoyltransferase (OCT), lactate, and creatinine were measured as indices of hepatocellular injury, anaerobic metabolism, and renal function, respectively. At 1 h post-resuscitation (PR), MAP was greater after SLOW and MEDIUM treatment (tx) than after other txs (P < 0.05). OCT increased earliest after FAST tx to values greater than those after other txs from 30 min to 24 h PR (P < 0.01). Plasma lactate was elevated immediately before resuscitation in all groups (P < 0.01) and returned to baseline at 3 h PR after SLOW tx compared to 5 h PR after FAST tx (P < 0.05). Creatinine at 5 h PR was less in the groups treated with intravenous fluid compared to the NO RESUS group, P < 0.05. Survival at 72 h was reduced in the FAST (57%) and NO RESUS (58%) groups compared to the SLOW (87%) and MEDIUM (85%) groups (P < 0.05). Thus, overly aggressive fluid tx accelerates hepatocellular injury, is no better than lesser rates of resuscitation at correcting plasma lactate and preserving renal function, and provides no overall survival benefit.
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PMID:Detrimental effects of rapid fluid resuscitation on hepatocellular function and survival after hemorrhagic shock. 1235 25

Studies on the neuroprotective effect of magnesium treatment in animal models of focal and global cerebral ischemia have produced inconsistent results. Nevertheless, two magnesium acute stroke phase III trials (IMAGES and FAST-MAG) have either been completed or are planned. Therefore, we decided to re-evaluate the efficacy of magnesium following focal cerebral ischaemia in rats. Two experiments were carried out in two independent laboratories based in Australia. Both used the intraluminal thread method to induce focal cerebral ischemia in the rat. In the Perth study the middle cerebral artery (MCA) was occluded for 45 min and body temperature was controlled during and after ischemia. In the Canberra laboratory the MCA was occluded for 2 h and body temperature was only controlled during surgery. Three different doses (180, 360, or 720 micromol/kg) of MgSO4 in the Perth study and two different MgSO4 doses (370 or 740 micromol/kg) in the Canberra study were intravenously or intra-arterially administered immediately before ischemia. Control animals were given an equal volume of normal saline just before ischemia in both studies. Twenty-four or 72 h post-ischemia, infarct volume was determined following 2',3',5'-triphenyl-2H-tetrazolium chloride (TTC) staining. No significant differences (P > 0.05) in total, cortical and striatal infarct volumes between saline and MgSO4 treated animals were observed in either study. We conclude MgSO4 does not reduce infarct volume when administered before focal cerebral ischemia in rats.
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PMID:Magnesium sulfate fails to reduce infarct volume following transient focal cerebral ischemia in rats. 1519 83