Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.5 (5'-nucleotidase)
 3,167 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Both ischemic preconditioning and pretreatment with the endotoxin derivative monophosphoryl lipid A (MLA) protect the heart against infarction, yet the cellular mechanisms responsible for the cardioprotection achieved with either intervention are unknown. Using pentobarbital-anesthetized dogs, we tested the hypothesis that increased activity of 5'-nucleotidase (5'-NT), the enzyme that catalyzes the formation of adenosine from AMP, may play a role. Twenty-two dogs underwent 1 h of coronary occlusion and 4 h of reperfusion: eight controls received no intervention, seven animals were preconditioned with four 5-min episodes of brief ischemia, and seven received MLA (35 micrograms/kg iv) 24 h previously. Collateral blood flow was measured by injection of radiolabeled microspheres, infarct size was delineated by tetrazolium staining, and myocardial 5'-NT activities were measured by quantifying the release of adenosine from AMP. Despite comparable values of collateral blood flow in all groups, infarct size was reduced in preconditioned and MLA-treated dogs vs. controls. In addition, 5'-NT activities were increased throughout the heart with preconditioning and MLA treatment. However, single and multivariate regression analyses revealed no correlation between infarct size and 5'-NT activities for either treatment group. In fact, in the preconditioned cohort, animals with the highest enzyme activities developed the largest infarcts. This dissociation between infarct size and 5'-NT suggests that increased activity of 5'-NT is not the mechanism by which preconditioning or MLA treatment protects the canine heart against infarction.
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PMID:Cardioprotection with ischemic preconditioning and MLA: role of adenosine-regulating enzymes? 885 35

We examined whether ecto-5'-nucleotidase mediates infarct limitation by ischemic preconditioning in the rabbit heart. Ecto-5'-nucleotidase activity in ischemic region after ischemic preconditioning was greater than that in nonischemic regions (23.6 +/- 2.5 vs. 13.6 +/- 1.0 nmol/mg protein/min; p < 0.01). With an inhibitor of 5'-nucleotidase, alpha,beta-methylene adenosine 5'-diphosphate (AMP-CP), ecto-5'-nucleotidase activity in the ischemic region was comparable to that in the nonischemic region. Mean blood pressure was reduced from 73 +/- 2 to 62 +/- 3 mm Hg with intravenous AMP, whereas it did not change with coperfusion of AMP and AMP-CP, suggesting effective inhibition of ecto-5'-nucleotidase. Separately, myocardial infarction was created by 30-min coronary occlusion and 3 h of reperfusion. Infarct size expressed as percentage volume in risk area was reduced by ischemic preconditioning compared with that in the control (7.8 +/- 2.5% vs. 38.1 +/- 4.0%; p < 0.01). However, infarct size in the group given AMP-CP plus ischemic preconditioning was similar to that in the control (36.2 +/- 2.8% vs. 38.1 +/- 4.0%; NS), suggesting that ecto-5'-nucleotidase mediates infarct limitation by ischemic preconditioning in the rabbit.
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PMID:Ecto-5'-nucleotidase mediates infarct size-limiting effect by ischemic preconditioning in the rabbit heart. 943 17