Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Morphofunctional state of myocardial capillary bed and serum creatine kinase were measured in 70 white rats with coronary arterial occlusion. Four-day pretreatment with alpha-tocopherol and, particularly, intal, was conductive to the improvement of micro-circulation in the ischemized myocardium via an increase in the number, exchange surface area and capacity of functional capillaries. This effect became manifest since day 1 after coronary arterial occlusion and was accompanied by a stabilization of the creatine kinase level. The fact that the effect of intal was of basically the same type, but more pronounced, as compared to that of alpha-tocopherol, might be due to both the similarity of the drugs in terms of nonspecific antioxidant effect and specific properties of intal which has a membrane-protective effect on the mast cell, normalizing its stress-induced activation.
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PMID:[Effect of preliminary administration of alpha-tocopherol and intal on the course of experimental myocardial necrosis]. 250 47

Leukocyte-mediated myocardial reperfusion injury is characterized by the progressive migration and accumulation of polymorphonuclear leukocytes within the myocardium. In this study, we hypothesized that leukocytes normally resident to the myocardium also contribute to myocardial injury in the absence of migration and accumulation of peripheral polymorphonuclear leukocytes. In isolated crystalloid-perfused rat hearts, we found numerous resident cardiac leukocytes that were identified primarily as macrophages and mast cells, the latter staining avidly for peroxidase. When hypoxic perfused hearts (60 minutes, n = 16) were reoxygenated there was a prompt release of this peroxidase activity, the extent of which correlated closely with the degree of myocardial injury (total creatine kinase release, r = 0.96). When reoxygenation associated mast cell degranulation was prevented in six additional hypoxic hearts using 10 microM Lodoxamide Tromethamine, peroxidase release was reduced 7.8-fold (p less than 0.001) and creatine kinase release (injury) was reduced 5.9-fold (p less than 0.001). These results demonstrate that the isolated crystalloid-perfused rat heart is not a leukocyte-free preparation and suggest that mast cells resident to the heart play an important role in acute reoxygenation injury.
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PMID:Acute reoxygenation injury in the isolated rat heart: role of resident cardiac mast cells. 284 39

Dystrophin-deficient female mdx mice were bred with male Tsk+/+ pa mice to examine the role played by mast cells in the pathophysiology of dystrophin deficiency. Resultant mdx/Tsk double-mutant mice were then examined functionally, biochemically, and histologically. While mdx mice remained as strong as their normal counterparts, mdx/Tsk double-mutant mice became progressively weak with age. Serum creatine kinase activity was significantly elevated in both mdx and mdx/Tsk double-mutant mice over normal controls. However, mast cell-derived plasma tryptase activity was consistently higher in the double-mutant than in mdx mice. In addition, histological examination of gastrocnemius muscle revealed that while necrosis was persistent in both strains of mdx mice from 2 to 8 weeks of age, regeneration was significantly reduced in the double-mutant mice. Of particular interest was the fact that necrosis in the mdx/Tsk double mutant exceeded mdx values at 8 weeks of age, corresponding approximately with a second peak in tryptase activity. Therefore, heightened mast cell activity appears to elicit in the dystrophin-deficient mdx mouse a myopathy not unlike the human Duchenne disease.
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PMID:Duchenne-like myopathy in double-mutant mdx mice expressing exaggerated mast cell activity. 756 39

Species-specific differences in the inflammatory response, specifically with regard to mast cells, have been proposed to explain the phenotypic variation among dystrophin-deficient humans, and mdx mice (Gorospe et al., 1994). To test this hypothesis we have intramuscularly injected a mast cell secretogogue into both dystrophin-negative mdx and dystrophin-positive normal mice. Mast cell activity was determined by measuring the activity of mast cell tryptase, while creatine kinase activity was used to determine the course of muscle damage in vivo. Area of damage around the injection site was measured at autopsy, and used as an indication of relative sensitivity to the secretogogue effect of compound 48/80. Mdx mice exhibited more damage in response to intramuscular injection than normal control mice. In addition, mdx mice showed a substantial increase in plasma tryptase activity, followed by a large increase in muscle creatine kinase activity. On the other hand, dystrophin-positive normal controls injected with 48/80 liberated little CK or tryptase activity. These results are consistent with the hypothesis that species-specific differences in mast cell activity, or sensitivity to mast cell products could account for the variation in pathology seen in dystrophin-deficient animals.
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PMID:Enhanced sensitivity of mdx mice to intramuscular injection of compound 48/80. 793 7

In the present study, we evaluated the potential role of mast cell degranulation in acute hypoxia/reoxygenation-induced injury to cardiomyocytes in the isolated rat heart. Histamine release was determined to delineate the extent of mast cell degranulation, whereas the release of creatine kinase (CK) and lactate dehydrogenase (LDH) was assessed to quantitate the extent of irreversible injury to cardiomyocytes. The suitability of peroxidase (PO) as a marker for mast cell degranulation was also evaluated. Reoxygenation resulted in a release of histamine corresponding with 6.5% +/- 0.6% of total tissue content, whereas LDH, CK and PO release amounted to 30% +/- 2%, 28% +/- 2% and 32% +/- 3% of their respective tissue contents. Identical perfusion in the presence of the mast cell stabilizer lodoxamide tromethamine resulted in a reduced histamine release (2.8% +/- 0.1%) of total tissue content upon reoxygenation, but the release of LDH, CK or PO was not influenced. Cumulative histamine release did not correlate with the amount of LDH, CK or PO released. Treatment with consecutive bolus injections of the mast cell degranulating compound 48/80 during normoxic perfusion resulted in an almost complete histamine release, whereas PO release remained below detection limit. When the compound 48/80-treated hearts were subjected to hypoxia/reoxygenation, the release of LDH, CK or PO during reoxygenation again remained unchanged, whereas histamine release was negligible. Determination of PO activity of freshly isolated cardiomyocytes demonstrated that the bulk of PO in rat hearts was located in this particular cell type. Therefore we conclude that in the isolated rat heart, PO release is not a specific marker of mast cell degranulation. In addition, our data provide no firm evidence that in this experimental model, mast cell degranulation contributes to a significant extent to acute hypoxia/reoxygenation-induced injury to cardiomyocytes.
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PMID:Lack of evidence for a role of mast cell degranulation in acute hypoxia/reoxygenation-induced injury in the isolated rat heart. 872 68

Our study was designed to investigate the role of resident cardiac mast cells in the cardioprotective effect of ischemic preconditioning. Ischemic/compound 48/80 preconditioning and treatment with compound 48/80, a mast cell degranulator (1 microg/ml), produced cardioprotective and antiarrhythmic effects in isolated perfused rat heart subjected to 30-min global ischemia followed by 30-min reperfusion. Four episodes of ischemic/compound 48/80 preconditioning and compound 48/80 treatment markedly reduced the release of lactate dehydrogenase (LDH) and creatine kinase (CK) in coronary perfusate and the incidence of ventricular premature beats (VPBs) and ventricular tachycardia or fibrillation (VT/VF) during the reperfusion phase. The release of mast cell peroxidase (MPO), a marker of mast cell degranulation in coronary perfusate, increased immediately after ischemic and compound 48/80 preconditioning. The cardioprotective and antiarrhythmic effect of ischemic/compound 48/80 preconditioning was lost within 60 min. It is proposed that the cardioprotective effect of ischemic preconditioning, which lasts for 60 min in isolated rat heart, may be ascribed to degranulation of resident cardiac mast cells.
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PMID:Resident cardiac mast cells and the cardioprotective effect of ischemic preconditioning in isolated rat heart. 926 40

The present study was designed to investigate the effect of amiloride, a Na+/H+ exchange inhibitor on cardioprotective effect of ischaemic preconditioning in isolated rat heart. Four episodes of ischaemic preconditioning and amiloride (174 microM) treatment markedly decreased the release of lactate dehydrogenase (LDH) and creatine kinase (CK) in coronary effluent and infarct size in hearts subjected to 30 min of global ischaemia followed by 120 min of reperfusion. Amiloride (174 microM) administered during ischaemic preconditioning (Amiloride in Ischaemic Preconditioning), produced no marked effect on LDH and CK release and infarct size. Ischaemic preconditioning and amiloride treatment significantly reduced ischaemia/reperfusion induced release of mast cell peroxidase (MPO). Four episodes of pH (20 mm of ammonium chloride) preconditioning also produced cardioprotection and decreased ischaemia/reperfusion induced release of MPO. It is interesting to note that a significant increase in release of MPO was observed immediately after ischaemic preconditioning and the release was inhibited by amiloride. Moreover, similar increase in MPO release was noted immediately after pH preconditioning. These findings tentatively suggest that ischaemic preconditioning and pH preconditioning produced cardioprotective effect by activating Na+/H+ exchange and consequent degranulation of resident cardiac mast cells. Amiloride administered during ischaemic preconditioning attenuated the cardioprotective effect of ischaemic preconditioning.
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PMID:Effect of amiloride A Na+/H+ exchange inhibitor on cardioprotective effect of ischaemic preconditioning: possible involvement of resident cardiac mast cells. 934 36

This study was designed to investigate the effect of disodium cromoglycate (DSCG), a mast cell stabilizer, on cardioprotective effect of ischemic preconditioning. Isolated rat heart was subjected to 30 min of global ischemia followed by 30 min of reperfusion. Ischemic preconditioning was provided by four episodes of 5-min global ischemia followed by 5 min of reperfusion before sustained ischemia. Ischemic preconditioning and DSCG (10 and 100 microM) treatment markedly decreased the release of lactate dehydrogenase (LDH) and creatine kinase (CK) in coronary effluent and percentage incidence of ventricular premature beats (VPBs) and ventricular tachycardia/fibrillation (VT/VF) during reperfusion. Ischemic preconditioning and DSCG treatment also significantly reduced ischemia/reperfusion-induced mast cell peroxidase (MPO) release, a marker of mast cell degranulation. A significant increase in MPO release was observed immediately after ischemic preconditioning, and the release was found to be inhibited in hearts perfused with DSCG (10 and 100 microM) during ischemic preconditioning. DSCG administered during ischemic preconditioning (DSCG in ischemic preconditioning) attenuated the cardioprotective and antiarrhythmic effects of ischemic preconditioning. DSCG in ischemic preconditioning produced no marked effect on ischemia/reperfusion-induced MPO release. These findings tentatively suggest that DSCG administration during ischemic preconditioning abolishes its cardioprotective effect, perhaps by stabilizing resident cardiac mast cells.
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PMID:Cardiac mast cell stabilization and cardioprotective effect of ischemic preconditioning in isolated rat heart. 959 79

The present study was designed to investigate the role of adrenergic component and cardiac mast cell degranulation in the cardioprotective effect of ischaemic preconditioning. Isolated rat hearts were subjected to 30 min of global ischaemia followed by 30 min of reperfusion. Ischaemic/norepinephrine (100 microm) preconditioning markedly reduced ischaemia-reperfusion-induced release of lactate dehydrogenase (LDH) and creatine kinase (CK) in coronary effluent and the incidence of ventricular premature beats (VPBs) and ventricular tachycardia/fibrillation (VT/VF) during the reperfusion phase. Moreover, ischaemic/norepinephrine preconditioning significantly reduced ischaemia-reperfusion-induced release of mast cell peroxidase (MPO), a marker of mast cell degranulation. Prazosin (0.1 microm), a alpha(1)adrenoceptor blocker, administered during ischaemic/norepinephrine preconditioning attenuated the cardioprotective and antiarrhythmic effect of ischaemic/norepinephrine preconditioning. MPO release increased immediately after ischaemic/norepinephrine preconditioning and the release was found to be inhibited in hearts subjected to ischaemic/norepinephrine preconditioning in the presence of prazosin. However, prazosin (0.1 microm) treatment per se produced cardioprotective and antiarrhythmic effects and reduced ischaemia-reperfusion-induced MPO release. These findings tentatively suggest that ischaemic preconditioning produced cardioprotective and antiarrhythmic effect by activating alpha(1)adrenoceptors and consequent degranulation of cardiac mast cells. Prazosin administered during ischaemic preconditioning abolished its ameliorative effect.
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PMID:Possible role of adrenergic component and cardiac mast cell degranulation in preconditioning-induced cardioprotection. 1043 71

Our study is designed to correlate nitrite concentration, an index of nitric oxide (NO) release with mast cell peroxidase (MPO), a marker of cardiac mast cell degranulation and cardioprotective effect of ischaemic preconditioning in isolated perfused rat heart subjected to 30 min of global ischaemia and 30 min of reperfusion. Ischaemic preconditioning, comprised of four episodes of 5 min global ischaemia and 5 min of reperfusion, markedly reduced the release of lactate dehydrogenase (LDH) and creatine kinase (CK) in coronary effluent and incidence of ventricular premature beats (VPBs) and ventricular tachycardia and fibrillation (VT/VF) during reperfusion phase. Ischaemia-reperfusion induced release of MPO was markedly reduced in ischaemic preconditioned hearts. Increased release of nitrite was noted during reperfusion phase after sustained ischaemia in preconditioned hearts as compared to control hearts. No alterations in the release of nitrite was observed immediately after ischaemic preconditioning. However, ischaemic preconditioning markedly increased the release of MPO prior to global ischaemia. It is proposed that cardioprotective and antiarrhythmic effect of ischaemic preconditioning may be ascribed to degranulation of cardiac mast cells. Depletion of cytotoxic mediators during ischaemic preconditioning and consequent decreased release of these mediators during sustained ischaemia-reperfusion may be associated with preservation of structures in isolated rat heart responsible for NO release.
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PMID:Possible role of cardiac mast cell degranulation and preservation of nitric oxide release in isolated rat heart subjected to ischaemic preconditioning. 1054 45


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