Myeloperoxidase Activity as a Quantitative Marker of Polymorphonuclear Leukocyte Accumulation into an Experimental Myocardial Infarct—The Effect of Ibuprofen on Infarct Size and Polymorphonuclear Leukocyte Accumulation

Allan, Geoffrey; Bhattacherjee, P.; Brook, Christopher; Read, Nicholas G.; Parke, A

doi:10.1097/00005344-198511000-00022

Cited by 68 publications

(36 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Myeloperoxidase activity in tissues has been shown to correlate directly with the number ofneutrophils present (Allan et al 1985) and the data reported here indicate that the neutrophil content of the reperfused muscles would be increased (Table 3). Howevcr, such an increase was prevented by all of the compounds tested.…”

Section: Discussionsupporting

confidence: 59%

Ischemia-reperfusion-induced muscle damage: Protective effect of corticosteroids and antioxidants in rabbits

Bushell

Klenerman

Davies

et al. 1996

Acta Orthopaedica Scandinavica

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 59%

Ischemia-reperfusion-induced muscle damage: Protective effect of corticosteroids and antioxidants in rabbits

Bushell

Klenerman

Davies

et al. 1996

Acta Orthopaedica Scandinavica

View full text Add to dashboard Cite

“…MPO activity was assayed according to methods by Allan et al (1). Change in absorbance at 460 nm was monitored with a spectrophotometer, with 1 unit of MPO defined as that yielding a change in absorbance of 1.0 and expressed as units per gram of wet weight.…”

Section: Methodsmentioning

confidence: 99%

Xanthine oxidase and activated neutrophils cause oxidative damage to skeletal muscle after contractile claudication

Judge

Dodd

2004

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Judge, A. R., and S. L. Dodd. Xanthine oxidase and activated neutrophils cause oxidative damage to skeletal muscle after contractile claudication. Am J Physiol Heart Circ Physiol 286: H252-H256, 2004. First published September 11, 2003 10.1152/ajpheart.00684. 2003.-We previously showed oxidative damage and edema within skeletal muscle after contractile claudication. To investigate the sources of this oxidative damage in the gastrocnemius muscle, we administered allopurinol (Allo, to inhibit xanthine oxidase) and cyclophosphamide (Cyclo, to deplete neutrophils) before inducing contractile claudication in male Sprague Dawley rats. Contractile claudication (ligated stimulated, LS) caused a significant increase in xanthine oxidase activity [sham ligated stimulated (SS) ϭ 2.57 Ϯ 0.07; LS ϭ 3.22 Ϯ 0.07] and neutrophil infiltration (SS ϭ 0.47 Ϯ 0.03; LS ϭ 0.91 Ϯ 0.10) compared with controls (SS), and this was associated with increased lipid peroxidation, protein oxidation, muscle damage, and edema. Pretreatment with Allo attenuated the increase in xanthine oxidase activity and attenuated lipid hydroperoxides (control LS ϭ 12.85 Ϯ 0.50; Allo LS ϭ 9.96 Ϯ 0.71), muscle damage, and neutrophil infiltration (control LS ϭ 0.91 Ϯ 0.10; Allo LS ϭ 0.61 Ϯ 0.07). This latter finding suggests that xanthine oxidasederived oxidants are chemotactic to neutrophils. Pretreatment with Cyclo reduced neutrophil infiltration (control LS ϭ 0.91 Ϯ 0.10; Cyclo LS ϭ 0.55 Ϯ 0.02) and attenuated lipid peroxidation (control LS ϭ 12.85 Ϯ 0.50; Cyclo LS ϭ 6.462 Ϯ 0.62), protein oxidation (control LS ϭ 2.59 Ϯ 0.47; Cyclo LS ϭ 1.77 Ϯ 0.60), muscle damage, and edema. Together, these data indicate that contractile claudication causes an increase in xanthine oxidase activity and neutrophils in muscle and that inhibition of these oxidant sources protects against oxidative stress, muscle damage, and edema. occlusion; free radicals; reactive oxygen species; muscle contraction SEVERAL STUDIES HAVE SHOWN that ischemia-reperfusion (I/R) caused by exercise claudication elevates markers of oxidative damage in the plasma. Hickman et al. (16) exercised claudicant patients for 10 min and found an increase in plasma malondialdehyde levels after exercise, whereas Silvestro et al. (32) showed an increase in thiobarbituric acid-reactive substances, as a marker of lipid peroxidation, after maximal, but not submaximal, exercise in claudicants.Likewise, markers of oxidative damage are also elevated in skeletal muscle after claudication. We recently found (21) an increase in protein oxidation and lipid peroxidation and a reduction in total glutathione levels 1 h after exercise with an animal model of claudication. This was associated with an increase in xanthine oxidase activity and neutrophils-both sources of oxidizing species.To further explore these findings and determine the relative contributions of each pathway, we chose to 1) inhibit xanthine oxidase activity and 2) deplete neutrophils and then measure markers of oxidative damage. Thus the purpose of this study wa...

show abstract

“…In previous studies we have demonstrated that in anaesthetized dogs, coronary reperfusion following a I h period of occlusion results in salvage of ischaemic tissue with maximum infarct reduction occurring following 2 h of coronary reperfusion (Allan et al, 1985). Using this experimental protocol we have now demonstrated that by increasing the haemoglobinoxygen affinity with BW12C, and hence reducing oxygen delivery to the jeopardized myocardium, reperfusion salvage is compromised with the result that infarct size is dramatically increased.…”

Section: Discussionmentioning

confidence: 85%

“…A concentrated solution of Evans blue dye (approximately 30 ml) was administered systemically via the femoral vein, followed immediately by a saturated solution of potassium chloride to induce cardiac arrest. By using this procedure, all but the LAD coronary bed perfused with saline was stained blue, hence effectively demarcating the area at risk (Allan et al, 1985).…”

Section: Experimental Myocardial Infarction Studiesmentioning

confidence: 99%

“…Transmural extension of the infarct was commonly seen in myocardium nearer the apex of the heart, whereas epicardial involvement from the mid-myocardium to the base of the heart was negligible. The histological features of the myocardial infarction were essentially as previously described for experimentally induced infarcts in the dog (Allan et al, 1985). Briefly, the infarcted myocardium stained more intensely with eosin than the surrounding normal tissue and frequently showed prominent myofibrillar contraction bands and tissue oedema.…”

Section: Effects Of Bw12c On Myocardial Infarct Sizementioning

confidence: 99%

See 1 more Smart Citation

Effects of an increase in haemoglobin O₂ affinity produced by BW12C on myocardial function in the erythrocyte‐perfused rabbit heart in vitro and myocardial infarct size in the dog

Allan

Chapple

Hughes

1986

British J Pharmacology

View full text Add to dashboard Cite

1The effects of BW12C on myocardial function in the erythrocyte-perfused rabbit heart and on myocardial infarct size in the anaesthetized dog have been evaluated. 2 Perfusion of rabbit hearts with erythrocytes pretreated with BW12C (10-3 M-4 x 10-3 M) produced concentration-dependent decreases in left ventricular pressure (LVP), LVP dP/dt and coronary perfusion pressure. A concomitant decrease in Po2 and an increase in lactate production by the myocardium was also observed.3 Perfusion of rabbit hearts with Krebs Henseleit buffer containing BW12C (10-5_10-4 M) caused no change in measured variables. Although BW12C (I0-3 M) caused a small decrease in LVP, coronary perfusion pressure and heart rate, these changes were not significant. 4 In anaesthetized dogs, an infusion of BW12C (total dose 50mgkg-', i.v.) caused small, but significant, changes in haemodynamic status. The oxygen saturation curve was shifted to the left and relative % oxygenation (P20) was shifted to the left throughout the course of the experiment. (P20, control 16.3 ± 0.4 mmHg; after BW12C 7.9 ± 1.4 mmHg). 5 Pretreatment with BW12C (total dose 50mg kg ')caused no change in area at risk but significantly increased the myocardial infarct size by 410%. 6 These studies with BW12C demonstrate that alteration in haemoglobin-oxygen affinity can induce adaptive physiological changes in tissue function and metabolism and can assume a critical role when oxygen supply may be impaired due to a flow-limiting stenosis.

show abstract

Myeloperoxidase Activity as a Quantitative Marker of Polymorphonuclear Leukocyte Accumulation into an Experimental Myocardial Infarct—The Effect of Ibuprofen on Infarct Size and Polymorphonuclear Leukocyte Accumulation

Cited by 68 publications

References 0 publications

Ischemia-reperfusion-induced muscle damage: Protective effect of corticosteroids and antioxidants in rabbits

Ischemia-reperfusion-induced muscle damage: Protective effect of corticosteroids and antioxidants in rabbits

Xanthine oxidase and activated neutrophils cause oxidative damage to skeletal muscle after contractile claudication

Effects of an increase in haemoglobin O₂ affinity produced by BW12C on myocardial function in the erythrocyte‐perfused rabbit heart in vitro and myocardial infarct size in the dog

Contact Info

Product

Resources

About

Myeloperoxidase Activity as a Quantitative Marker of Polymorphonuclear Leukocyte Accumulation into an Experimental Myocardial Infarct—The Effect of Ibuprofen on Infarct Size and Polymorphonuclear Leukocyte Accumulation

Cited by 68 publications

References 0 publications

Ischemia-reperfusion-induced muscle damage: Protective effect of corticosteroids and antioxidants in rabbits

Ischemia-reperfusion-induced muscle damage: Protective effect of corticosteroids and antioxidants in rabbits

Xanthine oxidase and activated neutrophils cause oxidative damage to skeletal muscle after contractile claudication

Effects of an increase in haemoglobin O2 affinity produced by BW12C on myocardial function in the erythrocyte‐perfused rabbit heart in vitro and myocardial infarct size in the dog

Contact Info

Product

Resources

About

Effects of an increase in haemoglobin O₂ affinity produced by BW12C on myocardial function in the erythrocyte‐perfused rabbit heart in vitro and myocardial infarct size in the dog