Abstract
The feasibility of polymorphonuclear leucocytes as a potential source of free radicals during reperfusion of ischaemic myocardium was evaluated. Isolated rat heart was perfused in the presence of f-Met-Leu-Phe-activated and normal polymorphonuclear leucocytes for 30min. To Judge the degree of cellular injury which might result from activated polymorphonuclear leucocytes during per fusion, isolated hearts were also perfused with superoxide onions, hydroxyl radicals, and hypochlorous acid-generating systems in the absence or presence of their corresponding scavengers, superoxide dismutase plus catalase, dimethylthiourea, and allo-purinol, respectively. Activated polymorphonuclear leucocytes stimulated the release of lactate dehydro-genase, a biological marker of cellular injury, and malondialdehyde, a presumptive marker for lipid peroxidation; increased tissue injury, as evidenced by morphologic examinations using light and electron microscopy; decreased dryjwet ratios of heart, signifying oedema formation; and reduced myocardial adenosine triphosphate and creatine phosphate content as well as coronary flow, indicating decreased myocardial performance. These biological, physiological, and morphologic parameters were reversed significantly, but not completely, by treating the heart with scavengers, superoxide dismutase plus catalase or allopurinol, but were reversed completely by simultaneous treatment with superoxide dismutase, catalase, and allopurinol. Comparable results were obtained when the hearts were treated with each of these free radical-generating systems and their corresponding scavengers. Generation of free radicals was confirmed either by cytochrome c reduction or by examining the chemiluminescence response using a luminometer. These results indicate that activated polymorphonuclear leucocytes can cause myocardial cellular injury equivalent to the damage caused by free radicals and oxidants which are present in an ischaemic-reperfused heart, suggesting that polymorphonuclear leucocytes may be a potential source of free radicals in the reperf used heart.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 800-813 |
| Number of pages | 14 |
| Journal | European Heart Journal |
| Volume | 11 |
| Issue number | 9 |
| DOIs | |
| State | Published - Jan 1 1990 |
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Keywords
- Free radical
- Heart
- Ischaemia
- Polymorphonuclear leucocytes
- Reperfusion injury
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
Cite this
Polymorphonuclear leucocytes as potential source of free radicals in the ischaemic-reperfused myocardium. / Bagchi, D.; Das, D. K.; Engelman, R. M.; Prasad, M. R.; Subramanian, Ramiah.
In: European Heart Journal, Vol. 11, No. 9, 01.01.1990, p. 800-813.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Polymorphonuclear leucocytes as potential source of free radicals in the ischaemic-reperfused myocardium
AU - Bagchi, D.
AU - Das, D. K.
AU - Engelman, R. M.
AU - Prasad, M. R.
AU - Subramanian, Ramiah
PY - 1990/1/1
Y1 - 1990/1/1
N2 - The feasibility of polymorphonuclear leucocytes as a potential source of free radicals during reperfusion of ischaemic myocardium was evaluated. Isolated rat heart was perfused in the presence of f-Met-Leu-Phe-activated and normal polymorphonuclear leucocytes for 30min. To Judge the degree of cellular injury which might result from activated polymorphonuclear leucocytes during per fusion, isolated hearts were also perfused with superoxide onions, hydroxyl radicals, and hypochlorous acid-generating systems in the absence or presence of their corresponding scavengers, superoxide dismutase plus catalase, dimethylthiourea, and allo-purinol, respectively. Activated polymorphonuclear leucocytes stimulated the release of lactate dehydro-genase, a biological marker of cellular injury, and malondialdehyde, a presumptive marker for lipid peroxidation; increased tissue injury, as evidenced by morphologic examinations using light and electron microscopy; decreased dryjwet ratios of heart, signifying oedema formation; and reduced myocardial adenosine triphosphate and creatine phosphate content as well as coronary flow, indicating decreased myocardial performance. These biological, physiological, and morphologic parameters were reversed significantly, but not completely, by treating the heart with scavengers, superoxide dismutase plus catalase or allopurinol, but were reversed completely by simultaneous treatment with superoxide dismutase, catalase, and allopurinol. Comparable results were obtained when the hearts were treated with each of these free radical-generating systems and their corresponding scavengers. Generation of free radicals was confirmed either by cytochrome c reduction or by examining the chemiluminescence response using a luminometer. These results indicate that activated polymorphonuclear leucocytes can cause myocardial cellular injury equivalent to the damage caused by free radicals and oxidants which are present in an ischaemic-reperfused heart, suggesting that polymorphonuclear leucocytes may be a potential source of free radicals in the reperf used heart.
AB - The feasibility of polymorphonuclear leucocytes as a potential source of free radicals during reperfusion of ischaemic myocardium was evaluated. Isolated rat heart was perfused in the presence of f-Met-Leu-Phe-activated and normal polymorphonuclear leucocytes for 30min. To Judge the degree of cellular injury which might result from activated polymorphonuclear leucocytes during per fusion, isolated hearts were also perfused with superoxide onions, hydroxyl radicals, and hypochlorous acid-generating systems in the absence or presence of their corresponding scavengers, superoxide dismutase plus catalase, dimethylthiourea, and allo-purinol, respectively. Activated polymorphonuclear leucocytes stimulated the release of lactate dehydro-genase, a biological marker of cellular injury, and malondialdehyde, a presumptive marker for lipid peroxidation; increased tissue injury, as evidenced by morphologic examinations using light and electron microscopy; decreased dryjwet ratios of heart, signifying oedema formation; and reduced myocardial adenosine triphosphate and creatine phosphate content as well as coronary flow, indicating decreased myocardial performance. These biological, physiological, and morphologic parameters were reversed significantly, but not completely, by treating the heart with scavengers, superoxide dismutase plus catalase or allopurinol, but were reversed completely by simultaneous treatment with superoxide dismutase, catalase, and allopurinol. Comparable results were obtained when the hearts were treated with each of these free radical-generating systems and their corresponding scavengers. Generation of free radicals was confirmed either by cytochrome c reduction or by examining the chemiluminescence response using a luminometer. These results indicate that activated polymorphonuclear leucocytes can cause myocardial cellular injury equivalent to the damage caused by free radicals and oxidants which are present in an ischaemic-reperfused heart, suggesting that polymorphonuclear leucocytes may be a potential source of free radicals in the reperf used heart.
KW - Free radical
KW - Heart
KW - Ischaemia
KW - Polymorphonuclear leucocytes
KW - Reperfusion injury
UR - http://www.scopus.com/inward/record.url?scp=0025082336&partnerID=8YFLogxK
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U2 - 10.1093/oxfordjournals.eurheartj.a059800
DO - 10.1093/oxfordjournals.eurheartj.a059800
M3 - Article
VL - 11
SP - 800
EP - 813
JO - European Heart Journal
JF - European Heart Journal
SN - 0195-668X
IS - 9
ER -