Reactive oxygen metabolite scavengers decrease functional coronary microvascular injury due to ischemia-reperfusion

1991 ◽  
Vol 260 (1) ◽  
pp. H42-H49
Author(s):  
I. M. Dauber ◽  
E. J. Lesnefsky ◽  
K. M. VanBenthuysen ◽  
J. V. Weil ◽  
L. D. Horwitz
Keyword(s):  
Blood Flow ◽  
Vascular Function ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Microvascular Dysfunction ◽  
Regional Myocardial Blood Flow ◽  
Coronary Microvascular Dysfunction ◽  
Reactive Oxygen Metabolites ◽  
Reactive Oxygen Metabolite ◽  
Microvascular Injury

The role of reactive oxygen metabolites in ischemia-reperfusion coronary microvascular injury is unclear. To investigate this problem, we tested the effects of the reactive oxygen metabolite scavengers superoxide dismutase (SOD) and dimethylthiourea (DMTU) on ischemia-reperfusion-induced coronary microvascular dysfunction. As an index of vascular function, we assessed microvascular permeability with a double radioisotope protein leak index (PLI) method. Anesthetized dogs underwent 60 min of ischemia via left anterior descending (LAD) occlusion followed by 60 min of reperfusion. Untreated animals (n = 7) received saline. SOD-treated animals (n = 6) received 140 U.kg-1.min-1 (6.6 mg.kg-1.min-1) bovine SOD throughout ischemia and reperfusion. DMTU-treated animals (n = 5) received a 500 mg/kg bolus 30 min before ischemia. At the beginning of reperfusion, radiolabeled autologous protein (113mIn transferrin) and red blood cells (99mTc) were given intravenously for the assessment of permeability. In untreated dogs, ischemia-reperfusion increased the PLI of ischemic (flow less than 20 ml.min-1.100 g-1) myocardium more than threefold compared with that of nonischemic (flow greater than 100 ml.min-1.100 g-1) myocardium (ischemic-to-nonischemic PLI ratio = 3.49 +/- 0.48). SOD reduced the PLI of ischemic myocardium by 45% and DMTU reduced it by 66% (PLI = 9.25 +/- 1.30, 5.04 +/- 1.18, and 3.16 +/- 0.94, untreated, SOD, and DMTU, respectively). The PLI was increased proportional to the regional severity of ischemic blood flow. Both SOD and DMTU reduced the increase in protein leak at all levels of regional ischemic blood flow. Neither SOD nor DMTU increased regional myocardial blood flow to the occluded LAD zone.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Redox Homeostasis and Metabolic Profile in Young Female Basketball Players during In-Season Training

Healthcare ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 368
Author(s):  
Rosamaria Militello ◽  
Simone Luti ◽  
Matteo Parri ◽  
Riccardo Marzocchini ◽  
Riccardo Soldaini ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Capacity ◽  
Training Session ◽  
Reactive Oxygen ◽  
Enzyme Linked Immunosorbent Assay ◽  
Reactive Oxygen Metabolites ◽  
Oxidative Stress Markers ◽  
Basketball Players ◽  
Reactive Oxygen Metabolite ◽  
Stress Markers

Background: Most studies on oxidative stress markers and antioxidant levels have been conducted in male athletes, although female participation in sport has increased rapidly in the past few decades. In particular, it could be important to assess oxidative stress markers in relation to the training load because the anaerobic path becomes predominant in high-intensity actions. Methods: Ten female professional basketball players, performing five 2 h-lasting training sessions per week, and 10 sedentary control women were investigated. Capillary blood and saliva samples were collected in the morning before the training session. The antioxidant capacity and the levels of reactive oxygen metabolites on plasma were determined measuring Reactive Oxygen Metabolite and Biological Antioxidant Potential (d-ROMs and the BAP Test). Salivary cortisol was detected by using commercial enzyme-linked immunosorbent assay kit. Results: The antioxidant capacity (BAP value) was significantly higher in elite basketball players (21.2%; p < 0.05). Conversely, cortisol (51%; p < 0.009) and the levels of oxidative species (d-ROM, 21.9%; p < 0.05) showed a significant decrease in elite athletes.

Beneficial actions of superoxide dismutase and catalase in stunned myocardium of dogs

1986 ◽  
Vol 250 (3) ◽  
pp. H372-H377 ◽  
Author(s):  
G. J. Gross ◽  
N. E. Farber ◽  
H. F. Hardman ◽  
D. C. Warltier
Keyword(s):  
Blood Flow ◽  
Superoxide Dismutase ◽  
Free Radicals ◽  
Oxygen Free Radicals ◽  
Ischemia Reperfusion ◽  
Free Radical Scavengers ◽  
Stunned Myocardium ◽  
Regional Myocardial Blood Flow ◽  
Control Group ◽  
Myocardial Segment

Recent evidence suggests that oxygen free radicals may partially mediate irreversible ischemia-reperfusion injury in the myocardium. In the present study, the effect of a combination of two oxygen free radical scavengers, superoxide dismutase plus catalase (SOD + CAT), on the recovery of subendocardial segment function following 15 min of coronary artery occlusion followed by 3 h of reperfusion ("stunned" myocardium) was compared with a control group in barbital-anesthetized dogs. Myocardial segment shortening (%SS) in the subendocardium of nonischemic and ischemic areas was measured by sonomicrometry and regional blood flow by radioactive microspheres. SOD and CAT were infused into the left atrium 30 min before and throughout the occlusion period. Compared with the control group, %SS in the subendocardium of the ischemic region was significantly (P less than 0.05) greater in the SOD plus CAT-treated group during occlusion and throughout reperfusion. Since there were no significant differences in hemodynamics or regional myocardial blood flow between the SOD plus CAT and the control groups, these results suggest that toxic oxygen free radicals may be partially involved in the reversible ischemic injury that occurs during short periods of coronary occlusion followed by reperfusion.

Microvascular ischemia-reperfusion injury in striated muscle: significance of "no reflow"

1992 ◽  
Vol 263 (6) ◽  
pp. H1892-H1900 ◽  
Author(s):  
M. D. Menger ◽  
D. Steiner ◽  
K. Messmer
Keyword(s):  
Shear Rate ◽  
Striated Muscle ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Capillary Density ◽  
Wall Shear Rate ◽  
Reactive Oxygen Metabolites ◽  
Capillary Perfusion ◽  
No Reflow ◽  
Oxygen Metabolites

“No reflow” has been implicated as prominent phenomenon in microvascular injury associated with ischemia-reperfusion (I/R). The objectives of this study were 1) to elucidate the significance of no reflow in microvascular I/R injury of striated muscle and 2) to determine whether reactive oxygen metabolites play a role in the development of postischemic no reflow. By use of the hamster dorsal skinfold preparation and intravital microscopy, microvascular perfusion of capillaries and postcapillary venules of striated muscle was quantitatively assessed before and 30 min, 2 h, and 24 h after 4 h of tourniquet-induced ischemia. I/R was characterized by a significant reduction (P < 0.01) in functional capillary density to 35% of baseline values during initial reperfusion, with incomplete recovery after 24 h (n = 9). In addition, capillary perfusion was found to be extremely heterogeneous, and wall shear rate in postcapillary venules was significantly decreased (P < 0.01). Treatment with either superoxide dismutase (SOD; n = 9) or allopurinol (n = 9) resulted in maintenance of capillary density of 60% of baseline (P < 0.05). Furthermore, I/R-induced capillary perfusion inhomogeneities and decrease of wall shear rate in venules were attenuated significantly (P < 0.01) by SOD and allopurinol. Thus part of capillary perfusion disturbances during I/R in striated muscle may be caused by increased postcapillary vascular resistance, probably mediated by reactive oxygen metabolites. However, the fact that in SOD- and allopurinol-treated animals 40% of the capillaries were still found to be nonperfused indicates that mechanisms other than oxygen radicals play an important role in the development of postischemic no reflow.

Microvascular ischemia-reperfusion injury in striated muscle: significance of "reflow paradox"

1992 ◽  
Vol 263 (6) ◽  
pp. H1901-H1906 ◽  
Author(s):  
M. D. Menger ◽  
S. Pelikan ◽  
D. Steiner ◽  
K. Messmer
Keyword(s):  
Striated Muscle ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Microvascular Permeability ◽  
Leukocyte Rolling ◽  
Reactive Oxygen Metabolites ◽  
Oxygen Metabolites ◽  
Reflow Paradox

Ischemia-reperfusion (I/R)-induced microvascular injury is characterized by capillary “no-reflow” and reflow-associated events, termed “reflow paradox,” including leukocyte-endothelium interaction and increase in microvascular permeability. The major objectives of this study were 1) to elucidate the significance of reflow paradox after 4 h of tourniquet-induced ischemia in striated muscle and 2) to determine the role of reactive oxygen metabolites in the pathogenesis of reflow paradox-dependent microcirculatory alterations. By use of in vivo fluorescence microscopy in a striated muscle preparation of hamsters, leukocyte-endothelium interaction in postcapillary venules and macromolecular extravasation from capillaries and venules were quantified before ischemia and after 30 min, 2 h, and 24 h of reperfusion. I/R elicited marked enhancement (P < 0.01) of leukocyte rolling during initial reperfusion and a 20-fold increase of leukocyte adherence (P < 0.01) lasting for the entire postischemic reperfusion period (n = 7). These phenomena were accompanied by significant leakage (P< 0.01) of macromolecules from capillaries and in particular from postcapillary venules (n = 9). Both superoxide dismutase (SOD, 20 mg/kg body wt, n = 7) and allopurinol (50 mg/kg body wt, n = 7) were effective in attenuating I/R-induced leukocyte rolling and adherence. In addition, microvascular leakage was significantly reduced by allopurinol (n = 9) and completely abolished by SOD (n = 9) (P < 0.01). These results support the concept that reactive oxygen metabolites contribute to I/R-induced reflow paradox, resulting in leukocyte accumulation, adherence, and increase in microvascular permeability.

n-3 fatty acids increase postischemic blood flow but do not reduce myocardial necrosis

1989 ◽  
Vol 257 (4) ◽  
pp. H1204-H1210 ◽  
Author(s):  
T. Force ◽  
C. D. Malis ◽  
J. L. Guerrero ◽  
G. S. Varadarajan ◽  
J. V. Bonventre ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Blood Flow ◽  
Polyunsaturated Fatty Acids ◽  
Myocardial Blood Flow ◽  
Fish Oil ◽  
Infarct Size ◽  
Ischemia Reperfusion ◽  
Saturated Fatty Acids ◽  
Regional Myocardial Blood Flow ◽  
Acute Ischemia

The effects of a fish oil-supplemented diet on infarct size and regional myocardial blood flow were examined in a rat model of acute ischemia followed by reperfusion. Thirty-five rats were fed a diet containing 20% by weight: fish oil (FO), rich in n-3 polyunsaturated fatty acids; corn oil (CO), with predominantly n-6 polyunsaturated fatty acids; or beef tallow (BT), containing large amounts of saturated fatty acids. After 6-12 wk on the diet, animals underwent 40 min of left coronary artery occlusion followed by 2 h of reperfusion. Regional transmural myocardial blood flow was determined with radioactive microspheres at 30 min of occlusion and again 30 min after reperfusion. Infarct size was determined with triphenyltetrazolium chloride. Blood flow was virtually undetectable within the ischemic zone in all groups during occlusion. With reperfusion, however, ischemic zone absolute blood flow and relative flow (normalized to nonischemic zone flow) were significantly greater in the fish oil group [2.4 +/- 0.25 ml.min-1.g-1, 44 +/- 4% vs. 1.7 +/- 0.3, 29 +/- 5% for CO (P less than 0.05 vs. FO), and 1.4 +/- 0.3, 29 +/- 5% for BT (P less than 0.05 vs. FO)]. Despite differences in reperfusion blood flow, average percent transmural extent of infarction was nearly identical (68 +/- 4, 68 +/- 5, and 64 +/- 3%) and overall infarct size was similar (38 +/- 3, 36 +/- 4, and 29 +/- 3%) for FO, CO, and BT groups, respectively. In conclusion, dietary supplementation with fish oils increases postischemic blood flow but has no effect on extent of myocardial infarction in this ischemia-reperfusion model in rats.

Myocardial hibernation: a delicate balance

2005 ◽  
Vol 288 (3) ◽  
pp. H984-H999 ◽  
Author(s):  
Gerd Heusch ◽  
Rainer Schulz ◽  
Shahbudin H. Rahimtoola
Keyword(s):  
Blood Flow ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Hibernating Myocardium ◽  
Regional Myocardial Blood Flow ◽  
Regional Energy ◽  
Myocardial Hibernation ◽  
Normal Blood Flow ◽  
Myocardial Ischemia Reperfusion ◽  
Regional Contractile Function

The pathophysiology of myocardial hibernation is characterized as a situation of reduced regional contractile function distal to a coronary artery stenosis that recovers after removal of the coronary stenosis. A subacute “downregulation” of contractile function in response to reduced regional myocardial blood flow exists, which normalizes regional energy and substrate metabolism but does not persist for more than 12–24 h. Chronic hibernation develops in response to one or more episodes of myocardial ischemia-reperfusion, possibly progressing from repetitive stunning with normal blood flow to hibernation with reduced blood flow. An upregulation of a protective gene program is seen in hibernating myocardium, putting it into the context of preconditioning. The morphology of hibernating myocardium is characterized by both adaptive and degenerative features.

scholarly journals Coronary microvascular dysfunction in diabetes mellitus

2017 ◽  
Vol 45 (6) ◽  
pp. 1901-1929 ◽  
Author(s):  
Aleksandar Kibel ◽  
Kristina Selthofer-Relatic ◽  
Ines Drenjancevic ◽  
Tatjana Bacun ◽  
Ivica Bosnjak ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Blood Flow ◽  
Endothelial Dysfunction ◽  
Microvascular Dysfunction ◽  
Coronary Microcirculation ◽  
Coronary Microvascular Dysfunction ◽  
Local Blood Flow ◽  
Physiological Processes ◽  
Wide Range ◽  
Vascular Beds

The significance, mechanisms and consequences of coronary microvascular dysfunction associated with diabetes mellitus are topics into which we have insufficient insight at this time. It is widely recognized that endothelial dysfunction that is caused by diabetes in various vascular beds contributes to a wide range of complications and exerts unfavorable effects on microcirculatory regulation. The coronary microcirculation is precisely regulated through a number of interconnected physiological processes with the purpose of matching local blood flow to myocardial metabolic demands. Dysregulation of this network might contribute to varying degrees of pathological consequences. This review discusses the most important findings regarding coronary microvascular dysfunction in diabetes from pre-clinical and clinical perspectives.

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