scholarly journals Myocardial injection of a thermoresponsive hydrogel with reactive oxygen species scavenger properties improves border zone contractility

2020 ◽  
Vol 108 (8) ◽  
pp. 1736-1746
Author(s):  
Kimberly A. Spaulding ◽  
Yang Zhu ◽  
Kiyoaki Takaba ◽  
Anusuya Ramasubramanian ◽  
Anusha Badathala ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Border Zone ◽  
Oxygen Species ◽  
Thermoresponsive Hydrogel ◽  
Reactive Oxygen Species Scavenger

scholarly journals Reactive oxygen species scavenger N-acetyl cysteine reduces methamphetamine-induced hyperthermia without affecting motor activity in mice

Temperature ◽  
2014 ◽  
Vol 1 (3) ◽  
pp. 227-241 ◽  
Author(s):  
Manuel Sanchez-Alavez ◽  
Nikki Bortell ◽  
Andrea Galmozzi ◽  
Bruno Conti ◽  
Maria Cecilia G. Marcondes
Keyword(s):  
Reactive Oxygen Species ◽  
Motor Activity ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Induced Hyperthermia ◽  
Acetyl Cysteine ◽  
Reactive Oxygen Species Scavenger

Mechanisms of pulmonary vasoconstriction induced by chemotactic peptide FMLP in isolated rabbit lungs

1992 ◽  
Vol 72 (4) ◽  
pp. 1549-1556 ◽  
Author(s):  
H. Tanaka ◽  
J. D. Bradley ◽  
L. J. Baudendistel ◽  
T. E. Dahms
Keyword(s):  
Reactive Oxygen Species ◽  
Polymorphonuclear Leukocytes ◽  
Reactive Oxygen ◽  
Cyclooxygenase Inhibitors ◽  
Oxygen Species ◽  
Chemotactic Peptide ◽  
Middle Segment ◽  
Pulmonary Vasoconstriction ◽  
Lipoxygenase Products ◽  
Reactive Oxygen Species Scavenger

The chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine (FMLP) has been shown to constrict both bronchial and coronary vascular smooth muscle through the action of cyclooxygenase or lipoxygenase products. We observed that intravenous FMLP increased pulmonary vascular resistance (PVR) in isolated buffer-perfused rabbit lungs. FMLP increased the PVR (primarily in the middle segment of the pulmonary vascular bed) at concentrations greater than or equal to 10(-7) M. Maximum vasoconstriction occurred at 5 min and then slowly declined to a level that remained above baseline at 30 min. Tachyphylaxis was observed in response to FMLP. When polymorphonuclear leukocytes (PMNs) were added to the perfusate, FMLP caused a greater increase in PVR. PMN depletion with dimethylmyleran significantly reduced the PVR response to FMLP. Pretreatment with two dissimilar cyclooxygenase inhibitors, meclofenamate and ibuprofen, and the leukotriene synthesis blocker MK 886 had no effect on the FMLP-induced vasoconstriction. However, the reactive oxygen species scavenger catalase significantly reduced the vasoconstriction. These results suggest that FMLP induces vasoconstriction that is dependent on PMNs and mediated by reactive oxygen species with no involvement of cyclooxygenase or lipoxygenase products.

scholarly journals The pH Hypothesis of Postconditioning

Circulation ◽  
2007 ◽  
Vol 115 (14) ◽  
pp. 1895-1903 ◽  
Author(s):  
Michael V. Cohen ◽  
Xi-Ming Yang ◽  
James M. Downey
Keyword(s):  
Reactive Oxygen Species ◽  
Mitochondrial Permeability Transition ◽  
Reactive Oxygen ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Oxygen Species ◽  
Risk Zone ◽  
Kinase C ◽  
Protective Signaling ◽  
Reactive Oxygen Species Scavenger

Background— It is unclear how reperfusion of infarcting hearts with alternating cycles of coronary reperfusion/occlusion attenuates infarction, but prevention of mitochondrial permeability transition pore (MPTP) formation is crucial. Acidosis also suppresses MPTP formation. We tested whether postconditioning protects by maintaining acidosis during early reoxygenation. Methods and Results— After 30-minute regional ischemia in isolated rabbit hearts, reperfusion with buffer (pH 7.4) caused 34.4±2.2% of the risk zone to infarct, whereas 2 minutes of postconditioning (6 cycles of 10-second reperfusion/10-second occlusion) at reperfusion resulted in 10.7±2.9% infarction. One minute (3 cycles) of postconditioning was not protective. Hypercapnic buffer (pH 6.9) for the first 2 minutes of reperfusion in lieu of postconditioning caused equivalent cardioprotection (15.0±2.6% infarction), whereas 1 minute of acidosis did not protect. Delaying postconditioning (6 cycles) or 2 minutes of acidosis for 1 minute aborted protection. Reperfusion with buffer (pH 7.7) blocked postconditioning protection, but addition of the MPTP closer cyclosporin A restored protection. Reactive oxygen species scavenger N-2-mercaptopropionyl glycine, protein kinase C antagonist chelerythrine, and mitochondrial K ATP channel closer 5-hydroxydecanoate each blocked protection from 2 minutes of acidosis as they did for postconditioning. Conclusion— Thus, postconditioning prevents MPTP formation by maintaining acidosis during the first minutes of reperfusion as reoxygenated myocardium produces reactive oxygen species that activate protective signaling to inhibit MPTP formation after pH normalization.

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