Shenlian extract protects against ultrafine particulate matter‐aggravated myocardial ischemic injury by inhibiting inflammation response via the activation of NLRP3 inflammasomes

2021 ◽  
Author(s):  
Shuiqing Qu ◽  
Kai Li ◽  
Ting Yang ◽  
Yuanmin Yang ◽  
Zhongyuzn Zheng ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Ischemic Injury ◽  
Inflammation Response ◽  
Myocardial Ischemic Injury ◽  
Ultrafine Particulate Matter ◽  
Nlrp3 Inflammasomes

Precordial S-T segment elevation mapping: An atraumatic method for assessing alterations in the extent of myocardial ischemic injury

1972 ◽  
Vol 29 (2) ◽  
pp. 223-230 ◽  
Author(s):  
Peter R. Maroko ◽  
Peter Libby ◽  
James W. Covell ◽  
Burton E. Sobel ◽  
John Ross ◽  
...  
Keyword(s):  
Ischemic Injury ◽  
Myocardial Ischemic Injury

Real-Time Prediction of Size-Resolved Ultrafine Particulate Matter on Freeways

2012 ◽  
Vol 46 (4) ◽  
pp. 2234-2241 ◽  
Author(s):  
Srijan Aggarwal ◽  
Ricky Jain ◽  
Julian D. Marshall
Keyword(s):  
Particulate Matter ◽  
Real Time ◽  
Time Prediction ◽  
Ultrafine Particulate Matter

A Novel nonpeptidic caspase-3/7 inhibitor, (S)-(+)-5-[1-(2-methoxymethylpyrrolidinyl)sulfonyl]isatin reduces myocardial ischemic injury

2002 ◽  
Vol 456 (1-3) ◽  
pp. 59-68 ◽  
Author(s):  
Justin G Chapman ◽  
William P Magee ◽  
Hans A Stukenbrok ◽  
Gretchen E Beckius ◽  
Anthony J Milici ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Ischemic Injury ◽  
Myocardial Ischemic Injury

Osmotic shock: modulation of contractile function, pHi, and ischemic damage in perfused guinea pig heart

1999 ◽  
Vol 276 (4) ◽  
pp. H1236-H1244 ◽  
Author(s):  
Douglas E. Befroy ◽  
Trevor Powell ◽  
George K. Radda ◽  
Kieran Clarke
Keyword(s):  
Nmr Spectroscopy ◽  
Guinea Pig ◽  
Intracellular Ph ◽  
Contractile Function ◽  
Osmotic Shock ◽  
Ischemic Injury ◽  
Ischemic Damage ◽  
Guinea Pig Heart ◽  
Myocardial Ischemic Injury ◽  
Developed Pressure

To determine the contribution of changes in extracellular osmolarity to ischemic injury, isolated guinea pig hearts were perfused with hyposmotic (220 mosM) or hyperosmotic (380 mosM) buffer.31P NMR spectroscopy was used to follow changes in intracellular pH (pHi) and energetics. Hyposmotic buffer decreased myocardial developed pressure by 30 ± 2% and pHi by 0.02 ± 0.01 unit, whereas hyperosmotic buffer increased myocardial developed pressure by 34 ± 1% and pHi by 0.14 ± 0.01 unit. All hearts recovered to control values on restoration of isosmotic (300 mosM) buffer. The hyperosmolar-induced intracellular alkalosis and developed pressure increase were not prevented by inhibition of Na+/H+exchange with use of 1 μM HOE-642 but were abolished with use of bicarbonate-free buffers. After 20 min of total global ischemia, hearts perfused with hyposmotic buffer showed significantly greater recoveries of developed pressure, phosphocreatine, and ATP than control hearts, but hearts perfused with hyperosmotic buffer did not recover after ischemia. In conclusion, buffer osmolarities between 220 and 380 mosM alter myocardial pHi and developed pressure but are not deleterious during perfusion. However, buffer osmolarity significantly alters the extent of myocardial ischemic injury.

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