PMID- 2171311
OWN - NLM
STAT- MEDLINE
DCOM- 19901105
LR  - 20190626
IS  - 0002-8703 (Print)
IS  - 0002-8703 (Linking)
VI  - 120
IP  - 4
DP  - 1990 Oct
TI  - DMPO and reperfusion injury: arrhythmia, heart function, electron spin resonance, 
      and nuclear magnetic resonance studies in isolated working guinea pig hearts.
PG  - 819-30
AB  - With the use of isolated working guinea pig hearts with normothermic global 
      ischemia, it was shown that 5,5-dimethyl-pirroline-N-oxide (DMPO), an organic 
      spin trap agent designed specifically to form stable adducts with oxygen free 
      radicals in electron spin resonance studies, can dramatically reduce the 
      vulnerability of the heart to reperfusion-induced arrhythmias. Studied in 
      concentrations ranging from 10 to 500 mumol/L, DMPO exerted a dose-dependent 
      protective effect. Thus, after 30 minutes of global ischemia, the incidence of 
      ventricular fibrillation (total) and tachycardia was reduced from control values 
      of 100% and 100% to 100% and 100%, 91% and 100%, 25% (p less than 0.001) and 50% 
      (p less than 0.05), and 25% (p less than 0.001) and 41% (p less than 0.05), 
      respectively, with DMPO concentrations of 10, 30, 100, and 500 mumol/L. Maximum 
      signals of DMPO-OH adduct, with the use of electron spin resonance studies, were 
      observed after 3 minutes of reperfusion in fibrillated hearts but were not 
      detected in nonfibrillated hearts. Results of nuclear magnetic resonance studies 
      of myocardial adenosine triphosphate, creatine phosphate, pH, and inorganic 
      phosphate showed that these parameters were not significantly changed by 
      treatment with DMPO, and consequently myocardial heart function was not improved, 
      although there was a dissociation between myocardial adenosine triphosphate 
      content and left ventricular developed pressure during reperfusion. The data 
      presented here indicate that oxygen free radicals play an important role in the 
      development of reperfusion-induced arrhythmias but trapping these cytotoxic free 
      radicals does not improve the recovery of postischemic heart function and 
      high-energy phosphate contents in isolated working guinea pig hearts.
FAU - Tosaki, A
AU  - Tosaki A
AD  - Institut Henri Beaufour, Les Ulis, France.
FAU - Braquet, P
AU  - Braquet P
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Am Heart J
JT  - American heart journal
JID - 0370465
RN  - 0 (Cyclic N-Oxides)
RN  - 0 (Free Radicals)
RN  - 0 (Phosphates)
RN  - 7170JZ1QF3 (5,5-dimethyl-1-pyrroline-1-oxide)
SB  - IM
MH  - Animals
MH  - Arrhythmias, Cardiac/etiology/*prevention & control
MH  - Cyclic N-Oxides/*therapeutic use
MH  - Electron Spin Resonance Spectroscopy
MH  - Free Radicals
MH  - Guinea Pigs
MH  - Hemodynamics/*drug effects
MH  - In Vitro Techniques
MH  - Magnetic Resonance Spectroscopy
MH  - Male
MH  - Myocardial Reperfusion Injury/complications/*drug therapy
MH  - Myocardium/chemistry
MH  - Phosphates/analysis
EDAT- 1990/10/01 00:00
MHDA- 1990/10/01 00:01
CRDT- 1990/10/01 00:00
PHST- 1990/10/01 00:00 [pubmed]
PHST- 1990/10/01 00:01 [medline]
PHST- 1990/10/01 00:00 [entrez]
AID - 0002-8703(90)90197-6 [pii]
AID - 10.1016/0002-8703(90)90197-6 [doi]
PST - ppublish
SO  - Am Heart J. 1990 Oct;120(4):819-30. doi: 10.1016/0002-8703(90)90197-6.