Title: Taurine protects the heart from neutrophil-induced reperfusio=
n
injury.
Title Abbreviation: Free Radic Biol Med Date of Pub: 1995 Oct
Author: Raschke P; Massoudy P; Becker BF;
Issue/Part/Supplement: 4 Volume Issue: Pagination: 461-71
19
MESH Headings: Animal; Antioxidants (*TU); Chemiluminescence; Corona=
ry
Vessels; Glutathione (BL); Guinea Pigs; Heart (DE/PH); Lactates (BL)=
;
Luminol (PD); Male; Myocardial Reperfusion Injury (*PC); Neutrophils
(DE/*PH); Oxidation-Reduction; Respiratory Burst (DE); Support, Non-=
U.S.
Gov't; Taurine (PD/*TU); -RN-;
Journal Title Code: FRE Publication Type: JOURNAL ARTICLE
Date of Entry: 951208N Entry Month: 9602
Country: UNITED STATES Index Priority: 2
Language: Eng Unique Identifier: 96015029
Unique Identifier:
96015029 ISSN: 0891-5849
Abstract: Deficiency of the amino acid taurine is implicated in vari=
ous
pathologic states of the heart. Besides other effects, taurine has b=
een
proposed to be an antioxidant. However, its benefit under conditions
associated with the generation of reactive oxygen species in the hea=
rt has
not been clearly demonstrated. To assess the potential of taurine to
influence neutrophil-dependent reperfusion injury, a model was devel=
oped
based on the isolated working guinea pig heart. After an initial wor=
k
phase, hearts were subjected to 15 min of global ischemia. Reperfusi=
on, in
a nonworking mode, was carried out in the absence or presence of
homologous neutrophils (PMN) and/or taurine. After 15 min, work was
resumed and percentage recovery of function was determined another 2=
0 min
later. During the reperfusion phase, coronary venous effluent was
collected to quantify release of lactate and glutathione, markers of
ischemic challenge and redox-stress, respectively. Furthermore, dire=
ct
effects of taurine on radical formation were investigated in a
chemiluminescence assay. Control hearts without application of PMN o=
r
taurine had a postischemic recovery of external heart work (EHW) of =
76%,
in the presence of taurine (15 mM) recovery was 72%. The application=
of
PMN for merely the first minute of reperfusion led to a significant
decrease in recovery to 30%, PMN having no effect without a foregoin=
g
ischemia. When taurine was additionally applied during reperfusion, =
EHW
recovered to 60%. Release of lactate and of oxidized glutathione (GS=
SG)
did not differ between the groups. In contrast, effluent concentrati=
ons of
reduced glutathione (GSH) were considerably elevated by the presence=
of
PMN in the sample and remained high even after PMN-washout. Taurine =
tended
to attenuate this PMN effect. At the 5th and 10th min of reperfusion=
, GSH
release of individual hearts correlated inversely with postischemic
recovery of EHW. Surprisingly, taurine, by itself, did not significa=
ntly
alter glutathione release. However, taurine (15 mM) markedly reduced
luminol-dependent chemiluminescence elicited by activated guinea pig=
PMN
as well as by chemically generated hypochlorous acid and hydroxyl
radicals, but not superoxide radicals. Our results demonstrate that
taurine protects the heart from PMN-induced reperfusion injury and
oxidative stress. Because respiratory burst activity of PMN was also
significantly reduced in the presence of taurine, the beneficial eff=
ect
appears to be mediated by antioxidative properties of taurine.
Abstract By: Author
Address: Physiologisches Institut, Universit=E4t M=FCnchen, Germany.
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