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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