title: Intracoronary infusion of reduced glutathione improves endothelial vasomotor response to acetylcholine in human coronary circulation.
abstract: BACKGROUND
  Oxygen free radicals have been shown to cause endothelial vasomotor dysfunction. This study examined the effect of reduced glutathione (GSH), an antioxidant, on human coronary circulation.
  
  
  RESULTS
  Responses of epicardial diameter and blood flow of the left anterior descending coronary artery to intracoronary infusion of acetylcholine (ACh, 50 microg/min) were measured by quantitative coronary angiography and Doppler flow-wire technique, respectively, before and during combined intracoronary infusion of GSH (50 mg/min) or saline in 26 subjects with no significant coronary stenosis. GSH infusion suppressed the constrictor response of epicardial diameter to ACh and enhanced the increase in blood flow response to ACh. Furthermore, GSH potentiated the coronary dilator effect of nitroglycerin. A beneficial effect of GSH on the epicardial diameter response to ACh was observed in a subgroup of subjects with > or = 1 coronary risk factors but not in a subgroup without risk factors. Saline infusion did not have any effects.
  
  
  CONCLUSIONS
  The results indicate that GSH improved coronary endothelial vasomotor function, particularly in subjects with coronary risk factors, and it potentiated the vasodilator effect of nitroglycerin in human coronary arteries.
authors.affiliation: Division of Cardiology, Kumamoto University School of Medicine, Kumamoto City, Japan. kiyo@gpo.kumamoto-u.ac.jp
authors.forename: K
authors.initials: K
authors.lastname: Kugiyama
authors.forename: M
authors.initials: M
authors.lastname: Ohgushi
authors.forename: T
authors.initials: T
authors.lastname: Motoyama
authors.forename: O
authors.initials: O
authors.lastname: Hirashima
authors.forename: H
authors.initials: H
authors.lastname: Soejima
authors.forename: K
authors.initials: K
authors.lastname: Misumi
authors.forename: M
authors.initials: M
authors.lastname: Yoshimura
authors.forename: H
authors.initials: H
authors.lastname: Ogawa
authors.forename: S
authors.initials: S
authors.lastname: Sugiyama
authors.forename: H
authors.initials: H
authors.lastname: Yasue
mesh_terms: D000109:Acetylcholine / Q000008:administration & dosage*; D000368:Aged; D000931:Antidotes / Q000008:administration & dosage*; D000975:Antioxidants / Q000008:administration & dosage; D017023:Coronary Angiography; D003326:Coronary Circulation / Q000187:drug effects* / Q000502:physiology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism; D005260:Female; D005609:Free Radicals / Q000378:metabolism; D005978:Glutathione / Q000008:administration & dosage*; D006801:Humans; D007261:Infusions, Intra-Arterial; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000378:metabolism; D005996:Nitroglycerin / Q000008:administration & dosage; D012965:Sodium Chloride / Q000008:administration & dosage; D014665:Vasodilator Agents / Q000008:administration & dosage; D014666:Vasomotor System / Q000187:drug effects* / Q000502:physiology
chemical_list: D000931:Antidotes; D000975:Antioxidants; D005609:Free Radicals; D014665:Vasodilator Agents; D009569:Nitric Oxide; D012965:Sodium Chloride; D005996:Nitroglycerin; D005978:Glutathione; D000109:Acetylcholine