Antioxidative properties of histidine and its effect on myocardial injury during ischemia/reperfusion in isolated rat heart

Qing Cai, Genzou Takemura, Muhammad Ashraf

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

We wished to determine whether histidine scavenges hydroxyl radical, H2O2, and superoxide anion in vitro and to investigate the protective effect of histidine on isolated perfused rat hearts after global ischemia (40 min) and reperfusion 30 min) (I/R). Left ventricular (LV) function was recorded and coronary effluent was collected for measurement of lactate dehydrogenase (LDH) before ischemia and at 5, 10, 15, and 30 min of reperfusion. At the end of the experiment, a portion of the LV wall was fixed with 2% glutaraldehyde for morphological analysis; the remaining heart was immediately frozen in liquid nitrogen for determination of adenine nucleotides. Histidine effectively quenched hydroxyl radicals and H2O2, but not superoxide anions, in in vitro and in vivo conditions. Hearts treated with histidine exhibited significantly greater functional recovery during reperfusion as compared with nontreated hearts (p < 0.05). Cell morphology was well preserved, and enzyme release was significantly attenuated by histidine treatment (p < 0.05). Histidine raised the ATP level to 73% and the creatine phosphate level to 68% of normal control during reperfusion. Total adenine nucleotide pool and energy charge rate in histidine-treated hearts significantly increased as compared with those in nontreated hearts (p < 0.05), but no effect on ATP and creatine phosphate was noted during ischemia, Histidine prevents postischemic reperfusion injury in isolated heart by inhibiting reactive O2species and preserving high-energy phosphates (HEP).

Original languageEnglish (US)
Pages (from-to)147-155
Number of pages9
JournalJournal of Cardiovascular Pharmacology
Volume25
Issue number1
DOIs
StatePublished - Jan 1 1995
Externally publishedYes

Fingerprint

Reperfusion Injury
Histidine
Reperfusion
Phosphocreatine
Ischemia
Adenine Nucleotides
Superoxides
Hydroxyl Radical
Adenosine Triphosphate
Glutaral
Left Ventricular Function
L-Lactate Dehydrogenase
Nitrogen
Phosphates
Enzymes

Keywords

  • Heart function
  • High-energy phosphates
  • Histidine
  • Ischemia/reperfusion
  • Reactive oxygen species

ASJC Scopus subject areas

  • Pharmacology
  • Cardiology and Cardiovascular Medicine

Cite this

Antioxidative properties of histidine and its effect on myocardial injury during ischemia/reperfusion in isolated rat heart. / Cai, Qing; Takemura, Genzou; Ashraf, Muhammad.

In: Journal of Cardiovascular Pharmacology, Vol. 25, No. 1, 01.01.1995, p. 147-155.

Research output: Contribution to journalArticle

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AB - We wished to determine whether histidine scavenges hydroxyl radical, H2O2, and superoxide anion in vitro and to investigate the protective effect of histidine on isolated perfused rat hearts after global ischemia (40 min) and reperfusion 30 min) (I/R). Left ventricular (LV) function was recorded and coronary effluent was collected for measurement of lactate dehydrogenase (LDH) before ischemia and at 5, 10, 15, and 30 min of reperfusion. At the end of the experiment, a portion of the LV wall was fixed with 2% glutaraldehyde for morphological analysis; the remaining heart was immediately frozen in liquid nitrogen for determination of adenine nucleotides. Histidine effectively quenched hydroxyl radicals and H2O2, but not superoxide anions, in in vitro and in vivo conditions. Hearts treated with histidine exhibited significantly greater functional recovery during reperfusion as compared with nontreated hearts (p < 0.05). Cell morphology was well preserved, and enzyme release was significantly attenuated by histidine treatment (p < 0.05). Histidine raised the ATP level to 73% and the creatine phosphate level to 68% of normal control during reperfusion. Total adenine nucleotide pool and energy charge rate in histidine-treated hearts significantly increased as compared with those in nontreated hearts (p < 0.05), but no effect on ATP and creatine phosphate was noted during ischemia, Histidine prevents postischemic reperfusion injury in isolated heart by inhibiting reactive O2species and preserving high-energy phosphates (HEP).

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