ROLE OF ONO-3144, A NEW CARDIOPLEGIC AGENT, IN THE REOXYGENATION INJURY IN THE ANOXIC MYOCARDIUM

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概要

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• We have investigated the effect of ONO-3144 (2-aminomethyl-4-tert-butyl-6-propionylphenol), which facilitates the conversion of prostaglandin G_2 to H_2 and acts as a scavenger of free radicals, on the reoxygenation injury in the anoxic heart. Rat hearts were perfused retrogradely with Krebs-Henseleit (KH) medium for 30 min (n=8). Group III hearts were similar to those in Group II except that 4 mg ONO-3144/liter was added to both anoxic and reoxygenation media (n=8). coronary effluent was collected for creatine kinase (CK) loss. four rats hearts in each group were fixed for electron microscopic study and the remaining hearts were frozen in liquid nitrogen for measurement of adenosine triphosphate (ATP). A six-fold increase in CK leakage, observed after reoxygenation of anoxic heart, was prevented by ONO-3144. Tissue ATP was reduced from 22.2±0.9μmol/g dry weight (Group I) to 5.5±1.1 μmol/g dry weight (Group II). A significant amount of ATP (9.05±1.22μmol/g dry weight) was preserved in the treated Group III. The number of normal cells obtained by morphometrical analysis increased significantly from 56.77.8% (Group II) to 86.21.0% (Group III) and moderately injured cells were reduced to 3% in Group III as compared to 16% in the untreated Group I. Injury to the severely injured cells was not prevented by the drug treatment. At electron microscopic level, the cellular membranes, mitochondria and glycogen deposits were well preserved in Group III. Thus, ONO-3144 treatment provides a protection against reoxygenation injury in the anoxic myocardium by scavenging. -OH or other closely related species of free radicals. Therefore, free radicals generated through the conversion of prostaglandin G_2 to H_2 might play an important role in the reoxygenation injury of the anoxic myocardium.

• 社団法人日本循環器学会の論文
• 1987-04-20

著者

• Kobayashi Hiroshi

  Central Institute for Electron Microscopic Research Lab. Nippon Medical School

• Ashraf Muhammad

  Central Institute For Electron Microscopic Researches Nippon Medical School

• RAHAMATHULIA MEYIAN

  Department of Pathology and Laboratory Medicine, University of Cincinnati Medical Center

• KOBAYASHI KAORU

  Central Institute for Electron Microscopic Researches, Nippon Medical School

• SCHWARTZ ARNOLD

  Department of Pharmacology and Cell Biophysics, University of Cincinnati Medical Center

• Schwartz Arnold

  Department Of Pharmacology And Cell Biophysics University Of Cincinnati Medical Center

• Rahamathulia Meyian

  Department Of Pathology And Laboratory Medicine University Of Cincinnati Medical Center

• Kobayashi Kaoru

  Central Institute For Electron Microscopic Researches Nippon Medical School

• Kobayashi Hiroshi

  Central Engineering Laboratories Nissan Motor Co. Ltd.

• KOBAYASHI Hiroshi

  Laboratory of Forest Utilization, Department of Forest Sciences, Graduate School of Agricultural and Life Sciences, The University of Tokyo

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