A ^<31>P NMR Study on HIbernating Myocardium

1991 Fiscal Year Final Research Report Summary

• Project/Area Number: 01480246
• Research Category: Grant-in-Aid for General Scientific Research (B)
• Allocation Type: Single-year Grants
• Research Field: Circulatory organs internal medicine
• Research Institution: Shiga University of Medical Science
• Principal Investigator: KINOSHITA Masahiko Shiga University of Medical Science The First Department of Internal Medicine, Professor, 医学部, 教授 (60093168)
• Co-Investigator(Kenkyū-buntansha): TSUTAMOTO Takayoshi Shiga University of Medical Science The First Department of Internal Medicine, A, 医学部, 助手 (40197695) ; TAKAHASHI Masayuki Shiga University of Medical Science The First Department of Internal Medicine, A, 医学部, 助手 (40179528) ; FUKUHARA Takehisa Shiga University of Medical Science The First Department of Internal Medicine, A, 医学部, 講師 (90156802) ; MITSUNAMI Kenichi Shiga University of Medical Science The First Department of Internal Medicine, A, 医学部, 助教授 (10127037)
• Project Period (FY): 1989 – 1991
• Keywords: Myocardial hibernation / Rapid ventricular pacing / ^<31>P NMR spectroscopy / Conductance catheter method / High energy Phosphate

Research Abstract

The term "hibernating myocardium" refers to chronic ischemia in which the blood supply to the myocardium is not low enough to cause tissue necrosis, but is low enough to result in chronic regional left ventricular dysfunction. The mechanism of left ventricular dysfunction in the hibernating myocardium is unknown mainly due to lack of adequate experimental models for it. The mechanism of left ventricular dysfunction induced by chronic rapid ventricular pacing also has not as yet been fully elucidated, but some investigators assume that it results from relative myocardial ischemia. So we investigated the mechanism of pacing-induced left ventricular dysfunction employing in vivo ^<31>P NMR spectroscopy using a chronically implanted radio frequency coil on the pericardium over the left ventricle in the dog, and tried to make it clear whether pacing-induced left ventricular dysfunction is considered as an adequate model for hibernating myocardium.
The heart was rapidly paced using chronicall y implanted pacing leads on the right ventricle at a rate 250 to 270 beats per minute for 3 to 5 weeks. The left ventricular end-diastolic pressure was high at the end of rapid pacing and remained high for a week after the cessation of pacing. The left ventricular dp/dt was decreased at the end of rapid pacing but increased significantly 1 hour after the cessation of pacing. Serial ^<3l>P NMR spectroscopy revealed a tendency of reduction in myocardial contents of adenosine triphosphate (ATP) and phosphocreatine (PCr) after the rapid ventricular pacing compared with before, but the recovery in their contents after the cessation of pacing seemed to be minimum during the following 3 hours. We measured the myocardial contents of ATP, ADP, AMP, and PCr by high-performance liquid chromatography after the NMR study in some cases, but couldn't find a significant reduction compared with the myocardium in shamoperated dogs which had normal left ventricular end-diastolic pressure and dp/dt. But this seemed to be due to a small number of cases measured. These findings may suggest the participation of myocardial ischemia in the mechanism of left ventricular dysfunction induced by chronic rapid ventricular pacing. Tbus, pacing-induced left ventricular dysfunction may be an adequate model for hibernating myocardium, but further investigation is necessary before reaching the definite conclusion.