Details

Autor(en) / Beteiligte

• YOSHIKAWA, TSUTOMU
• AKAISHI, MAKOTO
• IKEDA, FUMIHIKO
• HANDA, SHUNNOSUKE
• NAKAMURA, YOSHIRO

Titel

MECHANISMS OF TRANSIENT AUGMENTATION OF MYOCARDIAL CONTRACTION AFTER A BRIEF CORONARY OCCLUSION

Ist Teil von

• JAPANESE CIRCULATION JOURNAL, 1992/04/20, Vol.56(4), pp.404-411

Ort / Verlag

Kyoto: The Japanese Circulation Society

Erscheinungsjahr

1992

Link zum Volltext

Quelle

MEDLINE

Beschreibungen/Notizen

• The purpose of this study was 1) to clarify whether augmented myocardial contraction after a brief coronary occlusion, i.e. post-ischemic hypercontraction, depends on a transient increase in coronary blood flow or preceding myocardial ischemia, and 2) to identify the role of catecholamines or calcium flux in this phenomenon. Sixteen mongrel dogs were examined in open-chest anesthetized condition. One-minute reperfusion after two-minute total coronary occlusion of the left anterior descending artery resulted in a transient increase in segment shortening. Intracoronary administration of adenosine caused hyperemia without any changes in segment shortening. Two minutes of total coronary occlusion with adenosine caused post-ischemic hypercontraction to the same degree, but without any additional hyperemia. Two minutes of partial occlusion with 75% flow reduction caused less post-ischemic hypercontraction. Post-ischemic hypercontraction did not occur after partial occlusion with 50% flow reduction, irrespective of hyperemia with adenosine during reperfusion. Propranolol or verapamil did not prevent this phenomenon. Thus, post-ischemic hypercontraction is not dependent on the transient increase in coronary blood flow, but is related to the preceding myocardial ischemia. Local release of catecholamines is not likely to be the cause. A calcium antagonist, verapamil, did not modify this phenomenon. The precise mechanism of this phenomenon is still uncertain, although some alterations in cellular hemeostasis, such as ionic changes, are likely to be the cause.