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The antianginal agent, ranolazine, reduces myocardial infarct size but does not alter anatomic no-reflow or regional myocardial blood flow in ischemia/reperfusion in the rabbit.
J Cardiovasc Pharmacol Ther. 2008 Sep; 13(3):226-32.JC

Abstract

It has been suggested that ranolazine protects the ischemic/reperfused heart by reducing diastolic wall pressure during ischemia. However, there is limited information regarding the effect of ranolazine on the anatomic zone of no-flow in a model of acute myocardial occlusion/reperfusion. Before coronary artery occlusion (CAO), open-chest anesthetized rabbits were assigned to vehicle or ranolazine. Hearts received 60 minutes of CAO and 3 hours reperfusion. Ischemic risk zone was comparable in the 2 groups. Ranolazine significantly reduced infarct size. There was a non-significant trend for the no-reflow defect to be smaller in the ranolazine group. Regional myocardial blood flow was similar in both groups in the risk zone during ischemia and at 3 hours reperfusion. Heart rates were similar in both groups, whereas mean arterial pressure was reduced in the ranolazine group. While ranolazine was effective in reducing myocardial infarct size, the mechanism by which it did this was independent of improving perfusion during either ischemia or reperfusion, suggesting that ranolazine's effect of reducing infarct size involves alternative mechanisms.

Authors+Show Affiliations

Good Samaritan Hospital, Los Angeles, California 90017, USA. sharon.hale@netscape.comNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18625805

Citation

Hale, Sharon L., and Robert A. Kloner. "The Antianginal Agent, Ranolazine, Reduces Myocardial Infarct Size but Does Not Alter Anatomic No-reflow or Regional Myocardial Blood Flow in Ischemia/reperfusion in the Rabbit." Journal of Cardiovascular Pharmacology and Therapeutics, vol. 13, no. 3, 2008, pp. 226-32.
Hale SL, Kloner RA. The antianginal agent, ranolazine, reduces myocardial infarct size but does not alter anatomic no-reflow or regional myocardial blood flow in ischemia/reperfusion in the rabbit. J Cardiovasc Pharmacol Ther. 2008;13(3):226-32.
Hale, S. L., & Kloner, R. A. (2008). The antianginal agent, ranolazine, reduces myocardial infarct size but does not alter anatomic no-reflow or regional myocardial blood flow in ischemia/reperfusion in the rabbit. Journal of Cardiovascular Pharmacology and Therapeutics, 13(3), 226-32. https://doi.org/10.1177/1074248408320278
Hale SL, Kloner RA. The Antianginal Agent, Ranolazine, Reduces Myocardial Infarct Size but Does Not Alter Anatomic No-reflow or Regional Myocardial Blood Flow in Ischemia/reperfusion in the Rabbit. J Cardiovasc Pharmacol Ther. 2008;13(3):226-32. PubMed PMID: 18625805.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The antianginal agent, ranolazine, reduces myocardial infarct size but does not alter anatomic no-reflow or regional myocardial blood flow in ischemia/reperfusion in the rabbit. AU - Hale,Sharon L, AU - Kloner,Robert A, Y1 - 2008/07/14/ PY - 2008/7/16/pubmed PY - 2008/12/19/medline PY - 2008/7/16/entrez SP - 226 EP - 32 JF - Journal of cardiovascular pharmacology and therapeutics JO - J Cardiovasc Pharmacol Ther VL - 13 IS - 3 N2 - It has been suggested that ranolazine protects the ischemic/reperfused heart by reducing diastolic wall pressure during ischemia. However, there is limited information regarding the effect of ranolazine on the anatomic zone of no-flow in a model of acute myocardial occlusion/reperfusion. Before coronary artery occlusion (CAO), open-chest anesthetized rabbits were assigned to vehicle or ranolazine. Hearts received 60 minutes of CAO and 3 hours reperfusion. Ischemic risk zone was comparable in the 2 groups. Ranolazine significantly reduced infarct size. There was a non-significant trend for the no-reflow defect to be smaller in the ranolazine group. Regional myocardial blood flow was similar in both groups in the risk zone during ischemia and at 3 hours reperfusion. Heart rates were similar in both groups, whereas mean arterial pressure was reduced in the ranolazine group. While ranolazine was effective in reducing myocardial infarct size, the mechanism by which it did this was independent of improving perfusion during either ischemia or reperfusion, suggesting that ranolazine's effect of reducing infarct size involves alternative mechanisms. SN - 1074-2484 UR - https://www.unboundmedicine.com/medline/citation/18625805/The_antianginal_agent_ranolazine_reduces_myocardial_infarct_size_but_does_not_alter_anatomic_no_reflow_or_regional_myocardial_blood_flow_in_ischemia/reperfusion_in_the_rabbit_ L2 - https://journals.sagepub.com/doi/10.1177/1074248408320278?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -