CB-Receptor Agonist HU-210 Mimics the Postconditioning Phenomenon of Isolated Heart

CB receptor agonist HU-210 exhibits an infarction-limiting effect during in vitro reperfusion of the heart after focal ischemia. This effect is paralleled by a decrease in left-ventricular developed pressure and double product. In addition, HU-210 reduces end-diastolic pressure during the reperfusio...

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Veröffentlicht in:	Bulletin of experimental biology and medicine 2016-11, Vol.162 (1), p.27-29
Hauptverfasser:	Gorbunov, A. S., Maslov, L. N., Tsibulnikov, S. Yu, Khaliulin, I. G., Tsepokina, A. V., Khutornaya, M. V., Kutikhin, A. G.
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Arrhythmias, Cardiac - drug therapy Arrhythmias, Cardiac - metabolism Arrhythmias, Cardiac - physiopathology Biomedical and Life Sciences Biomedicine Blood pressure Blood Pressure - drug effects Calcium Calcium - metabolism Cardiac patients Cardiomyocytes Cell Biology Coronary Occlusion Coronary Vessels - surgery Dronabinol - analogs & derivatives Dronabinol - pharmacology Excitatory Amino Acid Antagonists - pharmacology Heart Heart attack Heart failure Heart Rate - drug effects Infarction Internal Medicine Ischemia Ischemic Postconditioning Laboratory Medicine Male Myocardial Reperfusion Injury - drug therapy Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - physiopathology Myocardium - metabolism Myocardium - pathology Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Neuroprotective Agents - pharmacology Organ Culture Techniques Pathology Rats Rats, Wistar Receptors, Cannabinoid - metabolism Reperfusion Shock Ventricle Ventricular Pressure - drug effects
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Beschreibung
Zusammenfassung:	CB receptor agonist HU-210 exhibits an infarction-limiting effect during in vitro reperfusion of the heart after focal ischemia. This effect is paralleled by a decrease in left-ventricular developed pressure and double product. In addition, HU-210 reduces end-diastolic pressure during the reperfusion period, which indirectly attests to reduced Ca 2+ overload of cardiomyocytes.
ISSN:	0007-4888 1573-8221
DOI:	10.1007/s10517-016-3536-6