title: Reperfusion at reduced flow rates enhances postischemic contractile recovery of perfused heart.
abstract: The effects of reperfusion at reduced flow rates on postischemic cardiac contractile function were examined in perfused rat hearts. Isolated hearts were subjected to 35-min ischemia followed by reperfusion at the preischemic flow rate (9.0 ml.g-1.min-1; ordinary flow rate) or at reduced flow rates (0.9-8.1 ml.g-1.min-1). Reperfusion at ordinary flow rate did not generate any left ventricular developed pressure (LVDP), whereas reperfusion at reduced flow rates (0.9-7.2 ml.g-1.min-1) elicited 13-57% of initial contractile force at reperfusion's end; optimal recovery occurred at 3.6 ml.g-1.min-1 (reduced flow rate). Reduced flow rate reperfusion attenuated ischemia-reperfusion-induced increase in left ventricular end-diastolic pressure (LVEDP) and perfusion pressure (PP), alteration in tissue Na+, K+, Ca2+, and Mg2+, release of creatine kinase and ATP metabolites, and development of triphenyltetrazolium chloride-unstained areas. Enhanced postischemic LVDP recovery was inversely related to higher coronary PP at the initial stage (4 min) of reperfusion (r = -0.763). The benefit of reduced flow rate reperfusion could not be attributed to rate of calcium delivery to the heart, formation of oxygen free radicals in myocardium, endothelium-dependent coronary artery dilation, or LVDEP reduction. Enhancement of postischemic LVDP recovery was associated with attenuation of ischemia-reperfusion-induced increases in myocardial sodium and calcium; failure of postischemic LVDP recovery was accompanied by an increase. Reduction in sodium and calcium overload may underlie the beneficial effects of reduced flow rate reperfusion in ischemic-reperfused heart.
authors.affiliation: Department of Pharmacology, Tokyo University of Pharmacy and Life Science, Hachioji, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Takeo
authors.forename: J X
authors.initials: JX
authors.lastname: Liu
authors.forename: K
authors.initials: K
authors.lastname: Tanonaka
authors.forename: Y
authors.initials: Y
authors.lastname: Nasa
authors.forename: K
authors.initials: K
authors.lastname: Yabe
authors.forename: H
authors.initials: H
authors.lastname: Tanahashi
authors.forename: H
authors.initials: H
authors.lastname: Sudo
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism; D003326:Coronary Circulation; D003402:Creatine Kinase / Q000378:metabolism; D003971:Diastole; D066298:In Vitro Techniques; D008274:Magnesium / Q000378:metabolism; D008297:Male; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000503:physiopathology*; D015425:Myocardial Reperfusion / Q000379:methods*; D009206:Myocardium / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000378:metabolism; D013997:Time Factors; D016277:Ventricular Function, Left
chemical_list: D000255:Adenosine Triphosphate; D012964:Sodium; D003402:Creatine Kinase; D008274:Magnesium; D011188:Potassium; D002118:Calcium