title: Postischemic [Ca2+] repletion improves cardiac performance without altering oxygen demands.
abstract: The positive inotropism expected with correction of postischemic hypocalcemia might be counterbalanced by potential aggravation of reperfusion injury, in particular by calcium overload. We evaluated the effect of normalizing blood calcium concentration ([Ca2+]) on postischemic left ventricular systolic and diastolic mechanics using oxygen consumption and indices derived from pressure-diameter relations. In 10 open-chest dogs on cardiopulmonary bypass, the hearts underwent 30 minutes of normothermic global ischemia followed by one hour of multidose hypothermic (4 degrees C), hypocalcemic (0.3 mmol/L) blood cardioplegia. After reperfusion, systemic [Ca2+] had decreased to 70% of control (p = 0.017). The left ventricular inotropic state was significantly depressed from baseline (control) values, but was restored to baseline levels by resumption of normocalcemia after one hour of reperfusion. Chamber stiffness increased by 308% (p = 0.006) after hypocalcemic reperfusion but decreased significantly after [Ca2+] correction. Recovery of left ventricular performance with [Ca2+] correction did not augment myocardial oxygen consumption from the postischemic uncorrected state (5.0 +/- 0.3 mL O2/min/100 g versus 5.3 +/- 0.3 mL O2/min/100 g). We conclude that normalizing [Ca2+] after blood cardioplegia improves postischemic left ventricular performance without adversely affecting compliance or oxygen consumption.
authors.affiliation: Department of Cardiothoracic Surgery, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC 27103.
authors.forename: H
authors.initials: H
authors.lastname: Yokoyama
authors.forename: J S
authors.initials: JS
authors.lastname: Julian
authors.forename: J
authors.initials: J
authors.lastname: Vinten-Johansen
authors.forename: W E
authors.initials: WE
authors.lastname: Johnston
authors.forename: T D
authors.initials: TD
authors.lastname: Smith
authors.forename: D S
authors.initials: DS
authors.lastname: McGee
authors.forename: A R
authors.initials: AR
authors.lastname: Cordell
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002118:Calcium / Q000097:blood*; D002122:Calcium Chloride / Q000008:administration & dosage / Q000627:therapeutic use*; D002302:Cardiac Output / Q000187:drug effects / Q000502:physiology; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology; D004285:Dogs; D006321:Heart / Q000502:physiology*; D006324:Heart Arrest, Induced; D006996:Hypocalcemia / Q000503:physiopathology; D009200:Myocardial Contraction / Q000187:drug effects* / Q000502:physiology; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption / Q000187:drug effects* / Q000502:physiology; D013318:Stroke Volume / Q000187:drug effects / Q000502:physiology
chemical_list: D002122:Calcium Chloride; D002118:Calcium