title: Effects of high plasma epinephrine and Ca2+ concentrations on neonatal myocardial function after ischemia.
abstract: Administration of catecholamines to newborn infants may potentiate reperfusion injury because of increased transsarcolemmal Ca2+ influx and the presence of less developed sarcoplasmic reticulum in the immature hearts. We investigated the effect of administration of epinephrine (1.5 micrograms/kg per minute for 120 minutes) before ischemia and modified serum ionized Ca2+ concentrations in the cardioplegic solution and perfusate on postischemic left ventricular systolic and diastolic function in 25 piglets (5 to 7 days old) undergoing 90 minutes of cold blood cardioplegic arrest. The piglets were divided into four groups; Ca2+ 1.2 mmol/L, group A (n = 6), Ca2+ 0.25 mmol/L, group B (n = 6), Ca2+ 1.2 mmol/L and epinephrine, group C (n = 6), Ca2+ 0.25 mmol/L and epinephrine, group D (n = 7). Left ventricular function was assessed by a conductance catheter in the left ventricle measuring end-systolic and end-diastolic pressure-volume relationships during transient vena caval occlusion. By analysis of covariance, only Ca2+ concentration was important in predicting ventricular function recovery after ischemia (p < 0.01). End-systolic elastance decreased in all groups after ischemia; the magnitude was significantly greater in the normal groups (51% versus 35%, p < 0.01). There was a significant increase in the chamber stiffness index after administration of epinephrine before ischemia (p < 0.05). Groups with low Ca2+ perfusate (B and D) had no change in chamber stiffness index after ischemia. In contrast, there was a significant increase in chamber stiffness in the normal Ca2+ groups with (C) or without (A) epinephrine after ischemia (p < 0.05). Adenosine triphosphate stores declined significantly in the normal Ca2+ groups--48% versus 18% in the low Ca2+ groups (p < 0.01). We conclude that low Ca2+ concentrations in the perfusate and cardioplegic solutions better preserve left ventricular function in the normal and in epinephrine-stressed neonatal heart after ischemia.
authors.affiliation: Division of Cardiovascular Surgery, Hospital for Sick Children, Toronto, Ontario, Canada.
authors.forename: J
authors.initials: J
authors.lastname: Caspi
authors.forename: J G
authors.initials: JG
authors.lastname: Coles
authors.forename: L N
authors.initials: LN
authors.lastname: Benson
authors.forename: S L
authors.initials: SL
authors.lastname: Herman
authors.forename: J
authors.initials: J
authors.lastname: Augustine
authors.forename: P
authors.initials: P
authors.lastname: Tsao
authors.forename: A
authors.initials: A
authors.lastname: Brezina
authors.forename: A
authors.initials: A
authors.lastname: Kolin
authors.forename: G J
authors.initials: GJ
authors.lastname: Wilson
mesh_terms: D000255:Adenosine Triphosphate / Q000737:chemistry; D000818:Animals; D000831:Animals, Newborn; D001706:Biopsy; D002118:Calcium / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D002302:Cardiac Output; D002314:Cardioplegic Solutions / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D003971:Diastole; D004195:Disease Models, Animal; D004353:Drug Evaluation, Preclinical; D004837:Epinephrine / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D006339:Heart Rate; D008854:Microscopy, Electron; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D009638:Norepinephrine / Q000097:blood; D012508:Sarcolemma / Q000737:chemistry; D013318:Stroke Volume / Q000187:drug effects*; D013552:Swine; D013599:Systole
chemical_list: D002314:Cardioplegic Solutions; D000255:Adenosine Triphosphate; D002118:Calcium; D009638:Norepinephrine; D004837:Epinephrine