title: Recovery of the chronically hypoxic young rabbit heart reperfused following no-flow ischemia.
abstract: The objective of this study was to test whether chronically hypoxic immature hearts exhibit greater tolerance to no-flow ischemia than normoxic hearts. Rabbits (N = 36) were raised from birth to 5 weeks of age in either hypoxic (10% O2/90% N2) or normoxic (room air) environment. Isolated, isovolumically beating hearts, with a fluid-filled balloon catheter in the left ventricular chamber, were perfused with a well-oxygenated buffer and studied during baseline [30 minutes; perfusion pressure, 60 mmHg; end diastolic pressure (EDP), 5 mmHg], no-flow ischemia (until onset of contracture or for 30 minutes), and Reperfusion (30 minutes; perfusion pressure, 60 mmHg). Time for onset of contracture (TOC) was defined by an increase in balloon pressure of 5 mmHg. The results were as follows: hypoxic vs normoxic: Hct, 56.4 +/- 2.5* vs 36.3 +/- 0.4%, (right ventricle/left ventricle) weight (dry) ratio, 0.50 +/- 0.04* vs 0.28 +/- 0.02. Baseline: developed pressure (DeltaP), 96 +/- 4 vs 93 +/- 5 mmHg; coronary flow, 90 +/- 10* vs 62 +/- 4 ml/min/gdry. No-flow ischemia: TOC, 12 +/- 1* vs 24 +/- 2 minutes. All hypoxic (no normoxic) hearts reached peak contracture. Reperfusion: Just after onset of contracture, DeltaP, 80 +/- 3* vs 67 +/- 4 mmHg; EDP, 5 +/- 1* vs 13 +/- 2 mmHg; after 30 minutes of no-flow ischemia, DeltaP, 58 +/- 5 vs 46 +/- 4 mmHg; EDP, 13 +/- 1* vs 24 +/- 3 mmHg; lactate release (LR), 0.15 +/- 0.01 vs 0.17 +/- 0.01 mmol/gdry, creatine kinase release (CKR), 46 +/- 8* vs 242 +/- 28 U/gdry. For hypoxic hearts reperfused after onset of contracture, LR was 0.11 +/- 0.03 mmol/gdry, comparable to that following 30 minutes of no-flow ischemia (*p < 0.05). Rabbit hearts subjected to hypoxia from birth developed ischemic contracture earlier and reached peak contracture, showed no significant increase in LR after onset of contracture, exhibited better recovery of EDP, and had markedly reduced CKR compared to normoxic controls.
authors.affiliation: Department of Pediatric Cardiology, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA, 70112, USA.
authors.forename: R G
authors.initials: RG
authors.lastname: Uy
authors.affiliation: Department of Pediatric Cardiology, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA, 70112, USA.
authors.forename: N T
authors.initials: NT
authors.lastname: Ross-Ascuitto
authors.affiliation: Department of Pediatric Cardiology, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA, 70112, USA. nascuit@tulane.edu.
authors.forename: R J
authors.initials: RJ
authors.lastname: Ascuitto
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001783:Blood Flow Velocity / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D002306:Cardiac Volume / Q000502:physiology; D002908:Chronic Disease; D003326:Coronary Circulation / Q000502:physiology*; D003402:Creatine Kinase / Q000097:blood; D000860:Hypoxia / Q000503:physiopathology*; D019344:Lactic Acid / Q000097:blood; D008955:Models, Cardiovascular; D017202:Myocardial Ischemia / Q000503:physiopathology*; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D010100:Oxygen / Q000097:blood; D011817:Rabbits; D012016:Reference Values; D016277:Ventricular Function, Left / Q000502:physiology; D016278:Ventricular Function, Right / Q000502:physiology
chemical_list: D019344:Lactic Acid; D003402:Creatine Kinase; D010100:Oxygen