Chronic hypoxia: A model for cyanotic congenital heart defects

Antonio F. Corno, Giuseppina Milano, Michele Samaja, Piergiorgio Tozzi, Ludwig K. Von Segesser

Research output: Contribution to journalArticle

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Abstract

Objective: The postoperative course of cyanotic children is generally more complicated than that of acyanotic children. A possible reason is reoxygenation injury at the beginning of cardiopulmonary bypass. In this study we tested the hypothesis that reoxygenation of chronically hypoxic hearts is worse than that of normoxic hearts. Methods: Two groups of rats (n = 9 each) were exposed to either room air (fraction of inspired oxygen, 0.21%) or chronic hypoxia (fraction of inspired oxygen, 0.10%) for 2 weeks. Hearts were then isolated and perfused for 30 minutes with hypoxic buffer (oxygen saturation, 10%), followed by 30 minutes of reoxygenation (oxygen saturation, 100%). Results: In hypoxic rats hematocrit values, hemoglobin concentrations, and red cells were higher (69% ± 6% vs 40% ± 6%, 219 ± 14 vs 124 ± 12 g/L, and 10.30 ± 0.6 vs 6.32 ± 0.5/μL/1000, respectively; P <.0001); the amount of ingested food was less (22.3 ± 4.8 vs 30.7 ± 3.9 g/d, P <.001), as was the amount of ingested water (21.0 ± 3.1 vs 50.4 ± 14.6 mL/d, P <.0001); and body weight was lower (182 ± 14.2 vs 351 ± 40.1 g, P <.0001), as was heart weight (1107 ± 119 vs 1312 ± 128 mg, P <.005). The heart weight/body weight ratio was higher (6.10 ± 0.8 vs 3.74 ± 0.1 mg/g, P <.0001). Systolic and diastolic functions, not different during the hypoxic baseline period, were more impaired in hypoxic than in normoxic hearts after the reoxygenation, whereas coronary resistance remained lower. During the hypoxic perfusion, the venous partial pressure of oxygen remained low in both groups, whereas during reoxygenation, partial pressure of oxygen was higher in hypoxic hearts, with a lower (P <.01) oxygen uptake. During hypoxic baseline adenosine triphosphate turnover, lactate production and lactate turnover were lower in hypoxic hearts (P <.005, P <.0001, and P <.0001, respectively). Conclusions: Body and blood values are severely affected by chronic hypoxia, and the cardiac effects of uncontrolled reoxygenation after chronic hypoxia are more severe than after acute hypoxia.

Original languageEnglish
Pages (from-to)105-112
Number of pages8
JournalJournal of Thoracic and Cardiovascular Surgery
Volume124
Issue number1
DOIs
Publication statusPublished - Jul 1 2002

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Congenital Heart Defects
Oxygen
Partial Pressure
Lactic Acid
Body Weight
Weights and Measures
Venous Pressure
Hypoxia
Cardiopulmonary Bypass
Hematocrit
Buffers
Hemoglobins
Perfusion
Adenosine Triphosphate
Air
Food
Water
Wounds and Injuries

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

Chronic hypoxia : A model for cyanotic congenital heart defects. / Corno, Antonio F.; Milano, Giuseppina; Samaja, Michele; Tozzi, Piergiorgio; Von Segesser, Ludwig K.

In: Journal of Thoracic and Cardiovascular Surgery, Vol. 124, No. 1, 01.07.2002, p. 105-112.

Research output: Contribution to journalArticle

Corno, Antonio F. ; Milano, Giuseppina ; Samaja, Michele ; Tozzi, Piergiorgio ; Von Segesser, Ludwig K. / Chronic hypoxia : A model for cyanotic congenital heart defects. In: Journal of Thoracic and Cardiovascular Surgery. 2002 ; Vol. 124, No. 1. pp. 105-112.
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AU - Von Segesser, Ludwig K.

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N2 - Objective: The postoperative course of cyanotic children is generally more complicated than that of acyanotic children. A possible reason is reoxygenation injury at the beginning of cardiopulmonary bypass. In this study we tested the hypothesis that reoxygenation of chronically hypoxic hearts is worse than that of normoxic hearts. Methods: Two groups of rats (n = 9 each) were exposed to either room air (fraction of inspired oxygen, 0.21%) or chronic hypoxia (fraction of inspired oxygen, 0.10%) for 2 weeks. Hearts were then isolated and perfused for 30 minutes with hypoxic buffer (oxygen saturation, 10%), followed by 30 minutes of reoxygenation (oxygen saturation, 100%). Results: In hypoxic rats hematocrit values, hemoglobin concentrations, and red cells were higher (69% ± 6% vs 40% ± 6%, 219 ± 14 vs 124 ± 12 g/L, and 10.30 ± 0.6 vs 6.32 ± 0.5/μL/1000, respectively; P <.0001); the amount of ingested food was less (22.3 ± 4.8 vs 30.7 ± 3.9 g/d, P <.001), as was the amount of ingested water (21.0 ± 3.1 vs 50.4 ± 14.6 mL/d, P <.0001); and body weight was lower (182 ± 14.2 vs 351 ± 40.1 g, P <.0001), as was heart weight (1107 ± 119 vs 1312 ± 128 mg, P <.005). The heart weight/body weight ratio was higher (6.10 ± 0.8 vs 3.74 ± 0.1 mg/g, P <.0001). Systolic and diastolic functions, not different during the hypoxic baseline period, were more impaired in hypoxic than in normoxic hearts after the reoxygenation, whereas coronary resistance remained lower. During the hypoxic perfusion, the venous partial pressure of oxygen remained low in both groups, whereas during reoxygenation, partial pressure of oxygen was higher in hypoxic hearts, with a lower (P <.01) oxygen uptake. During hypoxic baseline adenosine triphosphate turnover, lactate production and lactate turnover were lower in hypoxic hearts (P <.005, P <.0001, and P <.0001, respectively). Conclusions: Body and blood values are severely affected by chronic hypoxia, and the cardiac effects of uncontrolled reoxygenation after chronic hypoxia are more severe than after acute hypoxia.

AB - Objective: The postoperative course of cyanotic children is generally more complicated than that of acyanotic children. A possible reason is reoxygenation injury at the beginning of cardiopulmonary bypass. In this study we tested the hypothesis that reoxygenation of chronically hypoxic hearts is worse than that of normoxic hearts. Methods: Two groups of rats (n = 9 each) were exposed to either room air (fraction of inspired oxygen, 0.21%) or chronic hypoxia (fraction of inspired oxygen, 0.10%) for 2 weeks. Hearts were then isolated and perfused for 30 minutes with hypoxic buffer (oxygen saturation, 10%), followed by 30 minutes of reoxygenation (oxygen saturation, 100%). Results: In hypoxic rats hematocrit values, hemoglobin concentrations, and red cells were higher (69% ± 6% vs 40% ± 6%, 219 ± 14 vs 124 ± 12 g/L, and 10.30 ± 0.6 vs 6.32 ± 0.5/μL/1000, respectively; P <.0001); the amount of ingested food was less (22.3 ± 4.8 vs 30.7 ± 3.9 g/d, P <.001), as was the amount of ingested water (21.0 ± 3.1 vs 50.4 ± 14.6 mL/d, P <.0001); and body weight was lower (182 ± 14.2 vs 351 ± 40.1 g, P <.0001), as was heart weight (1107 ± 119 vs 1312 ± 128 mg, P <.005). The heart weight/body weight ratio was higher (6.10 ± 0.8 vs 3.74 ± 0.1 mg/g, P <.0001). Systolic and diastolic functions, not different during the hypoxic baseline period, were more impaired in hypoxic than in normoxic hearts after the reoxygenation, whereas coronary resistance remained lower. During the hypoxic perfusion, the venous partial pressure of oxygen remained low in both groups, whereas during reoxygenation, partial pressure of oxygen was higher in hypoxic hearts, with a lower (P <.01) oxygen uptake. During hypoxic baseline adenosine triphosphate turnover, lactate production and lactate turnover were lower in hypoxic hearts (P <.005, P <.0001, and P <.0001, respectively). Conclusions: Body and blood values are severely affected by chronic hypoxia, and the cardiac effects of uncontrolled reoxygenation after chronic hypoxia are more severe than after acute hypoxia.

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