Hyperglycemia during hypothermic canine cardiopulmonary bypass increases cerebral lactate

A. E. Feerick, W. E. Johnston, L. W. Jenkins, C. Y J Lin, H. Mackay, Donald Prough

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Background: Hyperglycemia frequently occurs during cardiopulmonary bypass (CPB), although its direct effects on cerebral perfusion and metabolism are not known. Using a canine model of hypothermic CPB, we tested whether hyperglycemia alters cerebral blood flow and metabolism and cerebral energy charge. Methods: Twenty anesthetized dogs were randomized into hyperglycemic (n = 10) and normoglycemic (n = 10) groups. The hyperglycemic group received an infusion of D50 W, and the normoglycemic animals received an equal volume of 0.9% NaCl. Both groups underwent 120 min of hypothermic (28°C) CPB using membrane oxygenators, followed by rewarming and termination of CPB. Cerebral blood flow (radioactive microspheres) and the cerebral metabolic rate for oxygen were measured intermittently during the experiment and brain tissue metabolites were obtained after bypass. Results: Before CPB, the glucose-treated animals had higher serum glucose levels (534 ± 12 mg/dL; mean ± SE) than controls (103 ± 4 mg/dL; P < 0.05), and this difference was maintained throughout the study. Cerebral blood flow and metabolism did not differ between groups at any time during the experiment. Sagittal sinus pressure was comparable between groups throughout CPB. Tissue high-energy phosphates and water contents were similar after CPB, although cerebral lactate levels were greater in hyperglycemic (37.2 ± 5.7 μmol/g) than normoglycemic animals (19.7 ± 3.7 μmol/g; P < 0.05). After CPB, pH values of cerebrospinal fluid for normoglycemic (7.33 ± 0.01) and hyperglycemic (7.34 ± 0.01) groups were similar. Conclusions: Hyperglycemia during CPB significantly increases cerebral lactate levels without adversely affecting cerebral blood flow and metabolism, cerebrospinal fluid pH, or cerebral energy charge.

Original languageEnglish (US)
Pages (from-to)512-520
Number of pages9
JournalAnesthesiology
Volume82
Issue number2
DOIs
StatePublished - 1995

Fingerprint

Cardiopulmonary Bypass
Hyperglycemia
Canidae
Lactic Acid
Cerebrovascular Circulation
Cerebrospinal Fluid
Membrane Oxygenators
Glucose
Rewarming
Microspheres
Energy Metabolism
Perfusion
Phosphates
Dogs
Oxygen
Pressure
Water
Brain
Serum

Keywords

  • Cardiopulmonary bypass
  • Cerebral blood flow
  • Cerebral metabolism
  • Hyperglycemia

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Hyperglycemia during hypothermic canine cardiopulmonary bypass increases cerebral lactate. / Feerick, A. E.; Johnston, W. E.; Jenkins, L. W.; Lin, C. Y J; Mackay, H.; Prough, Donald.

In: Anesthesiology, Vol. 82, No. 2, 1995, p. 512-520.

Research output: Contribution to journalArticle

Feerick, A. E. ; Johnston, W. E. ; Jenkins, L. W. ; Lin, C. Y J ; Mackay, H. ; Prough, Donald. / Hyperglycemia during hypothermic canine cardiopulmonary bypass increases cerebral lactate. In: Anesthesiology. 1995 ; Vol. 82, No. 2. pp. 512-520.
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AU - Feerick, A. E.

AU - Johnston, W. E.

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AU - Mackay, H.

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N2 - Background: Hyperglycemia frequently occurs during cardiopulmonary bypass (CPB), although its direct effects on cerebral perfusion and metabolism are not known. Using a canine model of hypothermic CPB, we tested whether hyperglycemia alters cerebral blood flow and metabolism and cerebral energy charge. Methods: Twenty anesthetized dogs were randomized into hyperglycemic (n = 10) and normoglycemic (n = 10) groups. The hyperglycemic group received an infusion of D50 W, and the normoglycemic animals received an equal volume of 0.9% NaCl. Both groups underwent 120 min of hypothermic (28°C) CPB using membrane oxygenators, followed by rewarming and termination of CPB. Cerebral blood flow (radioactive microspheres) and the cerebral metabolic rate for oxygen were measured intermittently during the experiment and brain tissue metabolites were obtained after bypass. Results: Before CPB, the glucose-treated animals had higher serum glucose levels (534 ± 12 mg/dL; mean ± SE) than controls (103 ± 4 mg/dL; P < 0.05), and this difference was maintained throughout the study. Cerebral blood flow and metabolism did not differ between groups at any time during the experiment. Sagittal sinus pressure was comparable between groups throughout CPB. Tissue high-energy phosphates and water contents were similar after CPB, although cerebral lactate levels were greater in hyperglycemic (37.2 ± 5.7 μmol/g) than normoglycemic animals (19.7 ± 3.7 μmol/g; P < 0.05). After CPB, pH values of cerebrospinal fluid for normoglycemic (7.33 ± 0.01) and hyperglycemic (7.34 ± 0.01) groups were similar. Conclusions: Hyperglycemia during CPB significantly increases cerebral lactate levels without adversely affecting cerebral blood flow and metabolism, cerebrospinal fluid pH, or cerebral energy charge.

AB - Background: Hyperglycemia frequently occurs during cardiopulmonary bypass (CPB), although its direct effects on cerebral perfusion and metabolism are not known. Using a canine model of hypothermic CPB, we tested whether hyperglycemia alters cerebral blood flow and metabolism and cerebral energy charge. Methods: Twenty anesthetized dogs were randomized into hyperglycemic (n = 10) and normoglycemic (n = 10) groups. The hyperglycemic group received an infusion of D50 W, and the normoglycemic animals received an equal volume of 0.9% NaCl. Both groups underwent 120 min of hypothermic (28°C) CPB using membrane oxygenators, followed by rewarming and termination of CPB. Cerebral blood flow (radioactive microspheres) and the cerebral metabolic rate for oxygen were measured intermittently during the experiment and brain tissue metabolites were obtained after bypass. Results: Before CPB, the glucose-treated animals had higher serum glucose levels (534 ± 12 mg/dL; mean ± SE) than controls (103 ± 4 mg/dL; P < 0.05), and this difference was maintained throughout the study. Cerebral blood flow and metabolism did not differ between groups at any time during the experiment. Sagittal sinus pressure was comparable between groups throughout CPB. Tissue high-energy phosphates and water contents were similar after CPB, although cerebral lactate levels were greater in hyperglycemic (37.2 ± 5.7 μmol/g) than normoglycemic animals (19.7 ± 3.7 μmol/g; P < 0.05). After CPB, pH values of cerebrospinal fluid for normoglycemic (7.33 ± 0.01) and hyperglycemic (7.34 ± 0.01) groups were similar. Conclusions: Hyperglycemia during CPB significantly increases cerebral lactate levels without adversely affecting cerebral blood flow and metabolism, cerebrospinal fluid pH, or cerebral energy charge.

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