BACKGROUND: Severe hypocapnia reduces cerebral blood flow (CBF) and is known to be a risk factor for diabetic ketoacidosis (DKA)-related cerebral edema and cerebral injury in children. Reductions in CBF resulting from hypocapnia alone, however, would not be expected to cause substantial cerebral injury. We hypothesized that either hyperglycemia or ketosis might alter the effects of hypocapnia on CBF and/or cerebral edema associated with CBF reduction. METHODS: We induced hypocapnia (pCO₂ 20 ± 3 mmHg) via mechanical ventilation in three groups of juvenile rats: 25 controls, 22 hyperglycemic rats (serum glucose 451 ± 78 mg/dL), and 15 ketotic rats (β-hydroxy butyrate 3.0 ± 1.0 mmol/L). We used magnetic resonance imaging to measure CBF and apparent diffusion coefficient (ADC) values in these groups and in 17 ventilated rats with normal pCO₂ (40 ± 3 mmHg). In a subset (n = 35), after 2 h of hypocapnia, pCO₂ levels were normalized (40 ± 3 mmHg) and ADC and CBF measurements were repeated. RESULTS: Declines in CBF with hypocapnia occurred in all groups. Normalization of pCO₂ after hypocapnia resulted in hyperemia in the striatum. These effects were not substantially altered by hyperglycemia or ketosis. Declines in ADC (suggesting brain cell swelling) during hypocapnia, however, were greater during both hyperglycemia and ketosis. CONCLUSIONS: We conclude that brain cell swelling associated with hypocapnia is increased by both hyperglycemia and ketosis, suggesting that these metabolic conditions may make the brain more vulnerable to injury during hypocapnia.
BACKGROUND: Severe hypocapnia reduces cerebral blood flow (CBF) and is known to be a risk factor for diabetic ketoacidosis (DKA)-related cerebral edema and cerebral injury in children. Reductions in CBF resulting from hypocapnia alone, however, would not be expected to cause substantial cerebral injury. We hypothesized that either hyperglycemia or ketosis might alter the effects of hypocapnia on CBF and/or cerebral edema associated with CBF reduction. METHODS: We induced hypocapnia (pCO₂ 20 ± 3 mmHg) via mechanical ventilation in three groups of juvenile rats: 25 controls, 22 hyperglycemicrats (serum glucose 451 ± 78 mg/dL), and 15 ketotic rats (β-hydroxy butyrate 3.0 ± 1.0 mmol/L). We used magnetic resonance imaging to measure CBF and apparent diffusion coefficient (ADC) values in these groups and in 17 ventilated rats with normal pCO₂ (40 ± 3 mmHg). In a subset (n = 35), after 2 h of hypocapnia, pCO₂ levels were normalized (40 ± 3 mmHg) and ADC and CBF measurements were repeated. RESULTS:Declines in CBF with hypocapnia occurred in all groups. Normalization of pCO₂ after hypocapnia resulted in hyperemia in the striatum. These effects were not substantially altered by hyperglycemia or ketosis. Declines in ADC (suggesting brain cell swelling) during hypocapnia, however, were greater during both hyperglycemia and ketosis. CONCLUSIONS: We conclude that brain cell swelling associated with hypocapnia is increased by both hyperglycemia and ketosis, suggesting that these metabolic conditions may make the brain more vulnerable to injury during hypocapnia.
Authors: Nicole S Glaser; Daniel J Tancredi; James P Marcin; Ryan Caltagirone; Yvonne Lee; Christopher Murphy; Nathan Kuppermann Journal: J Pediatr Date: 2013-07-18 Impact factor: 4.406
Authors: Joan S Roberts; Monica S Vavilala; Kenneth A Schenkman; Dennis Shaw; Lynn D Martin; Arthur M Lam Journal: Crit Care Med Date: 2006-08 Impact factor: 7.598
Authors: Nicole S Glaser; James P Marcin; Sandra L Wootton-Gorges; Michael H Buonocore; Arleta Rewers; John Strain; Joseph DiCarlo; E Kirk Neely; Patrick Barnes; Nathan Kuppermann Journal: J Pediatr Date: 2008-06-27 Impact factor: 4.406
Authors: Hatem Hamed Elshorbagy; Naglaa Fathy Barseem; Akram Elshafey Elsadek; Ashraf Hamed Al-shokary; Yehia Hamed Abdel Maksoud; Sameh Elsayed Abdulsamea; Iman M. Talaat; Hany Abdelaziz Suliman; Naglaa M. Kamal; Waleed E. Abdelghani; Sanaa Mohammed Azab; Dalia Mohamed Nour El Din Journal: J Clin Res Pediatr Endocrinol Date: 2019-05-09