Use of polyethylene glycol-bound superoxide dismutase, polyethylene glycol-bound catalase, and nimodipine to prevent hypoxic ischemic injury to the brain of newborn pigs

Huang

Patel

et al. 1994

Stroke

Background and Purpose Giving glucose before hypoxic ischemia worsens brain injury in piglets. Does giving glucose after hypoxic ischemia affect severity of injury?Methods Forty-three 0-to 3-day-old pigs were used. All piglets received 2 U/kg insulin before injury to prevent stressinduced hyperglycemia. Hypoxic ischemic brain damage was induced by clamping both carotid arteries and reducing arterial blood pressure to two thirds of normal by hemorrhage at time 0. At 15 minutes the fraction of inspired oxygen (Fio?) was reduced to 6%. At 30 minutes FiOj was increased to 100%, the carotids were released, and the withdrawn blood was reinfused. The piglets were then randomized to receive either 2 mL/kg of 50% dextrose followed by 2 mL/kg per hour for 2 hours or an equal volume of saline.

“…(n=ll), 10 [9,10]; hippocampus (n = ll), 10 [9.5, 10]; sum (n=ll), 29 [27.5, 29], as previously reported. …”

Section: Resultsmentioning

confidence: 57%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Glucose given after hypoxic ischemia does not affect brain injury in piglets.

Huang

Patel

et al. 1994

Stroke

“…All this strongly suggests that glucose caused the change in outcomes seen in our previous experiments associated with differences in serum glucose level. [8][9][10][11] How are the results of this experiment clinically applicable? Does …”

Section: Discussionmentioning

confidence: 99%

Glucose affects the severity of hypoxic-ischemic brain injury in newborn pigs.

Huang

Vig

et al. 1993

Stroke

Background and Purpose: The administration of glucose has been shown to worsen brain injury in adult animals but has no effect on the severity of injury in newborn rats. We wished to see whether the results in newborn rats could be extended to another newborn animal.Methods: In 44 0-to 3-day-old piglets, hypoxic-ischemic central nervous system damage was induced by ligation of both carotid arteries and reduction of their blood pressure to two-thirds normal for one-half hour. In the last 15 minutes of this half hour, oxygen concentration was reduced to 6%. The piglets were randomized to receive either 2 mLVkg 50%o dextrose in water followed by 2 mLlkg per hour for 2.5 hours beginning before ischemia or enough insulin to reduce their resting blood sugar to approximately 2 mmol/L.

“…The 30-min arterial pH was about 0.1 unit higher in the current experiment than in our previous stud ies due to a somewhat lower arterial pCCL and arterial blood lactate. In previous experi ments, there was only a very weak correlation between these values and pathological out come, so no significant change in outcome was expected [44], Although the rectal tem perature of the two current groups at 30 min was statistically higher than one of the pre vious groups, the magnitude of the difference was so small as to be unlikely to have affected our results in a significant way.…”

Section: Discussionmentioning

confidence: 50%

The Effect of Glucose during Ischemia on Brain ATP, Lactate, and Glutamate in Piglets

Qian²,

Cai³

1997

Neonatology

Self Cite

Glucose worsens hypoxic-ischemic brain injury in 0- to 3-day-old piglets. Piglets were randomly assigned to have blood glucose increased with glucose infusion (n = 12), or decreased with insulin (n = 13), or a sham group (n = 10). In the insulin and glucose groups at time 0, both carotid arteries were clamped, and blood was withdrawn to reduce the blood pressure one third. At time 15 min F_iO₂ was reduced to 6%. At time 30 min cerebrospinal fluid (CSF) was taken for glutamate, and the brains were frozen. The shams had CSF removed and brains frozen without hypoxia or ischemia. Brain ATP was 1.7 ± 0.09 μmol/g wet weight in the shams, 0.98 ± 0.09 in the glucose group (p < 0.01 vs. sham), and 0.52 ± 0.10 in the insulin group (p < 0.01 vs. glucose). Brain lactate levels were 4.3 ± 1.0 μmol/g wet weight in the shams, 18.3 ± 1.9 in the insulin group (p < 0.01 vs. sham), and 29.4 ± 2.6 in the glucose group (p < 0.01 vs. insulin). CSF glutamate was 9.3 ± 3.6 μM in the glucose group, 9.6 ± 3.5 in the insulin group, and 2.2 ± 0.9 in the shams (p < 0.05, glucose and insulin > sham). The B_max for MK-801 binding was 2.3 ± 0.2 pmol/mg protein in the glucose group, 2.6 ± 0.1 in the insulin group (p < 0.05 vs. sham), and 2.0 ± 0.2 in the shams, and the K_d was the same in the three groups (p = nonsignificant). Brain Na⁺, K⁺-ATPase was the same in the three groups (p = nonsignificant). Providing additional glucose preserves ATP during hypoxic-ischemic brain injury in the piglet but does not change CSF glutamate or brain-801 binding and probably worsens outcome by elevating brain lactate levels above the threshold for cellular injury.