Hypertonic saline dextran improves outcome after hypothermic circulatory arrest: a study in a surviving porcine model.
BACKGROUND
Hypertonic saline dextran (HSD) has been shown to have neuroprotective properties. In the present study we have assessed its potential neuroprotective efficacy in the setting of hypothermic circulatory arrest in a surviving porcine model.


METHODS
Twenty-four pigs were randomized to receive two 5-minute intravenous infusions (4 mL/kg) of either HSD (7.5 % saline, 6% dextran 70) or normal saline immediately after and 4 hours after a 75-minute period of hypothermic circulatory arrest at a brain temperature of 18 degrees C.


RESULTS
The 7-day survival was 75% in the HSD group and 66% in the control group (p > 0.9). Brain total histopathologic score was lower in the HSD group (p = 0.01). Postoperative behavioral scores were higher in the HSD group on the second day after surgery (p = 0.03). Intracranial pressure was lower in the HSD group from 45 minutes to 8 hours after hypothermic circulatory arrest (p = 0.03). Cerebral perfusion pressure was higher in the HSD group from 45 minutes to 3 hours after hypothermic circulatory arrest (p = 0.06). Brain lactate concentration was lower in the HSD group when compared with controls (p = 0.05). Furthermore, brain glucose levels tended to be higher and brain lactate-pyruvate ratio and lactate-glucose ratio were lower in the HSD group. Brain tissue oxygen partial pressures were somewhat higher in the HSD group (p = 0.08).


CONCLUSIONS
The use of HSD in experimental hypothermic circulatory arrest is associated with significantly better neurologic recovery, better histopathology, lower intracranial pressure, higher cerebral perfusion pressure, and better preservation of brain metabolism.
Kaakinen
Timo
T
Department of Surgery, Oulu University Hospital, University of Oulu, Oulu, Finland.
Alaoja
Hanna
H
Heikkinen
Janne
J
Dahlbacka
Sebastian
S
Laurila
Päivi
P
Kiviluoma
Kai
K
Salomäki
Timo
T
Tuominen
Hannu
H
Ohtonen
Pasi
P
Biancari
Fausto
F
Juvonen
Tatu
T
D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D001831:Body Temperature; D001921:Brain / Q000473:pathology; D001923:Brain Chemistry; D002315:Cardiopulmonary Bypass / Q000009:adverse effects; D050792:Circulatory Arrest, Deep Hypothermia Induced / Q000009:adverse effects*; D003911:Dextrans / Q000008:administration & dosage / Q000627:therapeutic use*; D004334:Drug Administration Schedule; D004353:Drug Evaluation, Preclinical; D005260:Female; D005947:Glucose / Q000032:analysis; D020925:Hypoxia-Ischemia, Brain / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D007262:Infusions, Intravenous; D007427:Intracranial Pressure / Q000187:drug effects; D007773:Lactates / Q000032:analysis; D018696:Neuroprotective Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D010100:Oxygen / Q000032:analysis; D010313:Partial Pressure; D011773:Pyruvates / Q000032:analysis; D011897:Random Allocation; D015427:Reperfusion Injury / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D012462:Saline Solution, Hypertonic / Q000008:administration & dosage / Q000627:therapeutic use*; D012965:Sodium Chloride / Q000008:administration & dosage / Q000627:therapeutic use*; D034421:Sus scrofa
D003911:Dextrans; D007773:Lactates; D018696:Neuroprotective Agents; D011773:Pyruvates; D012462:Saline Solution, Hypertonic; C104375:hypertonic saline-dextran solution; D012965:Sodium Chloride; D005947:Glucose; D010100:Oxygen