title: Hypertonic fluid resuscitation from subarachnoid hemorrhage in rats.
abstract: OBJECTIVE
  Increased intracranial pressure (ICP) and decreased cerebral blood flow leading to global cerebral ischemia are the primary causes of death after severe subarachnoid hemorrhage (SAH). Hypertonic saline has been demonstrated to exert neuroprotective properties after traumatic brain injury by osmotic mobilization of parenchymal water and improvement of microcirculation. We used a rat model to investigate the effects of hypertonic fluid resuscitation after SAH on ICP, cerebral blood flow, body weight, neurological recovery, and morphological damage.
  
  
  METHODS
  Sixty rats were subjected to SAH induced by an endovascular filament. ICP and local cerebral blood flow were recorded continuously. Animals were assigned to three groups: 1) NaCl 0.9%; 2) NaCl 7.5% (4 ml/kg); and 3) NaCl 7.5% plus 6% dextran 70 (4 ml/kg) given 30 minutes after SAH. Body weight and neurological deficits were assessed daily. Morphological damage was evaluated on Day 7.
  
  
  RESULTS
  SAH resulted in an immediate increase of ICP to approximately 60 mm Hg initially, and then to approximately 30 mm Hg for the next 90 minutes. Although NaCl 7.5% alone and in combination with dextran led to an immediate, significant, and lasting decrease of ICP to 15 to 20 mm Hg, only the combined therapy significantly increased body weight and improved neurological recovery. Furthermore, the group that received combined therapy exhibited significantly more surviving neurons in hippocampus, cortex, caudoputamen, and cerebellum. Mortality was reduced nonsignificantly, from approximately 65% in groups I and II to 35% in Group III.
  
  
  CONCLUSIONS
  Treatment with NaCl 7.5% plus 6% dextran 70 is significantly effective for reducing the initial harmful sequelae of SAH. The regimen resulted in lowered ICP, improved neurological recovery, and less morphological damage after SAH in the rat.
authors.affiliation: Department of Neurosurgery, Ludwig-Maximilians-Universität, Klinikum Grosshadern, Munich, Germany. Stefan.Zausinger@med.uni-muenchen.de
authors.forename: Stefan
authors.initials: S
authors.lastname: Zausinger
authors.forename: Serge C
authors.initials: SC
authors.lastname: Thal
authors.forename: Uwe
authors.initials: U
authors.lastname: Kreimeier
authors.forename: Konrad
authors.initials: K
authors.lastname: Messmer
authors.forename: Robert
authors.initials: R
authors.lastname: Schmid-Elsaesser
mesh_terms: D000818:Animals; D001921:Brain / Q000098:blood supply / Q000187:drug effects / Q000473:pathology; D002545:Brain Ischemia / Q000473:pathology / Q000503:physiopathology; D002470:Cell Survival / Q000187:drug effects; D002560:Cerebrovascular Circulation / Q000187:drug effects; D003911:Dextrans / Q000494:pharmacology; D004359:Drug Therapy, Combination; D019586:Intracranial Hypertension / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D009460:Neurologic Examination / Q000187:drug effects; D009474:Neurons / Q000187:drug effects / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology*; D051381:Rats; D012151:Resuscitation / Q000379:methods*; D012462:Saline Solution, Hypertonic / Q000494:pharmacology*; D013345:Subarachnoid Hemorrhage / Q000473:pathology / Q000503:physiopathology*; D015996:Survival Rate
chemical_list: D003911:Dextrans; D018696:Neuroprotective Agents; D012462:Saline Solution, Hypertonic