title: Impact of shock and fluid resuscitation on the morphology and apoptosis of bone marrow: an experimental study.
abstract: BACKGROUND
  We hypothesized that bone marrow failure after hemorrhagic shock might be secondary to impaired apoptosis regulation. Our objective was to assess the morphologic alterations and the rate of apoptosis in bone marrow after hemorrhagic shock and resuscitation.
  
  
  METHODS
  Under pentobarbital anesthesia, Wistar rats (n = 70) underwent femoral vessel cannulation. The hemorrhagic shock model involved a controlled retrieval of blood, maintaining mean blood pressure at 40 +/- 5 mm Hg during 50 minutes. During the resuscitation period, lactated Ringer's (twice the blood volume retrieved, group LR) or NaCl 7.5% (4 mL/kg, group HS) was infused, followed by the previously retrieved blood. Bone marrow was collected through left femoral puncture. Morphology was assessed by Leishmann-stained smears, and apoptosis was assessed through terminal deoxynucleotide transferase-mediated dUTP nick-end labeling assay. Analysis of variance and Tukey's test were applied for statistical treatment, considering p < 0.05 as significant.
  
  
  RESULTS
  LR animals presented a statistically significant decrease in the lymphocytic series (LR, 24.2 +/- 4.2%; Sham, 55.1 +/- 6.6%), together with an increase in the percentage of granulocyte (LR, 51.4% +/- 2.3%; Sham, 31.5 +/- 2.9%) and monocyte precursors (LR, 7.3 +/- 1.3%; Sham, 3.3 +/- 1.1%), detected 72 hours after shock (p < 0.05). Both LR and HS groups presented a significant increase in apoptosis, when compared with the sham group (LR, 13.1 +/- 0.5%; HS, 12.2 +/- 0.7%; Sham, 6.8 +/- 0.4%). The alterations detected in the bone marrow morphology of LR group were not observed in HS animals.
  
  
  CONCLUSIONS
  There was an increase in bone marrow apoptosis after hemorrhagic shock. The type of resuscitation scheme used did influence bone marrow morphology.
authors.affiliation: Emergency Service, Department of Surgery, Santa Casa Medical School, and Heart Institute (InCor), LIM11, Sao Paulo, Brazil. jgparreira@oul.com.br
authors.forename: José Gustavo
authors.initials: JG
authors.lastname: Parreira
authors.forename: Samir
authors.initials: S
authors.lastname: Rasslan
authors.forename: Luiz F
authors.initials: LF
authors.lastname: Poli de Figueiredo
authors.forename: Thereza Christina
authors.initials: TC
authors.lastname: Bortolheiro
authors.forename: Sueli
authors.initials: S
authors.lastname: Sinosaki
authors.forename: Daniela
authors.initials: D
authors.lastname: Hardt
authors.forename: Margareth Yada
authors.initials: MY
authors.lastname: Langui
authors.forename: Milene N
authors.initials: MN
authors.lastname: Rocha
authors.forename: Carlos Alberto
authors.initials: CA
authors.lastname: Longui
authors.forename: Carlos
authors.initials: C
authors.lastname: Chiattone
authors.forename: Maurício
authors.initials: M
authors.lastname: Rocha e Silva
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D017209:Apoptosis; D001794:Blood Pressure; D001854:Bone Marrow Cells / Q000166:cytology; D001855:Bone Marrow Diseases / Q000097:blood / Q000209:etiology / Q000473:pathology; D001856:Bone Marrow Examination; D004253:DNA Nucleotidylexotransferase; D004195:Disease Models, Animal; D004906:Erythrocyte Count; D005440:Fluid Therapy / Q000379:methods*; D006098:Granulocytes / Q000166:cytology; D007108:Immune Tolerance; D020287:In Situ Nick-End Labeling; D007552:Isotonic Solutions / Q000627:therapeutic use; D007958:Leukocyte Count; D008214:Lymphocytes / Q000166:cytology; D008297:Male; D009000:Monocytes / Q000166:cytology; D051381:Rats; D017208:Rats, Wistar; D012151:Resuscitation / Q000379:methods*; D000077325:Ringer's Lactate; D012771:Shock, Hemorrhagic / Q000150:complications / Q000628:therapy; D013997:Time Factors
chemical_list: D007552:Isotonic Solutions; D000077325:Ringer's Lactate; D004253:DNA Nucleotidylexotransferase