title: [Effect of hypotensive fluid resuscitation on microcirculation in an uncontrolled hemorrhagic shock of pregnant rabbits].
abstract: OBJECTIVE
  to study the effects of hypotensive resuscitation on microvascular perfusion in a clinically relevant model of uncontrolled hemorrhagic shock in pregnancy.
  
  
  METHODS
  thirty New Zealand white rabbits at 15 - 25 days, pregnanal age were randomly divided into three groups; Group normal saline traditional aggressive resuscitation (NS), traditional aggressive resuscitation in the prehospital phase with a large quantity of normal saline and Ringer's solution to maintain mean arterial pressure (MAP) at the approximately 80 mm Hg (1 mm Hg = 0.133 kPa) level: Group normal saline hypotensive resuscitation (NH) and group hypertonic hyperosmotic hypotension resuscitation (HHH), hypotensive resuscitation in the prehospital phase with a bolus dose of 4 ml/kg normal saline or hypertonic hydroxyl ethyl starch (10% hydroxyl ethyl starch +7.5% NaCl), followed by Ringer's solution to maintain MAP at 60 mm Hg. Production pregnant rabbit model with hemorrhagic shock. The experiment consisted of four phases:basic phase (0 miniutes), shock phase (0 - 30 miniutes), prehospital phase (30 - 90 miniutes) and hospital phase (90 - 180 miniutes).
  
  
  METHODS
  (1) arteriole and venule diameter were continuously monitored by microcirculatory detecting instrument; (2) functional capillary density (FCD) of each phase was expressed by the percentage of opening capillaries segments relative to basic phase; (3) blood pH, BE PCO(2), PO(2) in pregnant rabbits were determined with a Medica Easy Blood Gas Analyzer.
  
  
  RESULTS
  (1) there were no significant differences among three groups in arteriole and venule diameter at baseline (P > 0.05). After hemorrhagic shock arteriole diameter were NS (50.8 ± 5.6) µm, NH (47.6 ± 3.7) µm, HHH (51.3 ± 2.4) µm, respectively, with no significant differences between groups (P > 0.05). At the end of prehospital resuscitation phase and hospital resuscitation phase, significant differences were found in arteriole diameter in group NS (52.8 ± 4.9, 56.0 ± 3.8) µm, NH (61.3 ± 2.9, 65.4 ± 3.2)µm and HHH group (67.0 ± 4.1, 74.1 ± 4.8) µm (P < 0.05); after hemorrhagic shock venule diameter were NS (79.6 ± 7.0) µm, NH (75.3 ± 5.3) µm and HHH (76.2 ± 5.8) µm, respectively, with no significant differences between groups (P > 0.05). At the end of prehospital resuscitation phase and hospital resuscitation phase, venule diameter were NS (81.1 ± 6.7, 84.4 ± 6.0) µm, NH (82.8 ± 3.3, 85.4 ± 4.3) µm and HHH (86.9 ± 5.8, 89.4 ± 6.8) µm, respectively, with no significant differences between groups (P > 0.05). (2) The values of FCD in every groups were all 100%. After hemorrhagic shock FCD were NS (39.8 ± 6.8)%, NH (43.9 ± 4.0)%, HHH (44.0 ± 4.8)%, respectively, with no significant differences between groups (P > 0.05); at the end of prehospital resuscitation phase and hospital resuscitation phase, FCD were NS (54.5 ± 7.3, 59.7 ± 4.8)%, NH (63.1 ± 5.8, 70.3 ± 5.6)% and HHH (80.5 ± 6.9, 91.7 ± 4.7)%, respectively, with significant differences between groups (P < 0.05). (3) Blood gas parameter: the values of blood pH, BE, PO(2), PCO(2) in pregnant rabbits in all groups were within normal bounds at basic phase. Shock phase induced typical hyperventilation in all groups, with increase of arterial PO(2) and decrease of PCO(2); at the end of hospital resuscitation phase, there were no significant difference among the three groups in the values of blood PCO(2) (P > 0.05); the values of blood PO(2) at the hospital resuscitation phase were significantly lower in NS groups than corresponding values in the other groups (P < 0.05). After hemorrhagic shock there was significant metabolic acidosis as shown by decrease of pH, BE; at prehospital resucitation phase, pH, BE values tended to increase in all the groups but not reach to base period. At the end of hospital resucitation phase. The pH, BE value was significantly higher in NS group than those in the other two groups (P < 0.05). (4) Median survival time in NS (2.1 ± 0.2) days group was significantly shorter than NH (3.0 ± 0.3) days and HHH (3.6 ± 0.3) days group (P < 0.05). FCD at the end of the hospital resuscitation were significantly related with survival time (r = 0.655, P = 0.000).
  
  
  CONCLUSIONS
  compared with traditional aggressive fluid resuscitation, hypotensive resuscitation reduce constriction of arterial and venule diameter, increase FCD, alleviate metabolic acidosis and improve long-term survival. Hypertonic hydroxyl ethyl starch resuscitation ameliorate microcirculation without improving survival rate.
authors.affiliation: Department of Obstetric, Maternal and Child Health Hospital, Southern Medical University, Shenzhen 518028, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Qin
authors.forename: Yan-Hong
authors.initials: YH
authors.lastname: Yu
authors.forename: Chen-Hong
authors.initials: CH
authors.lastname: Wang
mesh_terms: D000818:Animals; D001784:Blood Gas Analysis; D001794:Blood Pressure; D004195:Disease Models, Animal; D005260:Female; D005440:Fluid Therapy / Q000379:methods*; D006895:Hydroxyethyl Starch Derivatives / Q000008:administration & dosage / Q000627:therapeutic use; D006982:Hypertonic Solutions / Q000008:administration & dosage / Q000627:therapeutic use; D008833:Microcirculation / Q000187:drug effects* / Q000502:physiology; D011247:Pregnancy; D011248:Pregnancy Complications / Q000401:mortality / Q000628:therapy*; D011817:Rabbits; D011897:Random Allocation; D012151:Resuscitation; D012771:Shock, Hemorrhagic / Q000401:mortality / Q000628:therapy*; D012965:Sodium Chloride / Q000008:administration & dosage / Q000627:therapeutic use; D015996:Survival Rate; D016896:Treatment Outcome
chemical_list: D006895:Hydroxyethyl Starch Derivatives; D006982:Hypertonic Solutions; D012965:Sodium Chloride