Objective To observe the effects of different levels of stroke volume variation (SVV)directed fluid therapy on prognosis in elderly patients.Methods One hundred and ten patients (male 67 cases,female 43 cases,aged 65-80 years,ASA grade Ⅰ or Ⅱ)undergoing abdominal sur-geries were randomized into three groups on the basis of SVV level:1 1%≤SVV≤14% (group H,n=37),7%≤SVV≤10% (group M,n = 37),3% ≤ SVV≤ 6% (group L,n = 36).Each group ac-cepted different fluid therapy strategy.Perioperative intake and outtake volume were recorded.Progno-sis indicators included gastrointestinal function recovery,post and total length of hospital stay and so on were collected.Postoperative complications were also recorded.Results Along with the level of SVV dropped,The volume of colloid and crystalloid among groups were significantly increased (P <0.05).There were no remarkable difference in the time interval of activity off bed,liquid diet,gastrointestinal decompres-sion and catheterization.Group L had a delayed exhaust time compared with group H (P <0.05).Patients in the group M had a shorter time to have semi-liquid diet.The transition of diet was also shortest in the group M.But these differences were not statistically significant.The group M also had a shorter time in first-degree or above nursing time and post and total length of hospital stay compared with group L (P <0.05).The incidence of postoperative infection in group L was higher than other two groups.Incidence of anastomosis leakage in group H was higher than that in other two groups (P <0.05).Conditions of compli-cations in group L were more severe and complicated compared with other two groups.Conclusion 3%≤SVV≤6% may increase the risk of postoperative infection and prolong the time of hospitalization.Patients in the level of 7%≤SVV≤10% may have a better postoperative recovery.This level could be a better goal of perioperative fluid therapy in elderly patients.

Objective To explore the effects of complement C1q on postsynaptic density protein 95(PSD95)and motor function of rats with cerebral ischemia-reperfusion injury.Methods Thirty-six clean male SD rats,aged 6-8 weeks,weighing 220-250 g,were randomly divided into three groups:sham group(group S),middle cerebral artery occlusion(MCAO)group(group M),and MCAO+C1q neutralization group(group A),12 rats in each group.Group S only received anatomical separation of common carotid ar-tery without insertion of monofilament,group M established the MCAO model was prepared by insertion of monofilament,and group A received C1q neutralizing antibody 10 μl injected into the lateral ventricle on the first day after establishing MCAO model.Three days after modeling,the adhesion removal experiment was used to record the adhesion stimulus removal time,and the balance beam experiment was used to evaluate the limb motor function of the rats.After the rats were sacrificed,the ELISA method was used to detect the C1q and C3 levels in the hippocampus tissue,the Western blot method was used to detect the C1q subcom-ponent subunit A(C1qa)and PSD95 protein levels in the hippocampus tissue,and the Nissl staining was used to record the number of Nissl bodies.Results Compared with group S,group M exhibited a signifi-cantly longer adhesion removal time,significantly elevated balance beam experiment score,significantly higher levels of C1q,C3,and C1qa in the hippocampus,and significantly lower levels of PSD95 and Nissl's body count in the hippocampus(P＜0.05).Compared with group M,group A exhibited significantly shor-ter adhesion removals,a significantly lower balance beam experiment score,significantly lower levels of C1q,C3,and C1qa in the hippocampus,significantly higher PSD95 content,and a significantly higher Nissl's body count in the hippocampus(P＜0.05).Conclusion Cerebral ischemia-reperfusion injury in rats can induce extensive activation of the complement system and aggravate the loss of synaptic protein PSD95 and motor dysfunction in rat hippocampal tissue through complement protein C1q.Neutralizing com-plement therapy can effectively improve cerebral ischemia-reperfusion injury in rats.