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Objective To investigate the effect of dexmedetomidine on cognitive dysfunction after offpump coronary artery bypass grafting in patients.Methods Fifty-eight ASA physical status Ⅱt or Ⅲ patients,aged 51-63 yr,weighing 52-83 kg,undergoing off-pump coronary artery bypass grafting,were randomly divided into 2 groups (n =29 each):control group (group C) and dexmedetomidine group (group D).Anesthesia was induced with midazolam,etomidate,sufentanil and pipecuronium.The patients were thracheal intubated and mechanically ventilated.Anesthesia was maintained with propofol,sufentanil,isoflurane and pipecuronium.A loading dose of dexmedetomidine 1 μg/kg was infused over 15 min after tracheal intubation,followed by dexmedetomidine infusion at 0.5 μg· kg-1 · h-1 until the end of operation in group D,while the equal volume of normal saline was infused in group C.Cognitive function was assessed by Mini-Mental State Examination (MMSE) at 24 h before operation and 24,48 and 72 h after operation.The development of postoperative cognitive dysfunction was recorded within 72 h after operation.The consumption of sufentanil and extubation time after extubation was recorded.Results Compared with group C,MMSE scores at 24 and 48 h after operation were significantly increased and the incidence of postoperative cognitive dysfunction within 72 h after operation was decreased (P ＜ 0.05),and no significant change was found in the consumption of sufentanil and extubation time in group C (P ＞ 0.05).Conclusion Dexmedetomidine can decrease the development of postoperative cognitive dysfunction after off-pump coronary artery bypass grafting in patients.
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Objective To study the effect of basic fibroblast growth factor(bFGF) on neuron-like differentiation of superparamagnetic iron oxide nanoparticles (SPIONs)-labeled amniotic membrane-derived mesenchymal stem cell.Methods Cells were cultured from enzymatic-digested amniotic membrane tissue.After that,the following steps were taken:(1) Mesenchymal stem cells derived from amniotic membrane were identified by using cell morphology,MTT method and flow cytometry.(2)SPIONs were used to label amniotic membrane-derived mesenchymal stem.(3)bFGF was imported to induce the neuron-like differentiation of SPIONs-labeled amniotic membrane-derived mesenchymal stem cell.Results (1) Primary cultures of P3,amniotic membrane-derived mesenchymal stem cell were fibroblast-like and expression of surface molecules CD29,CD44,CD90 and CD105 was detected,while expression of CD31,CD34,CD45 and CD106 was negative.(2) SPIONs of no more than 14.0 μg/ml are safe to label amniotic membrane-derived mesenchymal stem cells.Cell activity is more than 80％ and expression of surface molecules CD29,CD44,CD90 and CD105 is positive.(3)RT-PCR and immunocytochemistry analysis showed that 10.0 ng/ml bFGF induced neuron-like differentiation of amniotic membrane-derived mesenchymal stem cell (14 μg/ml SPIONs-labeled).Conclusions Enzymatic digestion and cell adherent culture method can be used to isolate mesenchymal stem cells from amniotic membrane.SPIONs of no more than 14.0 μg/ml are safe to label amniotic membrance-derived mesenchymal stem cells and have no effect on the cell activity.Neuron-like differentiation of amniotic membrane-derived mesenchymal stem cell can be induced with 10.0 ng/ml bFGF.
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Aim To investigate the inhibitory effect of atrase B on human platelet aggregation induced by activated complement.Methods By employing CVF to activate complement,the effect of atrase B on gel filtered platelet aggregation induced by activated complement was measured by turbidimetry and the expression of P-selectin and GPⅡb/Ⅲa on platelet membrane were detected by flow cytometry.Results Atrase B inhibited platelet aggregation and the expression of P-selectin and GPⅡb/Ⅲa on platelet membrane induced by activated complement.Conclusion Anticomplementary protein atrase B from Naja atra venom can significantly inhibit platelet activation and aggregation induced by activated complement.
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Aim To investigate the effect and mechanism of cobra venom metalloproteinase atrase A on inhibiting platelet aggregation.Methods Platelet aggregation induced by collagen,ADP,PAF,AA,ristocetin and thrombin,respectively,was measured turbimetrically after platelet incubated with atrase A.Western blot was used to detect the effect of atrase A on cleavage of platelet membrane glycoprotein and von Willebrand Factor.Results Atrase A significantly inhibited platelet aggregation induced by ristocetin and thrombin in a dose-and time-dependent manner.Meanwhile,atrase A just showed slight inhibitory effect on platelet aggregation induced by PAF,AA,collagen,and ADP after incubated with PRP for 5 min.After incubation time was prolonged to 30 min,significant inhibition was shown on platelet aggregation.Western blot revealed that atrase A cleaved platelet membrane glycoprotein GPIb.Conclusions Cobra venom metalloproteinase atrase A significantly inhibits platelet aggregation induced by ristocetin and thrombin due to the cleavage of platelet membrane glycoprotein Ib.And atrase A also has inhibitory effect on platelet aggregation induced by ADP,PAF,AA,and collagen.