ABSTRACT
Objective To investigate the effect of hydrogen-rich saline postconditioning on the expression of vascular endothelial growth factor receptor-1 (VEGFR1) during myocardial ischemiareperfusion (I/R) injury in rats.Methods Thirty-six adult male Sprague-Dawley rats,weighing 250-280 g,were randomly divided into 3 groups (n=12 each) using a random number table:sham operation group (group S),group I/R and hydrogen-rich saline group (group H2).Myocardial I/R was induced by 30 min ligation of anterior descending branch of the left coronary artery followed by 2 h reperfusion.In group H2,hydrogen-rich saline 5 ml/kg was injected intravenously at 5 min before reperfusion,while the equal volume of normal saline was given in group I/R.Left ventricular systolic pressure (LVSP),left ventricular enddiastolic pressure (LVEDP) and ± dp/dtmax were measured and recorded during reperfusion and at 120 min of reperfusion.The rats were sacrificed at 120 min of reperfusion,and myocardial specimens were obtained for determination of myocardial infarct size,contents of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) (using ELISA),and expression of VEGFR1 (by Western blot).At 120 min of reperfusion,blood samples were collected from the common carotid artery to measure cardiac troponin I (cTnI) concentrations in serum.Results Compared with group S,LVSP and ± dp/dtmax were significantly decreased,LVEDP was increased,the myocardial infarct size was enlarged,cTnI concentrations in serum and contents of IL-6 and TNF-α were increased,and the expression of VEGFR1 was down-regulated at 120 min of reperfusion in H2 and I/R groups.Compared with group I/R,LVSP and ± dp/dtmax were significantly increased,LVEDP and myocardial infarct size were decreased,cTnI concentrations in serum and contents of IL-6 and TNF-α were decreased,and the expression of VEGFR1 was up-regulated at 120 min of reperfusion in group H2.Conclusion Hydrogen-rich saline postconditioning can reduce myocardial I/R injury possibly by upregulating myocardial VEGFR1 expression and inhibiting inflammatory responses in the myocardium of rats.
ABSTRACT
Objective To determine the dose-response relationship of 0.2％ ropivacaine for ultrasoundguided stellate ganglion block (SGB).Methods Seventy-five ASA physical status [or Ⅱ patients with migraine,aged 23-55 yr,with body mass index of 22-28 kg/m2,scheduled for elective ultrasound-guided SGB,were randomly divided into R1-5 groups (n =15 each) using a random number table.In R1,R2,R3,R4 and R5 groups,the patients underwent ultrasound-guided SGB with 0.2％ ropivacaine 1,2,3,4 and 5 ml,respectively.A successful SGB block was confirmed by the onset of ptosis (Horner syndrome) on the injected side.Probit analysis was used to calculate the effective dose of 0.2 ％ ropivacaine in 50 ％ and 95 ％ of the patients (ED50 and ED95) and 95％ confidence interval (95％ CI).Results The ED50 of 0.2％ ropivacaine for ultrasound-guided SGB was 2.2 ml (95％CI 1.9-2.5 ml) and ED95 was 3.2 ml (95％CI 2.8-4.1 ml).Conclusion The ED50 and ED95 of 0.2％ ropivacaine for ultrasound-guided SGB are 2.2 and 3.2 ml,respectively.
ABSTRACT
<p><b>OBJECTIVE</b>To determine if locally administered bone morphogenetic protein-2 (BMP-2) and osteoprotegerin (OPG) improved osteogenesis and new bone formation by trans-sutural distraction osteogenesis.</p><p><b>METHODS</b>Twenty four dogs were divided into three groups randomly and received new internal trans-sutural distraction osteogenesis treatment. Five days after operation, infusion apparatus with double-tube was inserted to submucosa near the distracted zone to deliver controlled release agent of recombinant human bone morphogenetic protein-2/poly (lactic-co-glycolic acid)/fibrin sealant (rhBMP-2/PLGA/FS) in group A and group C. Recombinant human osteoprotegerin/fibrin sealant (rhOPG/ FS) was injected three weeks later in group B and group C. Histology staining and bone histomorphometry were used to measure the changes of maxillary bone sutura after distraction for 1, 2, 4 and 6 weeks.</p><p><b>RESULTS</b>New bone formation observed in distracted zone showed a significant increase in group A and C. Transmission electron microscope showed the osteoblast and osteocyte were active with dilated rough endoplasmic reticulum and a large number of chondriosomes and Golgi complex. After distraction for 6 weeks, indexes of osteoblast of group A, B, and C were 38.5 +/- 7.7, 35.7 +/- 6.5, and 41.7 +/- 11.0, indexes of osteoclast (Ioc) were 5.9 +/- 1.0, 1.2 +/- 0.3, and 2.8 +/- 0.4, bone trabecula thicknesses were (38.36 +/- 13.28), (66.20 +/- 9.16), and (51.85 +/- 9.92) microm respectively. Increased bone density and decreased Ioc were found in group B and C.</p><p><b>CONCLUSION</b>The new elastic distractor is effective in inducing new bone formation. BMP-2 and OPG combination acts synergistically, and leads to significant enhancement of bone formation and remodeling.</p>
Subject(s)
Animals , Dogs , Humans , Bone Density , Bone Morphogenetic Protein 2 , Lactic Acid , Maxilla , Osteoblasts , Osteogenesis , Osteogenesis, Distraction , Osteoprotegerin , Polyesters , Polyglycolic Acid , Polymers , Recombinant Proteins , Transforming Growth Factor betaABSTRACT
Aim To investigate whether Ca~(2+)/calmodulin-dependent kinase Ⅱ(CaMKⅡ)contribute to tumor necrosis factor α(TNF-α)-induced cardiomyocyte hypertrophy.Methods The protein content was assayed with Lowry's method.The cardiomyocytes volumes were measured by computer photograph analysis system.The protein synthesis was assayed with[~3H]-lencine incorporation method.[Ca~(2+)]_i transient was measured by Till image system by cell-loading Fura-2/AM.The expression of CaMKⅡδ_B was determined by Western blot.Results ① TNF-α significantly induced the increase of protein content, [~3H]-leucine incorporation and cell size;These responses were significantly suppressed by KN93, a selective CaMKⅡ inhibitor.② TNF-α increased the amplitude of the spontaneous Ca~(2+) transients in cultured ventricular myocytes from the neonatal rat;CaMKⅡ inhibitor KN93 can suppress the elevation induced by TNF-α.③ TNF-α significantly increased the expression of CaMKⅡδ_B.Concluslon CaMKⅡ signal pathway are involved in TNF-α-induced cardiomyocyte hypertrophy in rats.
ABSTRACT
Objective To evaluate the effect of dexmedetomidine on the efficacy of patient-controlled intravenous analgesia (PCIA) with morphine after elective radical gastrectomy. Methods One hundred and twenty ASA Ⅰ or Ⅱ patients aged 41-64 yr weighing 50-80 kg undergoing elective radical gastrectomy were randomly divided into 2 groups of 60 patients, according to the composition of PCIA solution:group I morphine (group M)and group Ⅱ morphine + dexmedetomidine (group MD). In group M the PCIA solution contained morphine 100 mg in 200 ml of normal saline (NS), while in group MD the PCIA solution contained morphine 100 mg+dexmedetomidine 200 μg in NS 200 ml. PCIA was started immediately after operation. A loading dose of 6 ml was given iv at the end of operation. PCIA setting was as follows:background infusion 1 ml/h, bolus dose 3 ml and lockout interval 10 min. VAS score was maintained at ≤4 and Ramsay score at 2-3. The total amount of morphine consumed, the number of attempts and successfully delivered doses within 24 and 48 h after operation were recorded. Postoperative complications including nausea, vomiting, bradycardia, hypotension, oversedation and respiratory depression were recorded. Results The total amount of morphine consumed, the number of attempts and successfully delivered doses within 24 and 48 h after operation were significantly smaller and the incidence of nausea and vomiting and pruritus was significantly lower in group MD than in Sroup M. No bradycardia,hypotension, oversedation or respiratory depression was observed in either group. Conclusion Dexmedetomidine added to intravenous morphine PCA can improve the analgesic efficacy after radical gastrectomy with less adverse effects.
ABSTRACT
Objective To investigate the dose-respeuse relationship of levobupivacaine for spinal anesthesia in patients undergoing cesarean section.Methods Sixty ASA Ⅰ or Ⅱ patients aged 25-35 yr weighing 60-90 kg scheduled for elective cesarean section under spinal anesthesia were enrolled in this study.Spinal puncture was performed at the L3,4 interspace.A 25 G spinal needle was inserted into the subarachnoid space cephalad.The patients were randomized to receive levobupivacaine 7.5 mg (group L1 ),10 mg (group L2),12.5 mg (group L3) or 15 mg (group L4) diluted to 3 ml with 5% glucose over 30 s (n = 15 each).The degree of pain was evaluated at the time of skin incision using visual analogue scales (VAS) (0 = no pain and 10 = worse pain ever).Effective analgesia was defined as VAS = 0.Spinal analgesia was inadequate when VAS≥1 and then 1% lidocaine 5-10 ml was given epidurally.The doses of levobupivacaine for effective analgesia in 50% and 95% of patients ( ED50 and ED95 ) and 95 % confidence interval were calculated by Probit method.Results The ED50 of levobupivacaine was 9.0 mg (95% confidence interval 7.8-9.9 mg) and ED95 13.2 mg (95% confidence interval 11.6-17.6 mg) for spinal anesthesia.Conclusion The ED50 and ED95 of levobupivacaine for spinal anesthesia in patients undergoing cesarean section are 9.0 mg and 13.2 mg respectively.
ABSTRACT
Aim To investigate whether Ca2+/calmodulin-dependent kinase Ⅱ(CaMKⅡ)contribute to tumor necrosis factor ?(TNF-?)-induced cardiomyocyte hypertrophy.Methods The protein content was assayed with Lowry's method.The cardiomyocytes volumes were measured by computer photograph analysis system.The protein synthesis was assayed with[3H]-lencine incorporation method.[Ca2+]i transient was measured by Till image system by cell-loading Fura-2/AM.The expression of CaMKⅡ?B was determined by Western blot.Results ① TNF-? significantly induced the increase of protein content,[3H]-leucine incorporation and cell size;These responses were significantly suppressed by KN93,a selective CaMKⅡ inhibitor.② TNF-? increased the amplitude of the spontaneous Ca2+ transients in cultured ventricular myocytes from the neonatal rat;CaMKⅡ inhibitor KN93 can suppress the elevation induced by TNF-?.③ TNF-? significantly increased the expression of CaMKⅡ?B.Concluslon CaMKⅡ signal pathway are involved in TNF-?-induced cardiomyocyte hypertrophy in rats.