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Objective:To evaluate the effect of intraoperative individualized systolic blood pressure (SBP) management on myocardial injury after hip replacement in elderly patients at high risks of hypertension.Methods:One hundred and eighty-two patients of either sex, aged 60-89 yr, with body mass index of 18-26 kg/m 2, with a history of hypertension requiring drug treatment and stratified high risk factors of cardiovascular risk factors, scheduled for elective hip replacement under general anesthesia, were divided into 2 groups ( n=91 each) using a random number table method: routine management group and individualized SBP management group. Individualized SBP management group maintained the intraoperative SBP at 90%-110% of the baseline value, and routine management group implemented blood pressure management according to the current routine clinical pathway.The intermedian cubital venous blood samples were collected before surgery and at 24, 48, and 72 h after surgery for determination of the serum concentrations of high sensitivity cardiac troponin T. Postoperative myocardial injury and myocardial infarction were also recorded. The 30-day all-cause mortality was recorded on day 30 after surgery. Results:The incidence of postoperative myocardial injury and serum concentrations of high sensitivity cardiac troponin T at 24, 48 and 72 h after surgery were significantly decreased, and the length of hospital stay was shortened in individualized SBP management group as compared with routine management group ( P<0.05). Conclusions:Intraoperative individualized SBP management can reduce the postoperative myocardial injury in elderly patients at high risk of hypertension undergoing hip replacement.
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Objective:To identify the risk factors for acute kidney injury (AKI) after lumbar surgery in elderly patients and develop a score prediction model.Methods:The elderly patients who underwent lumbar surgery were retrospectively analyzed.The patients were divided into AKI group and non-AKI group according to the diagnostic criteria in Kidney Disease: Improving Global Outcomes.Demographic data, history of underlying diseases, perioperative general status and related research laboratory tests were collected.Factors with statistically significant differences between groups were included in the logistic regression model.Risk factors were identified and the weighted score regression prediction model was developed.The receiver operating characteristic curve was drawn, and the model was evaluated.Results:AKI occurred in 87 patients (11.9%) after operation.Logistic regression results showed that increasing age, hypertension, anemia, hypoproteinemia, diabetes mellitus, duration of intraoperative low mean arterial pressure and blood transfusion were independent risk factors for AKI in elderly patients after lumbar surgery.The area under the receiver operating characteristic curve and 95% confidence interval were 0.909 (0.870-0.947), the sensitivity was 79.36%, the specificity was 92.74%, and the Youdon index was 0.719.The line chart prediction model was developed.The prediction analysis model was verified by Hosmer-Lemshow test, P=0.413, and the C-index visualized line chart prediction model was 0.908. Conclusions:Increasing age, hypertension, hypoproteinemia, diabetes mellitus, anemia, duration of intraoperative low mean arterial pressure and blood transfusion are independent risk factors for AKI after lumbar surgery in elderly patients.The risk prediction model developed can effectively predict the occurrence of AKI after lumbar surgery in elderly patients.
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Objective:To evaluate the relationship between declined preoperative left ventricular diastolic function and postoperative increased extravascular lung water (EVLW) in the patients undergoing transurethral resection of the prostate (TURP).Methods:A total of 116 patients, aged 55-90 yr, of American Society of Anesthesiologists physical status Ⅰ-Ⅲ, with body mass index of ≤30 kg/m 2, undergoing elective TURP under general anesthesia, without increased EVLW before surgery, were included in the study.Lung ultrasound examination was performed and lung ultrasound scores were assessed before leaving PACU.Increased EVLW was defined as lung ultrasound score ≥20.The occurrence of increased EVLW after operation was recorded, and patients were divided into increased EVLW group and non-increased EVLW group according to whether increased EVLW occurred.Multivariate logistic regression analysis was used to identify the risk factors for postoperative increased EVLW. Results:The results of multivariate logistic regression analysis showed that declined preoperative left ventricular diastolic function was an independent risk factor for postoperative increased EVLW ( P<0.05). Conclusions:Declined preoperative left ventricular diastolic function is an independent risk factor for postoperative increased EVLW in the patients undergoing TURP.
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Objective To study the incidence of moderate and severe preoperative anxiety and its related risk factors in patients undergoing elective general anesthesia.Methods A total of 562 pa-tients undergoing selective anesthesia 225 males and 337 females,aged 18-85 years,ASA physical status Ⅰ-Ⅲ,were selected in the affiliated hospital of Xuzhou medical university.State-trait anxiety inventory (STAI)was used to assess the degree of preoperative anxiety and the patients were divided into mild anxiety group (SAI ≤ 37,n=294)and moderate and severe anxiety group (SAI > 37,n=268)according to SAI score.The factors related to preoperative anxiety such as age,gender,edu-cational background,marital status,history of previous surgery,presence of pain,preoperative diag-nosis of tumor and presence or absence of hypertension were collected.Results The incidence of moderate and severe preoperative anxiety in our study was 268 (47.7%).Logistic regression analysis showed that female (OR=1.846,95%C I 1.298-2.624),single (OR=2.208,95%C I 1.218-4.004) might be the risk factors of preoperative anxiety.Conclusion Females and single individuals may be independent risk factors for preoperative anxiety.
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Objective To evaluate the effect of limb remote ischaemic preconditioning on pul-monary function in patients undergoing cardiac valve replacement surgery with cardiopulmonary by-pass.Methods Seventy patients,32 males and 38 females,aged 18-70 years,weighing 45-90 kg, ASA physical status Ⅱ or Ⅲ,scheduled for elective cardiac valve replacement surgery with cardiopul-monary bypass,were divided into 2 groups using a random number table,35 in each group.Patients in group R received three cycles of right upper-limb 5 min ischemia (blood-pressure cuff inflation to≥ 200 mm Hg)and 5 min reperfusion (blood-pressure cuff deflation to 0 mm Hg)at 10 min after in-tubation.In group C,the cuff was placed around the arm but not inflated.At 10 min after intubation (T0),at 1 h after aortic declamping (T1)and at 6 h (T2),12 h (T3),24 h (T4)after surgery,arte-rial blood was sampled to conduct gas analysis,PaO2/FiO2ratio and alveolar-arterial oxygen gradient (A-aDO2)were calculated,and the dynamic lung compliance (Cd)and static lung compliance (Cs) were also recorded.The occurrence of pulmonary adverse events was recorded until discharge. Results Compared with T0,PaO2/FiO2was decreased in the two groups at T1-T4,A-aDO2was de-creased at T2-T4,Cs and Cd were increased in group C at T3,and were increased in group R at T2, T3(P<0.05).Compared with group C,the Cs and Cd at T2,T3were increased in group R.There were no significant differences between the two groups in the PaO2/FiO2,A-aDO2at T0-T4.The oc-currence of the pulmonary adverse events was decreased significantly in group R than in group C (P<0.05).The occurrence of pulmonary adverse events was declined significantly in group R than in group C (P<0.05).Conclusion Limb remote ischemic preconditioning can improve the lung compli-ance and reduce the occurrence of the pulmonary adverse events in patients undergoing cardiac valve replacement surgery.
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Objective To compare the myocardial protective effects of post-treatment with sevoflurane and isoflurane on myocardial ischemia-reperfusion injury(MIRI) in adult rats.Methods Twenty-four adult male SD rats were divided into four groups (n =6) by using the random number table,control group (C),isehemia-reperfusion group (R),sevoflurane post-treatment (S) and isoflurane post-treatment group(I).The Langendorff isolated heart perfusion model was established.The heart rate(HR),left ventricular end-diastolic pressure(LLVEDP),left ventricular developed pressure(LVDP),maximum rate of rise of left ventricular pressure(LV+-dp/dtmax),and maximum rate of decrease of left ventricular pressure(LV-dp/dtmax) were recorded at the end of equilibrium perfusion,and at 30,90 min of reperfusion,respectively.At the end of infusion,1 mm3.of apical myocardial tissue was removed for observing mitochondrial structure under electron microscopy and scoring.The myocardial infarct size(MIS) in the remaining heart tissue was measured by TTC staining.Results Compared with the R group,the S and I groups showed improved cardiac function indicators,decreased MIS,and reduced mitochondrial damage after reperfusion(P＜0.05).Compared with the S group,the I group showed worse heart function,increased MIS,and more severe mitochondrial damage after reperfusion(P＜0.05).Conclusion Post-treatment with sevoflurane and isoflurane has a protective effect on MIRI in adult rats.Post-treatment with sevoflurane has a better cardioprotective effect than that with isoflurane.
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Objective To evaluate the effect of sevoflurane postconditioning on the expression of Pim-1 kinase during myocardial ischemia-reperfusion (I/R) in rats.Methods Male Sprague-Dawley rats,weighing 250-300 g,were used in this study.After the animals were anesthetized,their hearts were immediately removed and retrogradely perfused with an oxygenated K-H solution at 37 ℃ in a Langendorff apparatus.Thirty-six isolated rat hearts were assigned into 3 groups (n=12 each) using a random number table:control group (group C),group I/R and sevoflurane postconditioning group (group SP).The hearts were subjected to ischemia for 30 min followed by 120 min of reperfusion to establish the model of myocardial I/R injury.In group SP,the hearts were perfused with K-H solution saturated with 3％ sevoflurane for 15 min starting from the beginning of reperfusion.Heart rate (HR),left ventricular end-diastolic pressure (LVEDP),left ventricular developed pressure (LVDP) and the maximum rate of increase and decrease of left ventricular pressure (±dp/dtmax)were recorded at the end of equilibration and 30,60,90and 120 min of reperfusion.Myocardial tissues were obtained at T2 for determination of the expression of Pim-1 kinase,Bcl-2 and cytochrome c (Cyt c) in cytoplasm and mitochondria by Western blot.The hearts were selected at T4 for determination of myocardial infarct size (by TTC staining) and for examination of mitochondrial ultrastructure (with transmission electron microscope).Results Compared with group C,HR,LVDP and ±dp/dtmax were significantly decreased,and LVEDP was increased at T1-4,the myocardial infarct size was enlarged,the expression of Pim-1 and Bcl-2 in cytoplasm and mitochondria was down-regulated,the expression of Cyt c in cytoplasm was up-regulated,and the expression of Cyt c in mitochondria was down-regulated in group I/R (P＜0.05).Compared with group I/R,HR,LVDP and ±dp/ dtmax were significantly increased,and LVEDP was decreased at T1-4,the myocardial infarct size was decreased,the expression of Pim-1 kinase and Bcl-2 in cytoplasm and mitochondria was up-regulated,the expression of Cyt c in cytoplasm was down-regulated,and the expression of Cyt c in mitochondria was upregulated in group SP (P＜0.05).The damage to mitochondria was significantly attenuated in group SP as compared with group I/R,and was aggravated as compared with group C.Conclusion The mechanism by which sevoflurane postconditioning attenuates myocardial I/R may be related to up-regulation of Pim-1 kinase expression in rats.
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Objective To investigate the effect of sevoflurane postconditioning on mitochondrial connexin 43 (Cx43) during myocardial ischemia-reperfusion (I/R) in isolated rat hearts and the role of mitochondrial ATP-sensitive potassium (mito-KATP) channels in it.Methods Forty-five adult male SpragueDawley rats,weighing 200-250 g,were used in the study.Their hearts were excised and retrogradely perfused with K-H solution in a Langendorff apparatus.The 45 isolated hearts were assigned into 5 groups (n =9 each) using a random number table:control group (group C),I/R group,sevoflurane postconditioning group (group Sev),and sevoflurane postconditioning plus 5-hydroxydecanoate (5-HD,a specific mitoKATp channel blocker) group (group Sev+5-HD) and I/R plus 5-HD group (group I/R+5-HD).The hearts were subjected to 20 main of global ischemia followed by 90 min of reperfusion to establish the model of myocardial I/R injury.From the beginning of reperfusion,the hearts were perfused with K-H solution saturated with 3％ sevoflurane for 15 min in group Sev,with K-H solution saturated with 3％ sevoflurane and containing 100 μ mol/L 5-HD in group Sev+5-HD,and with K-H solution containing 100 μ mol/L 5-HD in group 5-HD.The heart rate (HR),left ventricular end-diastolic pressure (LVEDP),left ventricular developed pressure (LVDP) and the maximum rate of increase and decrease of ventricular pressure (±dp/dtmax) were recorded at the end of equilibration (T1) and 30 and 60 min of reperfusion (T2,3).At 90 min of reperfusion,the myocardial infarct size was measured by TTC staining,and the expression of total Cx43 (tCx43)and phosphorylated Cx43 (p-Cx43) in mitochondria was determined by Western blot analysis.The percentage of myocardial infarct size and p-Cx43/tCx43 ratio were calculated.Results Compared with group C,the HR,LVDP and ±dp/dtmax were significantly decreased,and the LVEDP was increased at T2,3,and the percentage of myocardial infarct size was increased in the other 4 groups,the expression of mitochondrial tCx43 and p-Cx43 was significantly down-regulated in I/R,Sev+5-HD and 5-HD groups (P＜0.05),and no significant change was found in the expression of mitochondrial tCx43 and p-Cx43 in group Sev (P＞0.05).Compared with group I/R,the HR,LVDP and ±dp/dtmax were significantly increased,and the LVEDP was decreased at T2,3,the percentage of myocardial infarct size was decreased,and the expression of mitochondrial tCx43 and p-Cx43 was up-regulated in group Sev (P＜0.05),and no significant change was found in the parameters mentioned above in Sev+5-HD and 5-HD groups (P＞0.05).Compared with group Sev,the HR,LVDP and ±dp/dt were significantly decreased,and the LVEDP was increased at T2,3,the percentage of myocardial infarct size was increased,and the expression of mitochondrial tCx43 and p-Cx43 was down-regulated in group Sev+5-HD (P＜0.05).There was no significant change in the pCx43/tCx43 ratio between the five groups (P＞0.05).Conclusion The mechanism by which sevoflurane postconditioning attenuates myocardial I/R injury may be related to induction of mito-KATP channel opening and up-regulation of the expression of mitochondrial Cx43 in cardiomyocytes of rats.
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Objective To evaluate the effects of sevoflurane preconditioning on wnt/glycogen synthase kinase-3 beta (GSK-3β)/β-catenin signaling pathway during myocardial ischemia-reperfusion (I/R) injury in rats in vitro.Methods Ault male Wistar rats,weighing 220-280 g,were heparinized and anesthetized with intraperitoneal 3％ pentobarbital 30 mg/kg.Their hearts were rapidly excised and perfused in a langendorff apparatus with oxygenated (95％ O2-5％ CO2) K-H solution at 37 ℃.After 15 min of equilibration,36 isolated hearts were randomly divided into 3 groups (n=12 each) using a random number table:sham operation group (group S),group I/R and sevoflurane preconditioning group (group SP).After 30 min of equilibration,the hearts were continuously perfused for 150 min in group S.The isolated hearts were subjected to 30 min of ischemia followed by 120 min of reperfusion.In SP group,the hearts were perfused for 15 min with K-H solution containing 2.4％ sevoflurane,followed by 5 min washout before reperfusion.At the end of equilibration and 30 min of reperfusion,HR,left ventricular end-diastolic pressure (LVEDP),left ventricular developed pressure (LVDP) and ± dp/dtmax were recorded.The severity of arrhythmias was assessed during reperfusion.At 60 min of reperfusion,3 hearts in each group were chosen for measurement of expression of wnt3a,phosphor-GSK-3β (p-GSK-3β) and β-catenin (by Western blot).At 120 min of reperfusion,6 hearts in each group were chosen for determination of myocardial infarct size by TTC staining.Results Compared with group S,HR,LVDP,+dp/dtmax and -dp/dtmax were significantly decreased,and LVEDP was increased at 30 min of reperfusion,arrhythmia scores and the percentage of myocardial infarct size were increased,and the expression of wnt3a,p-GSK-3β and β-catenin was down-regulated in I/R group.Compared with group I/R,HR,LVDP,+dp/dtmax and-dp/dtmax were significantly increased,and LVEDP was decreased at 30 min of reperfusion,arrhythmia scores and the percentage of myocardial infarct size were decreased,and the expression of wnt3a,p-GSK-3β and β-catenin was up-regulated in group SP.Conclusion Sevoflurane preconditioning attenuates myocardial I/R injury by activating wnt/GSK-3β/β-catenin signaling pathway in isolated rat hearts.
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Objective To evaluate the effects of sevoflurane preconditioning on zonula occludens-1 (ZO-1) during myocardial ischemia-reperfusion (I/R) in rats in vitro.Methods Adult male Wistar rats,weighing 250-300 g,were anesthetized with intraperitoneal pentobarbital 30 mg/kg and heparinized.Their hearts were excised and perfused in a Langendorff apparatus with K-H solution saturated with 95％ O2-5％ CO2 at 37 ℃.Eighteen isolated rat hearts were randomly assigned into 3 groups (n =6 each) using a random number table:control group (group C),group I/R and sevoflurane preconditioning group (group S).At 10 min of equilibration,the hearts were perfused with K-H solution for 110 min in group C,the hearts were perfused with K-H solution for 20 min,and then subjected to 30 min of ischemia followed by 60 min of reperfusion in group I/R,and the hearts were perfused with K-H solution saturated with 3％ sevoflurane for 15 min followed by 5 min washout,and then subjected to 30 min of ischemia followed by 60 min of reperfusion in group S.At the end of equilibration,immediately before ischemia,and at 15 and 60 min of reperfusion (T1,2),HR,left ventricular end-diastolic pressure (LVEDP),left ventricular developed pressure (LVDP),+ dp/dtmax and-dp/dtmax were recorded.The development of arrhythmias was recorded during reperfusion and scored.At 60 min of reperfusion,myocardial specimens were obtained from the apex of heart for determination of the expression of ZO-1 in myocardial tissues (by Western blot) and for observation of distribution of ZO-1 and connexin43 (Cx43) (by immunofluorescence).Results Compared with group C,HR,LVDP,+ dp/dtmax and-dp/dtmax were significantly decreased and LVEDP was increased at 15 and 60 min of reperfusion,scores of arrhythmia was increased,and ZO-1 expression was down-regulated in I/R group.Compared with group I/R,HR,LVDP,+ dp/dtmax and-dp/dtmax were significantly increased and LVEDP was decreased at 15 and 60 min of reperfusion,arrhythmia was decreased,and ZO-1 expression was up-regulated in group S.ZO-1 and Cx43 were co-localized at the intercalated disk.ZO-1 was redistributed in the lateralization of the membrane and co-localized with Cx43 in group I/R.The incidence of ZO-1 lateralization was significantly decreased in group S.Conclusion The mechanism by which sevoflurane preconditioning decreases reperfusion arrhythmia is related to inhibition of down-regulation of expression and redistribution of ZO-1 and inhibition of redistribution of Cx43 in rats.
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Objective To evaluate the relationship between calmodulin protein kinase Ⅱ (CaMK Ⅱ) and levosimendan against arrhythmias induced by myocardial ischemia-reperfusion (I/R) in rats in vitro.Methods Thirty male Wistar rats,weighing 250-300 g,were randomly divided into 3 groups (n =10 each) using a random number table:control group (group C),I/R group and levosimendan group (group L).Their hearts were rapidly excised and perfused in a langendorff apparatus with K-H solution saturated with 95％ O2-5％ CO2 at 36.5-37.5 ℃.At 20 min of equilibration,the hearts were perfused with K-H solution for 60 min in group C.The hearts were subjected to 30 min of ischemia followed by 30 min reperfusion with K-H solution in group I/R.The hearts were subjected to 30 min of ischemia followed by 30 min reperfusion with K-H solution containing 300 nmol/L levosimendan in group L.Left ventricle developed pressure (LVDP),left ventricle end-diastolic pressure (LVEDP),+ dP/dt-dP/dtmax and heart rate (HR) were recorded immediately before ischemia and at 15 and 30 min of reperfusion.Arrhythmia was recorded during reperfusion and scored.Specimens were obtained from the apex of heart at 30 min of reperfusion for determination of the intracellular calcium concentration ([Ca2 +] i).Myocardial specimens were obtained from the left ventricle at 30 min of reperfusion to detect CaMK Ⅱ activity.Results Compared with group C,arrhythmia score,[Ca2+]i and CaMK [Ⅱ activity were significantly increased,and LVDP,+ dP/dtmax,-dP/dtmax and HR were decreased,and LVEDP was increased at 15 and 30 min of reperfusion in group I/R.Compared with group I/R,the number of ventricular premature beat,arrhythmia score,[Ca2+] i and CaMK Ⅱ activity were significantly decreased,and LVDP,+ dP/dtmax,-dP/dtmax and HR were increased,and LVEDP was decreased at 15 and 30 min of reperfusion in group L.Conclusion Inhibition of CaMK Ⅱ activity is involved in the mechanism by which levosimendan decreases the development of arrhythmias induced by myocardial I/R in rats.
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ObjectiveTo investigate the protective effect of sevoflurane postconditioning (Sevo-Postcon)on the hearts isolated from rats with diabetes mellitus (DM) of different duration against ischemia-reperfusion (I/R)injury.MethodsSeventy-two pathogen-free male SD rats weighing 200-240 g were randomly divided into 3 groups ( n =24 each):group Ⅰ rats without DM (C) ; group Ⅱ rats with 2 week DM (2w DM) and group Ⅲ rats with 6 week DM (6w DM).DM was produced by intraperitoneal (IP) 1％ streptozocin (STZ) 60 mg/kg and confirmed by fasting blood glucose concentration ＞ 16.7 mmol/L in groups Ⅱ and Ⅲ.Hearts were isolated from rats and perfused with Krebs-Henseleit buffer (KHB) in a Langendorff apparatus.After a 15 min stabilization period,the isolated hearts were subjected to 30 min of global no-flow ischemia followed by 75 min of reperfusion.Twelve hearts in each group were perfused after ischemia with KHB saturated with 3％ Sevo for 15 min followed by perfusion with regular KHB for 60 min.LVEDP,LVDP, ± dp/dt and HR were measured and recorded after 15 min stabilization (T0,baseline) and at 15 and 75 min of reperfusion (T1,2 ).Myocardial specimens were obtained at 15 min of reperfusion (T1) for detection of p-Akt expression (by Western blot analysis).Infarct size was determined at 75 min of reperfusion (T2).ResultsSevo-Postcon significantly improved cardiac function,reduced infarct size and up-regulated p-Akt expression in groups Ⅰ (C) and Ⅱ (2w DM),while in group Ⅲ (6w DM) Sevo-Postcon did not cause any change in cardiac function,infarct size and p-Akt expression as compared with the isolated hearts without Sevo-Postcon.ConclusionThe cardioprotective effect of Sevo-Postcon can be attenuated with increasing duration of DM by impairing PI3K/Akt signaling pathway.
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Objective To investigate the role of phosphatidyl-inositol 3-kinase-Akt (PI3k-Akt) signal pathway in the attenuation of ischemia-reperfusion (I/R) injury by sevoflurane preconditioning in isolated rat hearts. Methods Ninety-six adult male SD rats weighing 220-280 g were randomly divided into 6 groups ( n = 16 each): sham operation group (group S); I/R group; sevoflurane preconditioning group (group SP); wortmannin group (group W); dimethyl sulfoxide (DMSO) group (group D) and sevoflurane preconditioning + wortmannin group (group SW) . Their hearts were excised and perfused in a Langendorff apparatus with K-H solution saturated with 95%O2-5%C02 at 37 ℃ . The hearts were continuously perfused for 180 min in group S. After 15 min of equilibration, the isolated hearts were subjected to 30 min of ischemia followed by 120 min of reperfusion in SP, W, D and SW groups. Croups SP, W, D and SW received 10 min of perfusion with K-H solution containing 2. 4% sevoflurane, 100 nmol/L wortmannin, 20 μmol/L DMSO, and 2.4% sevoflurane + 100 nmol/L wortmannin, respectively, followed by 5 min washout before I/R. Eight hearts in each group were selected and HR, left ventricular end-diabetic pressure (LVEDP), left ventricular developed pressure (LVDP), and ± dp/dtmax were recorded at the end of equilibration and at 15 min of reperfusion, Myocardial tissues were obtained at 15 min of reperfusion for determination of apoptosis (by TUNEL) and phosphorylated Akt (p-Akt) expression (by Western blot) . Another 8 hearts were selected at 120 min of reperfusion for determination of myocardial infarct size by TTC staining. Result Compared with group S, LVDP and ± dp/dt,
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<p><b>OBJECTIVE</b>To investigate the feasibility of endothelialization of bioprosthesis by transfer of vascular endothelial growth factor (VEGF) gene.</p><p><b>METHODS</b>Bovine pericardium treated with glutaraldehyde and L-glutamic acid was positioned into the pig right atrium. pcD(2)/hVEGF(121) gene (1 mg) was transferred into the right ventricular myocardium using surgical sutures Reverse transcri ption polymerase chain reaction (RT PCR) was employed to evaluate the expression of myocardial VEGF mRNA. The determination of concentrations of VEGF protein in blood from both the right atrium and peripheral vein, and histological and ultrastructural analysis of implanted bovine pericardium were completed simultaneously.</p><p><b>RESULTS</b>The concentration of VEGF derived from the right atrium in pcD(2)/hVEGF(121) group was significantly higher than that in the pcD(2) group 10 days after VEGF gene transfer (P < 0.01). The expression of myocardial VEGF mRNA in pcD(2)/hVEGF(121) group was much higher in comparison with that in the pcD(2) group. The morphological analysis demonstrated that the coverage rate of host endothelium in the pcD(2)/hVEGF(121) group was 2.6 times as fast as that in the pcD(2) group at 16 days after VEGF(121) gene transfer (P < 0.01). Entire endothelialization occurred at 30 days after VEGF gene transfer. In addition, higher expression of myocardial VEGF mRNA was still available.</p><p><b>CONCLUSIONS</b>VEGF gene transfer by surgical suture can remarkably accelerate endothelialization of bioprosthesis, which may provide a new approach for inhibiting biological valve calcification and improve biocompatibility and long-term durability of the bioprosthesis.</p>