ABSTRACT
Objective To investigate the role of induction of carbon monoxide (CO) with methylene chloride (MC) in recipients in ameliorating allograft rejection and prolonging allograft survival and to explore the possible mechanisms in a murine heart transplantation model.Methods Inbred male C57BL/6 mice were used as donors and inbred male Balb/c mice as recipients respectively to establish cervical heterotopic heart transplantation model.The experiments were divided into 3 groups.Recipients were treated with MC (100 mg/kg,per os) day 1 prior to transplantation to day 6 posttransplantation (group MC1w) or to day 13 posttransplantation (group MC2w),or treated with isovolumic olive oil day 1 prior to transplantation to cardiac arrest of allograft (group Tx).The serum TNF-α and IL-10 proteins,TNF-α and IL-10 mRNA,and Foxp3 mRNA and protein in cardiac grafts were measured respectively.The intercellular adhesion molecule-1 (ICAM-1) and Caspase-3 protein in cardiac grafts,and the histopathologic changes of cardiac grafts were also observed.Results Serum COHb levels in untreated mice were (0.85 ± 0.28)％.After MC application,serum COHb peaked within 3 h in recipients (5.24 ± 0,45)％ (P＜0.01 ).The median survival time of cardiac grafts in group MC1w(12.1 days) and group MC2w( 19.4 days) was longer than that in group Tx (6.3 days) (P ＜0.01). As compared with group Tx,induction of CO in group MC1w and group MC2w down-regulated significantly the levels of serum TNF-α (P＜0.01 ) and TNF-α mRNA (P＜0.01) of cardiac grafts and spleen in recipient mice,inhibited the protein expression of ICAM-1 (P＜0.01) and Caspase-3 (P＜0.01) of cardiac grafts,and inhibited,especially in group MC2w,the proliferation of lymphocytes and monocytes infiltration in cardiac grafts.There was no significant difference in serum IL-10 and Foxp3 mRNA and protein in cardiac grafts and spleen of recipients among the groups (P＞0.05).Conclusion Induction of CM in recipients could relieve cardiac allograft rejection and prolong cardiac allograft survival via its anti-inflammation and anti-apoptotic effects,not via up-regulation of Foxp3 in recipient mice.
ABSTRACT
Objective Pentamethylquercetin (PMQ) has a role in cardiovascular protection. We investigate the effects of 3,3' ,4' ,5,7-pentamethylquercetin, a derivative of PMQ, on intimal hyperplasia of the vein grafts in rats both in vivo and in vitro. Methods The proliferation of vascular smooth muscle cells ( VSMC ) was induced with Ang Ⅱ (0. 1μmol/L, 24 h)while PMQ was administrated at six different dosages (0. 1, 0.3, 1,3, 10 and 30 μmoL/L). Cell viability was identified with MTT; ROS was measured with DCFH-DA; and the expression of NADPH oxidase subunits Nox1, p47phox, and p22phox mRNA were measured with real-time PCR. For the experiment in vivo, 24 SD rats were randomly assigned to control group and PMQ groups, the latter was further divided into three different dosage groups. In the control group, solvent was administrated daily via gavage. In PMQ groups, PMQ ( 12.5 mg/kg, 25 mg/kg, 50 mg/kg) was administrated daily respectively in the same way.All SD rats received operation performed by one person. Reversed external jugular vein was implanted into the external carotid of the same side with interrupted suture. 4 weeks after operation, all vein grafts were harvested. Status of the vein grafts was observed and tissue sections were analyzed with HE staining. The intimal hyperplasia ( intima/media area index and intima/media thickness index) of the vein grafts was assessed. Results Cell viability and ROS of VSMC induced by Ang Ⅱ were suppressed by PMQ. Cell viability and ROS of VSMC were increased substantially when treated with Ang Ⅱ. The therapeutic effects of PMQ could be initially identified at dose of0. 3 μmol/L, with a peak at 3 μmol/L. The effects decreased from 30μmol/L to 10 μmol/L. PMQ at dose of 0.1 μmol/L had no effect on cell viability and ROS of VSMC induced by Ang Ⅱ. PMQ also downregulated the mRNA expression of NADPH oxidase subunits Nox1, p47phox and p22phox induced by Ang Ⅱ. A peak effect was observed at 3μmoL/L and decreased at 30 μmol/L. PMQ at o. 1 μmol/L had no effect on mRNA expression of NADPH oxidase subunits induced by Ang Ⅱ. As compared with control group, PMQ decreased intima/media area index ( 1. 64 ±0.20 in control, 0. 74 ±0.18 at 12.5 mg/kg, 1.09 ±0.17 at 25 mg/kg, 1.21 ± 0. 21 at 50 mg/kg) and intima/media thickness index ( 1.34 ± 0. 24 in control, 0.67 ± 0. 17 at 12.5 mg/kg, 0. 74 ± 0.14 at 25 mg/kg, 0.93 ± 0. 18 at 50mg/kg) at three dosages after implantation. Conclusion PMQ may suppress the proliferation of VSMC and inhibit neointima hyperplasia of vein grafts in rats. The effects may be attributed to the anti-oxidative activity and the downregulation of mRNA expression of NADPH oxidase subunits Noxl, p47phox and p22phox.
ABSTRACT
This study examined the adipocytokine-vascular interactions and link between epicardial adipose tissue and coronary artery atherosclerosis. Thirty-four patients undergoing open heart surgery were chosen randomly, and divided into group I (non-coronary artery disease group) and group II (coronary artery disease group). Blood samples were taken through peripheral vein prior to surgery. Plasma levels of a panel of proteins (adiponectin, IL-10, TNF-α) were detected by using ELISA. Epicardial adipose tissue was taken near the proximal tract of the right coronary artery and subcutaneous adipose was taken from the leg before cardiopulmonary bypassing, adiponectin and CD68 + were detected by using RT-PCR and immunohistochemistry. Our results showed that plasma adiponectin level was significantly lower in the group II as compared with group I (P<0.05). There were no differences in plasma concentration (IL-10, TNF-α, tatal-chol, HDL-chol, LDL-chol) between group I and group II. The number of CD68+ cells in epicardial adipose tissue of group II was significantly higher than that in subcutaneous adipose tissue. Adiponectin mRNA expression was 6 fold higher in subcutaneous adipose tissue than in epicardial adipose tissue of group II (P<0.01). Furthermore, the level of adiponectin mRNA in the epicardial adipose tissue in group II was also significantly lower than in group I (P<0.05). We are led to conclude that inflammation that occurs locally in epicardial adipose tissue of CAD contributes to the pathogenesis of coronary artery disease.
ABSTRACT
Objective To examine whether the increase of carbon monoxide (CO) induced by oral methylene chloride (MC) administration in recipients before heart transplantation would protect heart grafts against isehemia/reperfusion (I/R) injury associated with transplantation and to explore the possible mechanism.Methods Inbred male Balb/c mice were used as donors and recipients to establish cervical heart transplantation model Recipients were treated with either MC (100 mg/kg or 500 mg/kg,per os)(group MC 100 mg,n=10;group MC 500 mg,n=12) or olive oil(0.15 ml,per os.group olive,n=10) 3 h prior to anesthesia.Age-matched norwlal mice served as controls (group N,n=5).The serum COHb and the CO content of myocardial tissue were measured at 0,1,3,6,12,24 h after oral MC administration.Half of recipients were killed at 3 and 24h after transplantation for senum or cardiac graft samples.The serum cTnI levels,the mRNA levels of TNF-α,IL-10,Bcl-2,Bax.the protein levels of NF-κB and the ultrastructures of myocardium were examined.Results As tompared with group olive.the serum COHb and tissue CO were increased significantly and peaked within 3 h in group MC 100 mg and group MC 500 mg.The serum cTnI levels in group MC 100 mg and group MC 500 mg were significantly decreased (P<0. 01 ), especially in group MC 500 mg. The increase of CO in recipients of group MC100 mg and group MC 500 mg significantly inhibited the proinflammatory gene expression of TNF-α mRNA and the pro-apoptotic gene expression of Bax mRNA (P<0. 01), and increased the anti-apoptotic gene expression of Bcl-2 mRNA (P<0. 01), but did not increase the anti-inflammatory gene expression of IL-10 mRNA (P>0. 05) in the heart grafts. As compared with group N, the myocardial NF-κB activation was increased significantly in group olive,group MC 100 mg and group MC 500 mg (P<0. 01 ), but there was no significant difference among the later three groups (P>0. 05). The myocardial ultrastructure was also alleviated significantly in group MC 100 mg and group MC 500 mg as compared with group N. Conclusion The increase of CO induced by MC in recipients suppresses pro-inflammatory and pro-apoptotic gene expression and efficiently ameliorates transplant-induced heart I/R injury. The possible mechanism does not seem to be associated with down-regulation of the NF-κB signaling pathway.
ABSTRACT
Objective To compare the results of mitral valve reconstruction and replacement as treatments for moderate to severe ischemic mitral regurgitation(IMR), and report the mid-term outcome. Methods From June 2002 to May 2008, 83 pa-tients with moderate IMR(35 cases) and severe IMR (48 cases) underwent coronary artery bypass grafting(CABG) combined with mitral valvuloplasty (MVP) (n = 43) or mitral valve replacement (MVR) (n = 40). There were 49 males and 34 females with a mean age of (59.3±7.5) years(51 -77years). The procedures of MVP included annuloplasty with a Dacron or autologous per-icardium ring in 21cases, commissural annuloplasty in 9, quadrangular resection of the posterior leaflet in 9 and using St. Jude mitral annuloplasty ring in 4. In the cases underwent MVR, 28 patients received mechanical prostheses and 12 received biopros-theses. Results 30-day mortality rate was 2.3% for MVP and 5.0% for MVR (P >0.05). The 30-day complication rate was similar for the 2 groups but mechanical ventilation time was longer for MVR patients. Mild MR ocurred in 6 patients with MVP (P <0.05). Sevonty-six patients were followed by outpatient department visit or telephone for (20.2 ± 4.9) months (3 - 60 months). During the follow-up period, 7 patients with MVP had mild insufficiency but free off etber complications. All the valve prothesis functioned well. However, 3 cases had thromboembolic complications and 7 late deaths were recorded in MVR group. Five-year complication-free survival rate was 90% for MVP group and 61% for MVR. Conclusion MVP resulted in excellent durability and provided significant mid-term survival benefit over MVR. MVP should be the first choice for patients with chronic IMR.
ABSTRACT
AIM: To investigate the expression of heat shock protein 60(HSP60) and Toll-like receptor 4 transduction system in mouse cardiac transplantation. METHODS: The mouse cervical heart transplantation model was established. The animals were divided into control group (the donor and recipient were all C57BL/6 mice) and experimental group (the donor was BALB/c mice and recipient was C57BL/6 mice). The heart and blood were collected for study at 3 d and 7 d. The pathological analysis of the hearts was performed. The levels of cytokines in the serum were determined using ELISA. The expression of HSP60, TLR4, MyD88 and NF-κB in the myocardium was determined by immunohistochemistry and Western blotting. RESULTS: The expression levels of HSP60, TLR4, MyD88 and NF-κB were higher in experimental group than those in control group. Severe rejection was observed in experimental group, whereas no distinct rejection in control group was found. The cytokines (TNF-α, IFN-γ, IL-12) increased significantly in experimental group as compared to those in control group. CONCLUSION: HSP60 increases significantly after heart transplantation, which may activate Toll-like receptor 4 transduction system in a MyD88-dependent pathway and promote allograft rejection. Regulation of HSP60 signal transduction may be a novel way for treating allograft rejection.
ABSTRACT
BACKGROUND: The mouse model of cervical heart transplantation is an ideal medical research tool for study of transplant-induced ischemia/reperfusion injury and immunological rejection.However,technical problems have limited the widespread use of mouse cervical vascularized heart transplantation.OBJECTIVE: To improve the cervical heterotopic heart transplantation in mice using the tail-cuff technique.METHODS: Isogeneic transplantation was performed from Balb/c to BALB/c mice,and allogeneic transplantation from C57BL/6 to BALB/c mice.The right common carotid artery and the external jugular vein of the recipient were equipped with a tail cuff made from 24 G and 22 G intravenous catheter,and everted over the cuff,and then connected with the aorta and the pulonary artery of donor heart,respectively.RESULTS AND CONCLUSION: A total of 36 transplants for formal experiment,12 for isogeneic transplantation,and 24 for allogeneic transplantation,were performed with a surgical successful rate of 100%.The total surgical procedure was(49.6±7.4)minutes and total ischemic time of the grafts was(28.8±4.2)minutes.In particular,the average time for vascular everting and for the reconnection of both vessels was obviously shortened.This improved tail-cuff technique shows its superiority,and can serve as an ideal method for establishing cervical heterotopic heart transplantation model in mice.
ABSTRACT
The study summarizes the clinical experience of surgical treatments of various types of thoracic aneurysm and aortic dissection. Clinical data of 122 patients with thoracic aneurysm and aortic dissection during July 2005 to July 2008 were retrospectively analyzed. The elective operations were performed in 107 patients while emergency surgery was done in 15 cases. Different surgical strategies were employed on the basis of diseased region, including simple ascending aortic replacement (n=3), aortic root replacement (n=43), hemi-arch replacement /total arch replacement+elephant trunk technique (n=32), thoracic/thoracoabdominal aortic replacement (n=8) and endovascular repair (n=36). In this series, there is 4 cases of perioperative death due to massive cerebral hemorrhage (n=1), respiratory failure (n=1) and multiple organ dysfunction syndrome (MODS) (n=2). Three cases developed post-operative massive cerebral infarction and the relatives of the patients abandoned treatment. Instant success rate of endovascular repair was 100%. The intimal rupture was sealed. Blood flow was unobstructed in true lumen and no false lumen was visualized. It was concluded that aggressive surgery should be considered in the patients with thoracic aneurysm and aortic dissection. Surgical procedures should vary with the location and the nature of the lesions.
Subject(s)
Young Adult , Aortic Dissection/surgery , Aortic Aneurysm, Thoracic/surgery , Retrospective Studies , Vascular Surgical Procedures/methodsABSTRACT
The cell adhesive properties of decellularized valve scaffolds were promoted by immobilization of valve scaffold with arginine-glycine-aspartic acid (RGD)-containing peptides. Porcine aortic valves were decellularized with trypsin/EDTA, and detergent Triton X-100. With the help of a coupling reagent Sulfo-LC-SPDP, the valve scaffolds were immobilized with glycine-arginine-glycine-aspartic acid-serine-proline-cysteine (GRGDSPC) peptide. X-ray photoelectron spectroscopy (XPS) was used for surface structure analysis. Myofibroblasts harvested from rats were seeded onto the valve scaffolds. Cell count by using microscopy and modified MTT assay were performed to assess cell adhesion. Based on the spectra of XPS, the conjugation of GRGDSPC peptide with decellularized valve scaffolds was confirmed. Both cell count and MTT assay showed that myofibroblasts were much easier to adhere to the modified valve scaffolds, which was also confirmed histologically. Our findings suggest that it is feasible to immobilize RGD-containing peptides onto decellularized valve scaffolds. And the technique can effectively promote cell adhesion, which is beneficial for in vitro tissue engineering of heart valves.
ABSTRACT
Objective To explore the impact of hypoxia/reoxygenation stimulation on phenotype and immune activity of dendritic cells(DCs) cultured from murine bone marrow. Methods Mouse DCs were generated from bone marrow cells and were divided into control group and hypoxia/reoxygenation group. DC in control group was cultured at normal condition, and in hypoxia/reoxygenation group was cultured at hypoxic condition for 4 h followed by cultured at normal condition for 24 h. Flow cytometry and mixed lym-phocyte reaction(MLR) was used to detect the phenotype and functional properties of DCs. ELISA was used to detect the concentration of TNF-α, IFN-γ and IL-12 in the supernalant, Imrounochemistry was used to de-tect the concentration of NF-κB. Results Hypoxia/reoxygen stimulation increased the CD80, CD86, MHC Ⅱ in the cytomembrane of DCs and TNF-α, IFN-γ, IL-12 concentration in the supernalant. Hypoxia/reoxy-gen stimulation also promoted the shift of NF-κB to karyon. Conclusion Under hypoxia/reoxygen stimula-tion, DCs express high level of surface molecules, and possess strong immune activity.
ABSTRACT
Objective To study the impact of NF-kappaB activation on TNF-a and IL-1β expression in myocardial ischemia/reperfusion(I/R) injury.Methods Sixty-five Sprague-Dawley rats were randomly divided into three groups:sham,n=5;I/R:30 min of myocardial ischemia followed by 0,15,30,60,120.240 min of reperfusion,n=5 per subgroup;I/R+PDTC:PDTC(15 mg/kg)was given before ischemia,and the time points were the same as those in I/R group.TNF-a and IL-1β mRNA expression was detected by RT-PCR,activity of NF-KB was measured by electrophoretic mobility shift assay (EMSA),and MDA level in myocardium was assayed by TBA method.Results The expression of TNF-a and IL-1β was increased before reperfusion,reached their peak at the time point of reperfusion 30.60 min respectively.and remained high level at the 2nd h after reperfusion.NF-KB was activated 15 min after reperfusion,reached its peak at the first h after reperfusion.In I/R+PDTC group,NF-κB activation was blocked by PDTC.As compared with I/R group,the expression levels of TNF-a and IL-1β were decreased to varying degrees at each time point.and the content of MDA was also reduced in I/R+PDTC group.Conclusion NF-KB activation could play a pivotabrole in the expression of cytokine.Inhibition of NF-κB signal pathway might be a potential therapeutic strategy in reperfusion injury.
ABSTRACT
This is a comparative study on three groups. With the help of a coupling reagent Sulfo-LC-SPDP, the biological valve scaffolds were surface modified with one of arginine -glycine -aspartic acid (RGD) containing peptides by covalent bond(the treated group). After rat aortic myofibroblast seeding, MTT test showed that more cells of the treated group attached on the valve scaffolds coupled with RGD peptides when compared with the cells of the coated group and untreated group. Moreover, correlatioins of attachment with attaching time and peptide concentrations were observed. Light and electron microscopy and cell count also confirmed the findings. Therefore, immobilizing the RGD peptides on the decellularized valve scaffolds is effective for improving cell attachment, which is helpful to constructing tissue engineering heart valve.
Subject(s)
Animals , Rats , Aortic Valve , Cell Biology , Physiology , Bioprosthesis , Cell Adhesion , Coated Materials, Biocompatible , Chemistry , Pharmacology , Heart Valve Prosthesis , Oligopeptides , Pharmacology , Swine , Tissue Engineering , Methods , Tissue Scaffolds , ChemistryABSTRACT
Chronic rejection remains the leading cause of chronic allograft dysfunction and late mortality after lung transplantation. Adaptive immune system and its cellular-based rejection has been the focus in the development of obliterative bronchiolitis. Recent research has identified that humoral immunity, autoimmunity, and innate immunity also contribute to obliterative bronchiolitis. This paper presents an updated review of the immune mechanisms for obliterative bronchiolitis following lung transplantation.
ABSTRACT
To investigate whether peroxisome proliferators-activated receptor-y (PPARγ) ligand Troglitazone can reduce endothelial injury and activation during storage of harvested saphenous vein grafts. Segments of human saphenous vein graft were collected from 9 patients undergoing coronary bypass surgery and then divided into two equal parts of control and test specimens, were stored in ei-ther heparinized blood (control group) or heparinized blood containing 20 μmol/L troglitazone (test group) for 1 h at room temperature. Tissue distribution and protein expression of VCAM-1, ICAM-1, and endothelial nitric oxide synthase (eNOS) were compared using immunohistochemistry and West-ern blot analysis. Myeloperoxidase (MPO) activity, a marker of neutrophil sequestration in human saphenous vein grafts, was also measured in each group. The expression of ICAM-1 (753±132 versus 7201±934; P<0.01) , VCAM-1 (3731±294 versus 8292±793; P<0.01), and MPO activity (1.52±0.42 U/g, 5.04±1.26 U/g P<0.01) were significantly lower in test group. In contract, eNOS expression (7983±834 versus 3989±1008; P<0.01) was significantly higher in test group. PPARγ ligand troglita- zone might reduce endothelial injury during the storage period of human saphenous vein grafts.
ABSTRACT
The characteristics for the ex vivo expansion of the endothelial progenitor cells (EPCs)were explored. CD34+ cells were selected from umbilical cord blood mononuclear cells (MNC) by MiniMACS system, expanded under the same conditions as those for total MNC, coincubation of CD34+ and CD34- from the same donor for EPCs. In addition, the effects of vessel endothelial growth factor (VEGF) and passage on cell differentiation, expansion kinetics and apoptosis were examined.EPCs were determined and quantified by immunocytochemistry and flow cytometry. The results showed that both coculture of CD34+ and CD34 and total MNC led to a significant increase in the expansion of CD34+ cells as compared with CD34 enrichment (P＜0.05). There was a tendency toward decreased apoptosis in cultures when early passage was performed immediately after cord like structures appeared. VEGF had no significant effect on apoptosis (P＞0.05). These differentiated EPCs were positive for CD34+, von Willebrand factor (vWF), KDR, CD31 staining and phagocytized acetylated low-density lipoprotein (LDL). CD34+ cells accounted for (68.2±6.3) % of attaching (AT)cells at day 7 of culture. It was suggested the most efficient method to ex vivo expansion of EPCs was coculture of CD34+ and CD34- or total MNC. Early passage makes cell apoptosis rate decrease.VEGF had no significant effect on ex vivo expansion of EPCs.
ABSTRACT
Phrenic nerve injury after cardiac surgery increases postoperative pulmonary complications. The purpose of this study was to analyze the causes and effects of phrenic nerve injury after cardiac surgery. Prospectively collected data on 2084 consecutive patients who underwent cardiac surgery from Jan. 1995 to Feb. 2002 were analyzed. Twenty-eight preoperative and operation related variables were subjected to logistic analysis with the end point being phrenic nerve injury. Then phrenic nerve injury and 6 perioperative morbidities were included in the analysis as variables to determine their independent predictive value for perioperative pulmonary morbidity. An identical approach was used to identify the independent risk factors for perioperative mortality. There were 53 phrenic nerve injuries (2.5 %). There was no phrenic nerve injury in non-coronary surgery or coronary surgery using conduits other than the internal mammary artery. The independent risk factors for phrenic nerve injury were the use of internal mammary artery (Odds ratio (OR)=14.5) and the presence of chronic obstructive pulmonary disease (OR=2.9). Phrenic nerve injury was an independent risk factor (OR=8.1) for perioperative pulmonary morbidities but not for perioperative mortality. Use of semi-skeletonized internal mammary artery harvesting technique and drawing attention to possible vascular or mechanical causes of phrenic nerve injury may reduce its occurrence. Unilateral phrenic nerve injury, although rarely life-threatening, is an independent risk factor for postoperative respiratory complications. When harvesting internal mammary arteries, it should be kept in mind avoiding stretching, compromising, or inadvertently dissecting phrenic nerve is as important as avoiding damage of internal mammary artery itself.
ABSTRACT
Phrenic nerve injury after cardiac surgery increases postoperative pulmonary complications. The purpose of this study was to analyze the causes and effects of phrenic nerve injury after cardiac surgery. Prospectively collected data on 2084 consecutive patients who underwent cardiac surgery from Jan. 1995 to Feb. 2002 were analyzed. Twenty-eight preoperative and operation related variables were subjected to logistic analysis with the end point being phrenic nerve injury. Then phrenic nerve injury and 6 perioperative morbidities were included in the analysis as variables to determine their independent predictive value for perioperative pulmonary morbidity. An identical approach was used to identify the independent risk factors for perioperative mortality. There were 53 phrenic nerve injuries (2.5%). There was no phrenic nerve injury in non-coronary surgery or coronary surgery using conduits other than the internal mammary artery. The independent risk factors for phrenic nerve injury were the use of internal mammary artery (Odds ratio (OR) = 14.5) and thepresence of chronic obstructive pulmonary disease (OR = 2.9). Phrenic nerve injury was an independent risk factor (OR = 8.1) for perioperative pulmonary morbidities but not for perioperative mortality. Use of semi-skeletonized internal mammary artery harvesting technique and drawing attention to possible vascular or mechanical causes of phrenic nerve injury may reduce its occurrence. Unilateral phrenic nerve injury, although rarely life-threatening, is an independent risk factor for postoperative respiratory complications. When harvesting internal mammary arteries, it should be kept in mind avoiding stretching, compromising, or inadvertently dissecting phrenic nerve is as important as avoiding damage of internal mammary artery itself.
ABSTRACT
The characteristics for the ex vivo expansion of the endothelial progenitor cells (EPCs) were explored. CD34+ cells were selected from umbilical cord blood mononuclear cells (MNC) by MiniMACS system, expanded under the same conditions as those for total MNC, coincubation of CD34+ and CD34- from the same donor for EPCs. In addition, the effects of vessel endothelial growth factor (VEGF) and passage on cell differentiation, expansion kinetics and apoptosis were examined. EPCs were determined and quantified by immunocytochemistry and flow cytometry. The results showed that both coculture of CD34+ and CD34- and total MNC led to a significant increase in the expansion of CD34+ cells as compared with CD34 enrichment (P 0.05). These differentiated EPCs were positive for CD34+, von Willebrand factor (vWF), KDR, CD31 staining and phagocytized acetylated low-density lipoprotein (LDL). CD34+ cells accounted for (68.2 +/- 6.3)% of attaching (AT) cells at day 7 of culture. It was suggested the most efficient method to ex vivo expansion of EPCs was coculture of CD34+ and CD34- or total MNC. Early passage makes cell apoptosis rate decrease. VEGF had no significant effect on ex vivo expansion of EPCs.
ABSTRACT
The feasibility and safety of total arterial coronary revascularization with 2 arterial conduits in patients with impaired left ventricular function was evaluated. Data were prospectively collected on all patients with multiple vessel discase and moderately or severely impaired left ventricular function, who underwent coronary surgery with the intention of total arterial revascularization with 2 conduits between March 1995 and August 2002. One hundred and seventy-nine patients were included in the study. Acute coronary insufficiency was present in 3 patients and 43 had unstable angina. Severe left ventricular impairment was present in 29 patients. There were 17 redo operations including 3 redo-redo procedures. Eighty-two percent of patients had a Y graft configuration from the left internal mammary artery (right internal mammary artery 40.8%, radial artery 33.5%, other 7.8%). The perioperative mortality was 2.2%, myocardial infarction 1.7% and stroke 0.6%. Total arterial revascularization in patients with ischaemic left ventricular dysfunction can be safely performed with 2 arterial conduits. The radial artery provides conduit length greater than the right internal mammary artery and allows full revascularization despite left ventricular dilatation.
Subject(s)
Angina, Unstable/complications , Angina, Unstable/surgery , Coronary Artery Bypass/methods , Prospective Studies , Radial Artery/transplantation , Vascular Surgical Procedures/methods , Ventricular Dysfunction, Left/etiology , Ventricular Dysfunction, Left/surgeryABSTRACT
The feasibility and safety of total arterial coronary revascularization with 2 arterial conduits in patients with impaired left ventricular function was evaluated. Data were prospectively collected on all patients with multiple vessel disease and moderately or severely impaired left ventricular function, who underwent coronary surgery with the intention of total arterial revascularization with 2 conduits between March 1995 and August 2002. One hundred and seventy-nine patients were included in the study. Acute coronary insufficiency was present in 3 patients and 43 had unstable angina. Severe left ventricular impairment was present in 29 patients. There were 17 redo operations including 3 redo-redo procedures. Eighty-two percent of patients had a Y graft configuration from the left internal mammary artery (right internal mammary artery 40. 8 %, radial artery 33.5 %,other 7.8 % ). The perioperative mortality was 2.2 %, myocardial infarction 1.7 % and stroke 0. 6 %.Total arterial revascularization in patients with ischaemic left ventricular dysfunction can be safely performed with 2 arterial conduits. The radial artery provides conduit length greater than the right internal mammary artery and allows full revascularization despite left ventricular dilatation.