Biomedical subjects

Zongquan Sun

Publications and source records attributed to Zongquan Sun.

13 recordsLinked to original sources

PubMed2006

Total arterial revascularisation in left ventricular dysfunction.

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.

Adult↗

PubMed2006

Characteristics of ex vivo expansion of endothelial progenitor cells.

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.

Antigens, CD34↗

PubMed2006

Semi-skeletonized internal mammary grafts and phrenic nerve injury: cause-and-effect analysis.

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.

Adult↗

PubMed2006

Congenital cardiac diverticulum in the subaortic valve area.

OBJECTIVE: We report and review the clinical characteristics and operative techniques of the rare malformation of congenital cardiac diverticulum in the subaortic valve area. METHODS: Four male patients with congenital ventricular fibrous diverticula in the subaortic valve area are reported. RESULTS: The patients' ages ranged from 4 to 47 years (mean 39 years). The first case was complicated by rupture, pseudoaneurysm formation, and a hemopericardium, and was only diagnosed on the third surgical exploration. The second case was associated with endocarditis involving both aortic and mitral regurgitation. The diverticulum was suspected on 2-dimensional transthoracic echocardiography and confirmed at surgery. In the third case, the subaortic diverticulum was associated with a rupture of the left cusp of the aortic valve with severe regurgitation. In the fourth case, the diverticulum was located between the aortic and mitral valves with a diameter of approximately 30 mm and was associated with multiple perforations of an aortic valve leaflet and severe regurgitation. There were no other congenital thoracoabdominal or cardiac anomalies. At a mean follow-up of 1 year, all patients were well. CONCLUSIONS: Congenital cardiac diverticulum in the subaortic valve area is a rare anomaly. Transthoracic echocardiography and transesophageal echocardiography are reliable tools for the diagnosis and follow-up. Isolated congenital cardiac diverticula in the subaortic valve area tend to involve a benign clinical process, but may be complicated by spontaneous rupture or endocarditis. Surgical resection is performed when complications require surgical therapy.

Adolescent↗

PubMed2005

Chemical preconditioning by 3-nitropropionic acid reduces ischemia-reperfusion injury in rat heart.

This study was designed to investigate the cardioprotective effects of preconditioning with 3-nitropropionic acid, an inhibitor of mitochondrial succinate dehydrogenase. 16 isolated rat hearts were randomly divided into two groups, a treatment group and a control group. The rats of the treatment group were treated intraperitoneally with 3-nitropropionic acid (3-NPA, 4 mg/kg) and the rats of the control group were treated with saline. 24 h after the treatment, the isolated hearts were mounted on a Langendorff apparatus. After 30 min, the hearts were subjected to 30-min ischemia and 60-min reperfusion. The HR, LVDP and +/- dp/dt(max) were measured at pre-ischemia and 30 min, 60 min after the reperfusion. Coronary effluent was collected 15 min after the reperfusion for the determination of CK and LDH. At the end of the 60-min reperfusion the heart was removed for the determination of myocardial SOD and MDA. Our results showed that in the 3-NPA group LVDP and +/- dp/dt(max) recovered significantly better, myocardial MDA, CK and LDH were significantly lower and the myocardial SOD was significantly higher than in the control group. It is concluded that chemical preconditioning by 3-nitropropionate has cardioprotective effects against ischemia-reperfusion injury.

Animals↗

PubMed2005

Effect of L-carnitine on cardiomyocyte apoptosis and cardiac function in patients undergoing heart valve replacement operation.

The effects of L-carnitine, as an ingredient of cardioplegia solution, on cardiac function and cardiomyocyte apoptosis in patients undergoing heart valve replacement operation were investigated. Twenty-three cases undergoing heart valve replacement with cardiopulmonary bypass (CPB) were randomly allocated into two groups: L-carnitine group (n = 12, 12 g/L L-carnitine was put in the ST. Thomas cardioplegia) and control group (n = 11, identical to the L-carnitine group except that normal saline was administered instead of L-carnitine). Serum cardial troponin I (cTnI) levels, the left ventricular ejection fraction (LVEF), and cardiac index (CI) were measured perioperatively. A bit of myocardial tissue obtained from right atria was taken before CPB and by the end of intracardiac procedure to undergo electron microscopy examination and estimate apoptosis by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL). From the end of CPB to 3 days after operation, the serum levels of cTnI in the L-carnitine group was significantly lower than that in the control group (P < 0.05). Heart color ultrasonogram showed that the CI index and LVEF at 7th day postoperatively in the L-carnitine group were significantly higher than in the control group (P < 0.05). Compared to the control group, L-carnitine significantly alleviated the morphologic changes of cardiac muscle cells (electron microscopy examination) and decreased the amounts of apoptotic cardiac muscle cells (TUNEL). Furthermore, the dosage of vasoactive drugs used after operation was significantly less in the L-carnitine group (P < 0.01). It was concluded that L-carnitine cardioplegia solution could improve cardiac function in patients undergoing heart valve replacement operation and alleviate CPB-mediated apoptosis of cardiac muscle cells.

Adult↗

PubMed2005

Total arterial revascularization with internal mammary artery or radial artery pi graft configuration.

To investigate the clinical use of pi graft in total arterial revascularization and its outcomes, a retrospective analysis of 23 patients out of 1000 patients undergoing total arterial coronary bypass surgery with a pi graft between September 1994 and December 2004 was performed. In the selected patients for the management of triple vessel disease with middle diagonal/intermediate ramus disease such that a skip with the left internal mammary artery (LIMA) or radial artery (RA), the main stem of pi graft, to the left anterior descending coronary artery (LAD) will not work and the right internal mammary artery (RIMA) or right gastroepiploic artery (RGEA) cannot pick up the diagonal/intermediate ramus, hence the LAD and diagonal/intermediate ramus were grafted with a mini Y graft using the distal segment of LIMA, RIMA, RA or RGEA, together with the bilateral internal mammary artery (BIMA) or LIMA-RA T graft to compose pi graft. Twenty-three patients (18 males, 5 females) underwent the pi graft procedure. There were no deaths or episodes of myocardial infarction, stroke, and deep sternal wound infection. One patient required reopening for controlling bleeding. Until the end of 2004, during a mean follow-up of 81.0 +/- 28.4 months, no angina needing re-intervention or operative therapy or coronary related death occurred. In conclusion, in patients with specific coronary artery anatomy/stenosis, the BIMA (sometimes LIMA with RA or RGEA) pi graft can be successfully performed for total arterial revascularization with good midterm outcomes.

Aged↗

PubMed2005

Implantation of endothelial progenitor cells into laser-induced channels in rat ischemia hindlimb augments neovascularization.

The aim of this study was to investigate the effect of transmuscle laser revascularization (TMR) in combination with endothelial progenitor cell grafting on neovascularization of ischemic hindlimbs of nude rats. Mononuclear cells (MNCs) isolated from human umbilical cord blood (HUCB) by density gradient centrifugation were expanded in vitro. Spindle-shaped attaching (AT) cells and cord-like structures were developed from culture of MNCs. Acetylated low-density lipoprotein (Ac-LDL) incorporation by AT cells was performed. Phenotypic characterization was assessed by immunocytochemistry, and flow cytometry analysis. EPCs were labeled with 1, 1'-dioctadecyl-1 to 3,3, 3', 3'- tetramethyl-indocarbocyanine perchlorate (DiI) before being injected into the Nd:YAG laser channels or ischemic region. An acute ischemic limb model was created with the following four groups of nude rats by ligating the right external iliac artery: TMR + EPC group: rats with local transplantation of EPCs into laser channels; TMR group: those with transmuscular channels created without EPCs; EPC group: those with EPCs injected into the ischemic hindlimb; control group: an ischemic model without TMR or EPCs. All rats underwent femoral artery ultrasonic blood flow measurements of the ischemic and nonischemic limbs to obtain a flow ratio (femoral artery flow index [FAFI]: right femoral artery flow/left femoral artery flow) immediately after ligation of the artery (at baseline) and 28 days postoperation, and the ischemic limb muscle was sampled for histochemical and immunohistologic analysis. AT cells expressed AC 133 and endothelial cell (ECs) markers (KDR, CD34, CD31, and von Willebrand factor) and exhibited function similar to that of ECs as estimated by Ac-LDL incorporation. Flow cytometric analysis revealed that AT cells were positive for CD34 (62% +/- 7%) and AC133 (57.2% +/- 9.8%) at day 7 of culture. Twenty-eight days after the operation, the FAFI was significantly higher in the TMR+EPC group and EPC group than that in the control group. It was significantly higher in the TMR+EPC group, EPC group, and TMR group than that at their respective baselines. The FAFI in the control group was unchanged and no difference in FAFI was found between the TMR group and control group, and among the TMR+EPC, TMR, and EPC groups. TMR+EPC, TMR, and EPC treatment resulted in an increased number of capillaries in the treated regional area compared to the control group. Nd: YAG-laser transmuscle revascularization combined with the EPC grafting can significantly ameliorate perfusion and augment neovascularization in this ischemic hindlimb model of nude rats.

Animals↗

PubMed2004

Study on the relationship between heat shock protein 70 and toll-like receptor-4 of monocytes.

To explore the relation between human heat shock protein 70 (hsp70) and TLR4 in human monocytes in vitro, human monocytes were stimulated with various concentrations of HSP70, and TNF-alpha production in supernatants was measured by ELISA. Pre-incubated with or without anti-TLR4 mAb, and stimulated with hsp70 (5.0 microg/ml), NF-kappaB p65 of human monocytes in different time points were detected by immunohistochemistry and monocyte surface expression of TLR4 was measured by flow cytometry. After the human monocytes were pre-incubated with various concentrations of anti-TLR4 and stimulated with hsp70 (5.0 microg/ml), TNF-alpha production in supernatants was measured. The results showed that hsp70 enhanced NF-kappaB activation, which was clearly inhibited by anti-TLR4, with the positive cell ratios being 67.44%, 39.17%, 31.56% and 28.05 %, respectively. TLR4 was rapidly down-regulated in the presence of hsp70. MFI of TLR4 on monocytes in different time points were 87.77 +/- 5.38, 78.16 +/- 6.01 and 45.17 +/- 4.97 (P<0.05), 26.98 +/- 5.83 (P<0.01), respectively. Moreover, hsp70-induced TNF-alpha production by human monocytes was inhibited by anti-TLR4. It is suggested that TLR4 is involved in the hsp70-mediated activation of innate immunity.

HSP70 Heat-Shock Proteins↗

PubMed2004

St Thomas Hospital Cardioplegia #2 fails to suppress slow reaction pacemaker cell electrical activity.

BACKGROUND: Inadequate right atrial myocardial preservation during cardioplegic arrest may promote postoperative supraventricular arrhythmias (SVA). We determined (1). if oxygenated St. Thomas Hospital Cardioplegia #2 (STH2) alone causes slow reaction pacemaker cell (SR) quiescence; and (2). if hypothermia, higher [K(+)], lower [Ca(2+)], and verapamil in STH2 suppresses SR electrical activity. MATERIALS AND METHODS: A glass microelectrode recorded SA node SR membrane action potentials (AP) in rabbits (n = 23, 1.93 +/- 0.45 kg) randomized to normothermic STH2 (33 degrees C, n = 6), hypothermia (20 degrees C, n = 4), hypothermic STH2 (22 degrees C, n = 3), lower calcium STH2 (n = 3), higher potassium STH2 (n = 4), and STH2 plus Verapamil (n = 3). RESULTS: Normothermic STH2 depressed SR action potential amplitude and action potential duration (APD), but did not completely suppress action potential generation. Hypothermia alone prolonged APD and sinus cycle length and suppressed SR AP. STH2 with hypothermia (to 20 degrees C) completely suppressed propagating AP and STH2 plus 0.04 Ca(2+) mEq/L inhibited SR AP generation. STH2 plus 30 mEq K(+) and STH2 plus 2.5 mmol/L verapamil failed to generate SR AP. CONCLUSION: STH2 cannot prevent SA node SR myocardial cells from low-amplitude AP autogeneration above 21 degrees C. STH2 with 30 mEq/L K(+), STH2 with 0.02 mEq/L Ca(2+), and STH2 plus 2.5 mmol/L verapamil can arrest AP generation in SR and potentially prevent postoperative SVA.

Animals↗

PubMed2003

Protective effect of heparin-coated circuits on the platelets during cardiopulmonary bypass.

To observe the protective effect of heparin-coated circuits (HCC) on the platelet function during cardiopulmonary bypass (CPB), 23 patients with heart valve replacement were studied. The system heparin dose was 3 mg/kg in the control group (n = 15) and heparin-coated circuits in the HCC group (n = 8). Platelet count, alpha-granule membrane protein-140 (GMP-140) concentrations were determined before CPB, at 60 min of CPB, 30 and 60 min after protamine administration, first 12 h after CPB, respectively. At end of CPB the arterial filters in the circuits were observed by electron microscopy. The amount of first 12-h postoperative blood loss was measured. There was significant reduction in platelet loss during and after CPB in the HCC group in contrast to the control group during CPB (P<0.05). During the first 12 h, postoperative blood loss was reduced in the HCC group as compared with that in the control group (218+/-61 ml, vs. 332+/-118 ml, P<0.05). Electron microscopy showed that in the HCC group the filter meshes and their fringes were clear and fragments of floccules were occasionally seen, without adherent cells or only few adherent cells on their surfaces, whereas several cellular and fibrous components were found to adhere to the surfaces of the filter meshes in the control group. This study indicates that heparin-coated circuits might reduce the platelet loss and activation during CPB and improve hemocompatibility of cardiopulmonary bypass equipment.

Adult↗

PubMed2003

Carvedilol attenuates CPB-induced apoptosis in dog heart: regulationof Fas/FasL and caspase-3 pathway.

OBJECTIVE: To evaluate the effects of Carvedilol on cardiopulmonary bypass (CPB)-induced myocardiocyte apoptosis and its effects on regulation of Fas, FasL expression, caspase-3 activity and oxidative stress in the left ventricle (LV) in this setting. METHODS: Ten adult dogs undergoing conventional hypothermic CPB were randomly divided into control and Carvedilol treated groups (n = 5, respectively). Dogs in Carvedilol treated group received a bolus of Carvedilol (1 mg/kg) intravenously and a maintenance dosage of Carvedilol (3 micro g.min(-1).kg(-1)) for 3 hours after the reperfusion of the heart. Dogs in control group received no Carvediolol. LV samples were obtained before, during and 3 hours after CPB. In situ nick end-labeling (TUNEL) technique was used to detect the apoptotic cells. The expressions of Fas and FasL were detected immunohistochemically and quantified by fluorescence activated cell sorting (FACS). The activity of caspase-3 enzyme and malondialdehyde (MDA) level were measured by cleavage of Z-DEVD-AMC substrate and thiobarbituric acid reactive substance (TBARS) method, respectively. RESULTS: Before and during CPB, all the parameters were not significantly different intra- or between groups (P > 0.05). After CPB, these parameters in both groups were significantly elevated compared with those of before and during CPB (P < 0.028, respectively). However, the number of apoptotic cells in Carvedilol treated group was significantly decreased compared with that of the control group (P < 0.021). The expressions of Fas and FasL were significantly downregulated by Carvedilol (P < 0.001 and 0.003, respectively). The caspase-3 activity and the content of MDA in the Carvedilol treated group was also significantly reduced (P < 0.026 and 0.005, respectively). CONCLUSIONS: Carvedilol significantly reduces CPB-induced cardiomyocyte apoptosis in dog hearts and the reduction of cardiomyocyte apoptosis is associated with downregulation of Fas and FasL expression, inhibition of caspase-3 activity and oxidative stress in LV.

Adrenergic beta-Antagonists↗

PubMed2002

Regulatory effect of bcl-2 family proteins in CPB-induced cardiomyocyte apoptosis in dog hearts.

Whether conventional hypothermic CPB induces myocyte apoptosis in dog hearts and modulation of bcl-2, bcl-xl, bax, bad, and caspase-3 pathways in this setting was investigated. Ten healthy adult dogs were randomized into sham-operated and CPB groups. Samples of left ventricle were obtained before, during and 3 h after CPB. In situ TUNEL was used to detect apoptotic myocytes. Immunohistochemistry and flow cytometry were employed for detection of expressions of bcl-2, bcl-xl, bax and bad proteins. Z-DEVD-AMC substrate cleavage and TBARS methods were used to measure the activity of caspase-3 and the content of lipid peroxide in LV myocardium, respectively. After CPB, the number of apoptotic myocytes in CPB group was significantly increased. The results of immunohistochemistry demonstrated that bcl-2, bcl-xl, bax and bad proteins were constitutionally present on the sarcolemma of the LV myocytes. FACS results showed that, after CPB, expressions of bax and bad in CPB group were significantly upregulated, while the expressions of bcl-2 and bcl-xl were not significantly changed in both groups. The activity of caspase-3 and the content of lipid peroxide in LV myocardium in CPB group were also significantly increased after CPB. The present study shows that there exists myocardiocyte apoptosis in dog hearts undergoing conventional hypothermic CPB and the myocyte apoptosis is initiated by ischemia and performed during reperfusion. Moreover, the CPB-induced myocyte apoptosis was associated with upregulation of expressions of bax and bad proteins, activation of caspase-3 and increase of oxidative stress.

Animals↗