Biomedical subjects

Zhi-Yong Wu

Publications and source records attributed to Zhi-Yong Wu.

11 recordsLinked to original sources

PubMed2006

Effects of hemoglobin concentration on hyperdynamic circulation associated with portal hypertension.

BACKGROUND: Chronic anemia caused by different factors is a common complication in patients with portal hypertension, but attention has been rarely paid to its detrimental effect on hemodynamic status. This study was undertaken to investigate the effects of hemoglobin concentration on hyperdynamic disturbance associated with portal hypertension (PHT). METHODS: According to blood hemoglobin level of 120 g/L, 55 patients with portal hypertension were divided into two groups, anemic and nonanemic. Hemodynamic and clinical data of the patients were analyzed retrospectively. The data were analyzed separately according to the Child classification in an attempt to avoid the effects of differences on hepatic function. RESULTS: Compared with the nonanemic group, the anemic group had an increased cardiac output (7.4+/-1.7 L/min vs. 6.3+/-1.9 L/min, P=0.028), free portal pressure (29.1+/-3.1 mmHg vs. 26.8+/-3.3 mmHg, P=0.012), a decreased mean arterial pressure (84.0+/-10.7 mmHg vs. 97.1+/-12.0 mmHg, P<0.01), and systemic vascular resistance (866+/-215 dyn/s.cm5 vs. 1207+/-317 dyn/s.cm5, P<0.01). Similar results were obtained when Child A and Child B-C patients were analyzed separately. Multivariate logistic regression revealed that the concentrations of hemoglobin (standard coefficient=0.31, P=0.01) and albumin (standard coefficient=0.21, P=0.04) were independent factors influencing the systemic vascular resistance in PHT patients. CONCLUSIONS: Anemia aggravates the hyperdynamic circulation of portal hypertension. Hemoglobin concentration is an important variable for evaluating the degree of hemodynamic disturbance in PHT patients.

Analysis of Variance↗

PubMed2006

Expression of cyclooxygenase in hyperdynamic portal hypertensive rats.

BACKGROUND: By detecting hemodynamic changes, concentration of plasm prostacyclin (PGI2) and expression of cyclooxygenase (COX) in vasculature and splanchnic tissues, we evaluated the relative contributions of PGI2 and COX mRNA expression to the hyperdynamic circulatory state in chronic portal hypertensive rats. METHODS: Fifty male Sprague-Dawley rats were divided into 3 groups: intrahepatic portal hypertension (IHPH, n=18) by injection of CCl4, prehepatic portal hypertension (PHPH, n=18) by partial stenosis of the portal vein, and sham-operated controls (SO, n=14). Splanchnic hemodynamics was measured by radioactive microsphere techniques and the concentration of PGI2 was detected by specific radioimmunoassay for its stable hydrolysis product 6-keto-PGF1alpha. Semi-quantitive reverse transcriptase-polymerase chain reaction (RT-PCR) was performed to measure the levels of COX-1 mRNA and COX-2 mRNA in the thoracic aorta, superior mesenteric artery (SMA), and small intestine of IHPH, PHPH and SO rats, respectively. RESULTS: Hyperdynamic circulatory state was characterized by increased splanchnic blood flow and decreased splanchnic vascular resistance in IHPH and PHPH rats. The concentration of plasma 6-keto-PGF1alpha (pg/ml) in IHPH (1093.75+/-142.15) and PHPH (897.42+/-53.29) rats was significantly higher than that in SO rats (730.13+/-98.67) (P<0.05). The expression of COX-1 mRNA in the thoracic aorta, SMA and small intestine was enhanced, whereas COX-2 mRNA expression was not detected in either of these vessels or the small intestine. The plasma 6-keto-PGF1alpha concentration and the expression of COX-1 mRNA in these vessels and the small intestine were closely correlated with such hemodynamic parameters as portal venous inflow (PVI), splanchnic vascular resistance (SVR) and free portal venous pressure (FPP) (P<0.05). CONCLUSION: The expression of COX-1 mRNA and the levels of PGI2 were closely related to the hyperdynamic circulatory state of portal hypertensive rats.

Analysis of Variance↗

PubMed2006

Gene expression changes after hypoxic preconditioning in rat hepatocytes.

BACKGROUND: Hypoxic preconditioning can protect hepatocytes against hypoxic injury, but its mechanism has not been elucidated. The aim of this study was to profile gene expression patterns involved in hypoxic preconditioning and probable mechanism at the level of gene expression. METHODS: Hepatocytes were divided into 2 groups: control group and hypoxic preconditioning group. Biotin-labeled cRNA from the control group and the hypoxic preconditioning group was hybridized by oligonucleotide microarray. Genes that were significantly associated with hypoxic preconditioning were filtered, and validated at the level of transcript expression. RESULTS: Forty-three genes with significantly altered expression patterns were discovered and most of them had not been previously reported. Among these genes, genes encoding superoxide dismutase 2 (SOD2) and interleukin 10 (IL-10) in the hypoxic preconditioning group were confirmed to be up-regulated with real-time quantitative PCR. CONCLUSIONS: Many cytokines are involved in hypoxic preconditioning and protect hepatocytes from hypoxia-reoxygenation injury, and the increase of oxygen free-radical scavengers and anti-inflammatory factors may play a key role in this phenomenon. Diverse signal pathways are probably involved.

Animals↗

PubMed2006

Influence of nitric oxide synthase and cyclooxygenase blockade on expression of cyclooxygenase and hemodynamics in rats with portal hypertension.

BACKGROUND: The importance of nitric oxide (NO) in the pathogenesis of portal hypertension (PHT) has been extensively studied, but whether or not prostacyclin (PGI(2)) plays a role in formation and development of hyperdynamic circutatory state in PHT has not been verified. The present study was undertaken to investigate the possible interaction between prostacyclin (PGI(2)) and nitric oxide (NO) in the hyperdynamic circulatory state of rats with chronic portal hypertension (PHT), by measuring the hemodynamic changes and expression of cyclooxygenase (COX) mRNA in vessels and small intestine after administration of N(omega)-nitro-L-arginine (L-NNA) or indomethacin (INDO) either in the short-term (7 days) or long-term (15 days). METHODS: Ninety-seven male Sprague-Dawley rats were divided into three groups: intrahepatic portal hypertension (IHPH) induced by injection of CCl(4), prehepatic portal hypertension (PHPH) induced by partial stenosis of the portal vein, and sham-operated controls (SO). Animals of each group received L-NNA or INDO either for 7 or 15 days, with saline as control. Splanchnic hemodynamics was measured by the radioactive microsphere technique. The concentration of NO in serum was determined as the nitrate; nitrite ratio (NO(2)(-)/NO(3)(-), micromol/L) by a colorometric method, and that of PGI(2) was measured by specific radioimmunoassay for its stable hydrolysis product 6-keto-PGF(1alpha) (pg/ml). The reverse transcription-polymerase chain reaction measured the levels of COX-1 mRNA in the superior mesenteric artery, thoracic aorta, and small intestine of these rats. RESULTS: Compared with SO rats, COX-1 mRNA expression and the concentrations of plasma 6-keto-PGF(1alpha) and serum NO(2)(-)/NO(3)(-) were enhanced in both IHPH and PHPH rats; splanchnic vascular resistance (SVR) decreased, but portal venous inflow (PVI) markedly increased (P<0.05). Seven or 15 days of L-NNA treatment reduced COX-1 mRNA expression in these vessels and the small intestine, concomitant with a significant decrease in the concentration of plasma PGI(2) and serum NO in IHPH and PHPH rats (P<0.05). At the same time, PVI decreased but SVR increased significantly (P<0.05). In both IHPH and PHPH rats, the COX-1 mRNA expression and the concentration of plasma PGI(2) after No synthase (NOS) blockade for 15 days were higher than those for 7 days, whereas the hyperdynamic circulatory state was improved after NOS blockade for 15 days compared with 7 days. The concentration of PGI(2) treated by INDO for 15 days was not significantly different from that after 7-day COX blockade, and hemodynamics restored hyperdynamic circulatory state. CONCLUSIONS: The hyperdynamic circulatory state in rats with PHT is correlated with the concentration of serum NO. There is a possible interaction between PGI(2) and NO in the hyperhemodynamics of PHT. PGI(2) is probably not the mediator in the formation and development of the hyperdynamic circulatory state in rats with chronic PHT.

Animals↗

PubMed2005

Diaqua(2,2'-diamino-4,4'-bi-1,3-thiazole)oxosulfatovanadium(IV) tetrahydrate.

The title compound, [VO(SO(4))(C(6)H(6)N(4)S(2))(H(2)O)(2)].4H(2)O, displays a distorted octahedral coordination geometry. The 2,2'-diamino-4,4'-bithiazole ligand is present in the usual chelating bidentate mode. The sulfate ligand coordinates in a monodentate fashion to the V atom. A large displacement of the V atom from the equatorial plane towards the oxo group correlates with the strong V=O double bond. In the crystal structure, a three-dimensional supramolecular network is formed by hydrogen bonds.

Journal Article↗

PubMed2005

Role of PGI2 in the formation and maintenance of hyperdynamic circulatory state of portal hypertensive rats.

AIM: To investigate the role of prostacyclin (PGI(2)) and nitric oxide (NO) in the development and maintenance of hyperdynamic circulatory state of chronic portal hypertensive rats. METHODS: Ninety male Sprague-Dawley rats were divided into three groups: intrahepatic portal hypertension (IHPH) group by injection of CCl(4), prehepatic portal hypertension (PHPH) group by partial stenosis of the portal vein and sham-operation control (SO) group. One week after the models were made, animals in each group were subdivided into 4 groups: saline controlled group (n = 23), Nomega-nitro-L-arginine (L-NNA) group (n = 21) group, indomethacin (INDO) group (n = 22) and high-dose heparin group (n = 24). The rats were administrated 1 mL of saline, L-NNA (3.3 mg/kg.d) and INDO (5 mg/kg.d) respectively through gastric tubes for one week, then heparin (200 IU/Kg/min) was given to rats by intravenous injection for an hour. Splanchnic and systemic hemodynamics were measured using radioactive microsphere techniques. The serum nitrate/nitrite (NO(2)(-)/NO(3)(-)) levels as a marker of production of NO were assessed by a colorimetric method, and concentration of 6-keto-PGF1alpha, a stable hydrolytic product of PGI(2), was determined by radioimmunoassay. RESULTS: The concentrations of plasma 6-keto-PGF1alpha (pg/mL) and serum NO(2)(-)/NO(3)(-) (micromol/L) in IHPH rats (1123.85+/-153.64, 73.34+/-4.31) and PHPH rats (891.88+/-83.11, 75.21+/-6.89) were significantly higher than those in SO rats (725.53+/-105.54, 58.79+/-8.47) (P<0.05). Compared with SO rats, total peripheral vascular resistance (TPR) and spanchnic vascular resistance (SVR) decreased but cardiac index (CI) and portal venous inflow (PVI) increased obviously in IHPH and PHPH rats (P<0.05). L-NNA and indomethacin could decrease the concentrations of plasma 6-keto-PGF1alpha and serum NO(2)(-)/NO(3)(-) in IHPH and PHPH rats (P<0.05). Meanwhile, CI, FPP and PVI lowered but MAP, TPR and SVR increased (P<0.05). After deduction of the action of NO, there was no significant correlation between plasma PGI(2) level and hemodynamic parameters such as CI, TPR, PVI and SVR. However, after deduction of the action of PGI(2), NO still correlated highly with the hemodynamic parameters, indicating that there was a close correlation between NO and the hemodynamic parameters. After administration of high-dose heparin, plasma 6-keto-PGF(1alpha) concentrations in IHPH, PHPH and SO rats were significantly higher than those in rats administrated vehicle (P<0.05). On the contrary, levels of serum NO(2)(-)/NO(3)(-) in IHPH, PHPH and SO rats were significantly lower than those in rats administrated Vehicle (P<0.05). Compared with those rats administrated vehicle, the hemodynamic parameters of portal hypertensive rats, such as CI and PVI, declined significantly after administration of high-dose heparin (P<0.05), while TPR and SVR increased significantly (P<0.05). CONCLUSION: It is NO rather than PGI(2) that is a mediator in the formation and maintenance of hyperdynamic circulatory state of chronic portal hypertensive rats.

Animals↗

PubMed2005

Feature characterization of microfabricated microfluidic chips by PDMS replication and CCD imaging.

This paper presents a new approach for the metrological characterization of microfabricated features on microfluidic chips, based on a combination of poly(dimethylsiloxane) (PDMS) replication and charge-coupled device (CCD) imaging. A PDMS replicate was cast from the original chip sample, and a 2-mm thick sample slice was cut from the replica at the cross-section to be studied. The digital image of the revealed structural profile was captured by a CCD camera under a microscope, and the image was processed using specially-developed algorithms for CCD image calibration and edge detection. Depth and width measurements obtained using the method agreed well with those gained using a stylus profiler and universal measuring microscope, with a deviation of below 0.9 mum, while profile distortions of deeper structures using stylus profilers were avoided. The method is reliable, non-destructive, and cheap and simple to implement in any analytical laboratory.

Journal Article↗

PubMed2005

Magnetic resonance angiography in the management of patients with portal hypertension.

BACKGROUND: In recent years, MR techniques have been widely used for displaying hepatic vessels and measuring its hemodynamics, especially in the management of the patients with portal hypertension. The aim of this study was to evaluate the role of magnetic resonance angiography (MRA) in the treatment of patients with portal hypertension. METHODS: A series of 38 patients with portal hypertension and 12 control patients were enrolled in this study. Three dimensional dynamic contrast-enhanced (3D-DCE) MRA and two dimensional phase-contrast (2D-PC) MR were used for the study of portal venous anatomy and its hemodynamics, which were compared with those of indirect portal-venography (IPVG) and doppler ultrasonography (DUS). RESULTS: The anatomical imaging of the portal venous system could be displayed clearly in 3D-DCE MRA and the imaging quality of MRA was better than that of IPVG. The hemodynamic information from 2D-PC MR was closely related to that from DUS. CONCLUSIONS: As a non-invasive technique, MRA can display the anatomy of the portal venous system clearly and measure its hemodynamics exactly. It is very useful and can be applied if necessary in the management of patients with portal hypertension.

Adult↗

PubMed2005

Effects of combined splenorenal shunt devascularization and devascularization only on hemodynamics of the portal venous system in patients with portal hypertension.

BACKGROUND: Shunt and devascularization have totally different effects on hemodynamics of the portal venous system, and the actual results of combined shunt and devascularization should be determined by more clinical observations. This study aimed to evaluate effects on hemodynamics of the portal venous system after conventional splenorenal shunt combined with pericardial devascularization and pericardial devascularization only. METHODS: In 20 patients who had received conventional splenorenal shunt combined with pericardial devascularization(CP) and 18 who had received pericardial devascularization and splenectomy(PCDV), hemodynamic parameters of the portal venous system were studied by magnetic resonance angiography 1 week before and 2 weeks after operation. Free portal pressure was detected continuously by a transducer during the operation. RESULTS: Compared to the preoperative data, a decreased flow of the portal vein(PVF) (563.12+/-206.42 ml/min vs. 1080.63+/-352.85 ml/min, P < 0.05), a decreased diameter of the portal vein (PVD) (1.20+/-0.11 cm vs. 1.30+/-0.16 cm, P < 0.01), a decreased free portal pressure(FPP) (21.50+/-2.67 mmHg vs. 29.88+/-2.30 mmHg, P < 0.01) and an increased flow of the superior mesenteric vein (SMVF) (1105.45+/-309.03 ml/min vs. 569.13+/-178.46 ml/min, P < 0.05) were found in the CP group after operation; a decreased PVD (1.27+/-0.16 cm vs. 1.40+/-0.23 cm, P < 0.05), a decreased PVF(684.60+/-165.73 ml/min vs. 1175.64+/-415.09 ml/min, P < 0.05), a decreased FPP (24.40+/-3.78 mmHg vs. 28.80+/-3.56 mmHg, P < 0.05) and an increased SMVF (697.91+/-121.83 ml/min vs. 521.30+/-115.82 ml/min, P < 0.05) were found in the PCDV group. After operation, the PVF of CP group(563.12+/-206.42 ml/min vs. 684.60+/-165.73 ml/min, P > 0.05) was not decreased significantly while FPP (21.50+/-2.67 mmHg vs. 24.40+/-3.78 mmHg, P < 0.01) was decreased significantly as compared with that of the PCDV group. CONCLUSIONS: PVF and FPP could be decreased by both surgical procedures, but the effect of decreasing FPP is much better in the combined procedures than in PCDV. Since there is no significant difference in PVF between the two groups, the combined procedures could integrate advantages of shunt with those of the devascularization, maintaining the normal anatomy structure of the hepatic portal vein, and should be one of the best choices for patients with PHT when surgical interventions are considered.

Adult↗

PubMed2004

Diagnosis and surgical treatment of giant splenic artery aneurysms with portal hypertension: report of 4 cases.

BACKGROUND: Giant splenic artery aneurysm (GSAA) is a rare but clinically relevant disease. Its importance lies in potential rupture and hemorrhage. Early diagnosis and treatment before rupture of GSAA are crucial to GSAA patients especially to GSAA patients with portal hypertension(PHT). METHODS: Four patients of GSAA with PHT treated at our hospital from December 1999 to September 2001 were retrospectively reviewed. RESULTS: GSAA was found in all patients with digital substracted angiography (DSA) and/or magnetic resonance angiography (MRA) before operation. Resection of GSAA and treatment of PHT were carried out successfully with no perioperative mortality. CONCLUSIONS: Patients with GSAA are apt to have PHT or segmental PHT because of suppression of the splenic vein or formation of aneurysm-portal vein fistula. Operation should be focused on GSAA, and PHT complications.

Aged↗

PubMed2003

Microfluidic systems in proteomics.

We present the state-of-the-art in miniaturized sample preparation, immunoassays, one-dimensional and multidimensional analyte separations, and coupling of microdevices with electrospray ionization-mass spectrometry. Hyphenation of these different techniques and their relevance to proteomics will be discussed. In particular, we will show that analytical performances of microfluidic analytical systems are already close to fulfill the requirements for proteomics, and that miniaturization results at the same time in a dramatic increase in analysis throughput. Throughout this review, some examples of analytical operations that cannot be achieved without microfluidics will be emphasized. Finally, conditions for the spreading of microanalytical systems in routine proteomic labs will be discussed.

Electrophoresis↗