Observation about the effects of fluid management for patients with severe heart failure under the guidance of PICCO / 中国实用护理杂志

Objective To guide fluid management for sever heart failure patients by using PICCO indicators, in order to direct clinical fluid management and nursing care. Methods Sixty-four heart failure patients with level IV cardiac function were randomly divided into the control group and the experimental group according to random number table, and each one had 32 patients. Fluid management for patients in the control group was implemented with CVP monitoring technology, while the patients in the experimental group accepted PICCO monitoring technology as fluid management. Then compare these indicators between the two groups--length of stay in ICU, mortality rate of 28 days, daily fluid intake, output and time of achieving negative fluid balance, and observe the change of cardiac function index (CFI) and capacity indicators (ITBVI, GEDVI, EVLWI) in the experiment group before and after treatment. Results Indicators of ITBVI、GEDVI、EVLWI in the experiment group recovered to normal state and CFI improved. The indicators which had mentioned above was (1 203.41±111.08) ml/m2, (1 087.78±66.91) ml/m2, (12.91±3.54) ml/kg, (2.91±0.29) L·min-1·m-2 respectively when before the treatment, while the values after the treatment was (895.50 ± 50.27) ml/m2, (728.19 ± 73.33) ml/m2, (6.51 ± 0.75) ml/kg, (4.61 ± 0.69) L · min-1 · m-2, the difference was significant (t=-18.52-54.42, P<0.05). The length of stay in ICU, mortality rate of 28 days, daily fluid intake, output and time of achieving negative fluid balance of the experimental group were significantly lower than those in the control group(t=-17.19,-76.80,-12.38, χ2=3.26, P<0.05). Conclusions PICCO monitoring indicators are better than CVP method in the aspect of fluid management for patients with sever heart failure, which can increase the rescue success rate, promote the treatment effect, improve prognosis, and promote the rehabilitation of patients.

Lentivirus-mediated angiotensin-converting enzyme 2 overexpression inhibits angiotensin II-induced albumin down-regulation and enhancement of migration in rat hepatocytes / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the inhibitory effect of angiotensin-converting enzyme 2 (ACE2) on angiotensin II (Ang II)-induced down-regulation of albumin expression and enhancement of cell migration in rat hepatocytes.</p><p><b>METHODS</b>Cultured rat hepatocyte were treated with Ang II (10-7 mol/L) for different time lengths, and the protein expressions of vimentin and albumin and cell migration were detected. The cells transfected with lentiGFP or lentiACE2 were treated with A779 for 1 h and then with Ang II, and Western blotting and immunofluorescent cytochemistry were used to detect the protein levels; the cell migration was evaluated by Transwell assay.</p><p><b>RESULT</b>Ang II induced significantly increased vimentin expression and reduced albumin expression in rat hepatocytes in a time-dependent manner. Overexpression of ACE2 obviously inhibited the up-regulation of vimentin expression, reduction of albumin expression, and enhancement of cell migration induced by Ang II.</p><p><b>CONCLUSION</b>ACE2 overexpression can inhibit Ang II-induced up-regulation of vimentin, reduction of albumin expression, and enhancement of cell migration in rat hepatocytes.</p>

Epithelial to mesenchymal phenotype transition in the liver of rats with bile duct ligation / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the occurrence of epithelial to mesenchymal phenotype transition (EMT) in the liver of rats following bile duct ligation (BDL).</p><p><b>METHODS</b>Twenty-four male Wistar rats were randomized into sham-operated group and BDL group. Liver fibrosis of the rats was evaluated by HE staining and Masson's trichrome staining. Western blotting was used to detect the expression levels of the epithelial markers albumin and E-cadherin and the mesenchymal markers type I collagen and vimentin in the liver tissue. Immunofluorescence was employed to determine the co-localizations of FSP-1+vimentin, FSP-1+type I collagen, FSP-1+albumin, and albumin+type I collagen in cells.</p><p><b>RESULTS</b>Compared with those in sham-operated group, the rats in BDL group showed significantly increased ISHAK fibrosis score (4.42+1.16 vs 0, P+0.000), METAVIR fibrosis score (3.42+0.67 vs 0, P+0.000) and type I collagen levels (0.30+0.06 vs 0.11+0.07, P+0.000) with up-regulated protein levels of albumin (0.53+0.63 vs 1.12+0.01, P+0.000) and E-cadherin (0.21+0.01 vs 0.44+0.01, P+0.000) and down-regulated type I collagen (8.21+0.12 vs 0.24+0.01, P+0.000) and vimentin (3.14+0.01 vs 0.37+0.01, P+0.000). The number of cells with co-localizations of FSP-1+vimentin, FSP-1+type I collagen, FSP-1+albumin, and albumin+type I collagen was also significantly increased in BDL group.</p><p><b>CONCLUSION</b>BDL causes significantly decreased expression of epithelial markers and increased expressions of the mesenchymal markers in rats, indicating the occurrence of EMT in some of the liver cells.</p>

Prolonged angiotensin-(1-7) infusion inhibits hepatic fibrosis in rats with bile duct ligation / 南方医科大学学报

<p><b>OBJECTIVE</b>To observe the inhibitory effect of angiotensin-(1-7) on liver fibrosis induced by bile duct ligation in rats.</p><p><b>METHODS</b>Eighteen Wistar rats were randomized into 3 groups and subject to sham operation, bile duct ligation (BDL), or BDL with angiotensin-(1-7) treatment. An osmotic minipump was implanted intraperitoneally for administration of saline in the sham-operated and BDL groups and angiotensin-(1-7) (25 µg·kg(-1)·h(-1)) in angiotensin-(1-7) treatment group. After a 4-week treatments, the fibrosis score, Masson staining, and hydroxyproline assay were used to evaluate the level of liver fibrosis in the rats, and immunohistochemistry was used to detect expression of α-smooth muscle actin (α-SMA) in the liver tissue.</p><p><b>RESULTS</b>Compared with BDL group, a 4-week treatment with angiotensin-(1-7) following BDL significantly reduced the fibrosis score (2.33±0.52 vs 5.17±0.75), hydroxyproline content (0.36±0.03 vs 0.52±0.04) and α-SMA expression (54.11±17.55 vs 191.84±31.72) in the liver tissue of the rats (P<0.01).</p><p><b>CONCLUSION</b>Prolonged infusion of angiotensin-(1-7) inhibit the formation of hepatic fibrosis in rats following bile duct ligation.</p>

Spironolactone inhibits hepatic sinusoid angiogenesis in rats with hepatic fibrosis / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the inhibitory effects of spironolactone against hepatic sinusoid angiogenesis in rats with hepatic fibrosis.</p><p><b>METHODS</b>Twenty-four male Wistar rats were randomly divided into sham-operated group, bile duct ligation (BDL) group, and BDL+SP group in which the rats received daily spironolactone injection (20 mg/kg) the day after BDL. Four weeks after the operation, the rats were sacrificed for examination of liver histology using Masson staining and the expression of vascular endothelial growth factor A (VEGF-A) mRNA in the liver using real-time quantitative PCR. Immunohistochemistry was used to detect the expression of von Willebrand factor (vWF) in the hepatic tissues.</p><p><b>RESULTS</b>Spironolactone significantly inhibited liver fibrogenesis in rats after BDL (METAVIR liver fibrosis scores 2.84∓0.44 vs 19.73∓3.54, P=0.00). Real-time PCR and immunohistochemistry showed that compared with BDL group, spironolactone treatment significantly inhibited the expression of VEGF-A mRNA (0.71∓0.12 vs 1.75∓0.15, P=0.00) and vWF (1.15∓0.09 vs 3.08∓0.17, P=0.00) in the liver. The expression of VEGF-A mRNA was highly correlated with the expression of vWF (r=0.890, P=0.000).</p><p><b>CONCLUSION</b>Spironolactone can inhibit hepatic sinusoid angiogenesis in rats with BDL-induced hepatic fibrosis by inhibiting the expression of VEGF-A.</p>