Evaluation of a modified ultrasound-assisted technique for mid-thoracic epidural placement: a prospective observational study.

BACKGROUND: Although mid-thoracic epidural analgesia benefits patients undergoing major surgery, technical difficulties often discourage its use. Improvements in technology are warranted to improve the success rate on first pass and patient comfort. The previously reported ultrasound-assisted technique using a generic needle insertion site failed to demonstrate superiority over conventional landmark techniques. A stratified needle insertion site based on sonoanatomic features may improve the technique. METHODS: Patients who presented for elective abdominal or thoracic surgery requesting thoracic epidural analgesia for postoperative pain control were included in this observational study. A modified ultrasound-assisted technique using a stratified needle insertion site based on ultrasound images was adopted. The number of needle passes, needle skin punctures, procedure time, overall success rate, and incidence of procedure complications were recorded. RESULTS: One hundred and twenty-eight subjects were included. The first-pass success and overall success rates were 75% (96/128) and 98% (126/128), respectively. In 95% (122/128) of patients, only one needle skin puncture was needed to access the epidural space. The median [IQR] time needed from needle insertion to access the epidural space was 59 [47-122] seconds. No complications were observed during the procedure. CONCLUSIONS: This modified ultrasound-assisted mid-thoracic epidural technique has the potential to improve success rates and reduce the needling time. The data shown in our study may be a feasible basis for a prospective study comparing our ultrasound-assisted epidural placements to conventional landmark-based techniques.

Platelet CFTR inhibition enhances arterial thrombosis via increasing intracellular Cl- concentration and activation of SGK1 signaling pathway.

Platelet hyperactivity is essential for thrombus formation in coronary artery diseases (CAD). Dysfunction of the cystic fibrosis transmembrane conductance regulator (CFTR) in patients with cystic fibrosis elevates intracellular Cl- levels ([Cl-]i) and enhanced platelet hyperactivity. In this study, we explored whether alteration of [Cl-]i has a pathological role in regulating platelet hyperactivity and arterial thrombosis formation. CFTR expression was significantly decreased, while [Cl-]i was increased in platelets from CAD patients. In a FeCl3-induced mouse mesenteric arteriole thrombosis model, platelet-specific Cftr-knockout and/or pre-administration of ion channel inhibitor CFTRinh-172 increased platelet [Cl-]i, which accelerated thrombus formation, enhanced platelet aggregation and ATP release, and increased P2Y12 and PAR4 expression in platelets. Conversely, Cftr-overexpressing platelets resulted in subnormal [Cl-]i, thereby decreasing thrombosis formation. Our results showed that clamping [Cl-]i at high levels or Cftr deficiency-induced [Cl-]i increasement dramatically augmented phosphorylation (Ser422) of serum and glucocorticoid-regulated kinase (SGK1), subsequently upregulated P2Y12 and PAR4 expression via NF-κB signaling. Constitutively active mutant S422D SGK1 markedly increased P2Y12 and PAR4 expression. The specific SGK1 inhibitor GSK-650394 decreased platelet aggregation in wildtype and platelet-specific Cftr knockout mice, and platelet SGK1 phosphorylation was observed in line with increased [Cl-]i and decreased CFTR expression in CAD patients. Co-transfection of S422D SGK1 and adenovirus-induced CFTR overexpression in MEG-01 cells restored platelet activation signaling cascade. Our results suggest that [Cl-]i is a novel positive regulator of platelet activation and arterial thrombus formation via the activation of a [Cl-]i-sensitive SGK1 signaling pathway. Therefore, [Cl-]i in platelets is a novel potential biomarker for platelet hyperactivity, and CFTR may be a potential therapeutic target for platelet activation in CAD.

Milrinone is better choice for controlled low central venous pressure during hepatectomy: A randomized, controlled trial comparing with nitroglycerin.

BACKGROUND: To explore the feasibility and effectiveness of controlled low central venous pressure(CLCVP)induced by milrinone during hepatectomy, and its influence on perioperative hemodynamics, blood loss and patients' recovery, comparing with the traditional method by nitroglycerin. METHODS: 52 patients who underwent elective open hepatectomy were enrolled in the study and randomly divided into two groups: milrinone (M) group and nitroglycerin (NG) group. Milrinone was infused with the rate of 0.5 µg/kg/min in group M, while nitroglycerin was given 0.2-0.5 µg/kg/min in group NG to maintain CVP≤ 5 mmHg during liver resection. The demographic variables, data of the operative procedure and intraoperative hemodynamics were recorded. The postoperative recovery profiles and pre- and post-operative haematological markers of vital organs were also collected and compared. RESULTS: 1. The blood loss of group M, no matter during liver resection or in the whole procedure, was both less than that of group NG (P < 0.05), so did the hemoglobin detected by blood gas analysis (P < 0.05). Meanwhile, time of hepatectomy and hepatic hilum occlusion were shorter in group M (P < 0.05). 2. Compared with the NG group, cardiac index (CI) and stroke volume index (SVR) were higher in group M in the operation. The norepinephrine dosage necessary in the operation was of no difference in two groups (P > 0.05). 3. Drainage indwelling time and postoperative hospital stay of group M were shorter than that of group NG (P < 0.05). Most of the blood biomarkers increased on postoperative day (POD)-1, and returned to the preoperative level on POD-7 without inter-group difference (P > 0.05). Brain natriuretic peptide precursor (Pro-BNP) in group M was higher than NG group on POD-1 (P < 0.05), and the statistical difference disappeared on POD-7. CONCLUSION: Milrinone can effectively maintain a controlled low central venous pressure during hepatectomy. Compared with nitroglycerin, milrinone can reduce the amount of blood loss, with the benefit of better manifestation of hemodynamics and enhanced postoperative recovery.

Bibliometric and Visual Analysis of Vascular Calcification Research.

Background: Extensive studies related to vascular calcification (VC) were conducted in recent years. However, no bibliometric analysis has systematically investigated this topic. Our study aimed to determine the hotspots and frontiers of VC research in the past decade and provide a reference for future scientific research directions and decision-making in the VC field. Methods: VC studies were acquired from the Web of Science Core Collection. Bibliometric and visual analyses were performed using CiteSpace, VOSviewer, and Microsoft Excel software. Results: A total of 8,238 English articles on VC research published in 2011-2020 were obtained. In the past decade, annual publications and citations showed a significant growth trend, especially in 2018-2020. The most productive country, institution, journal and author are the United States, the University of California System, PLOS ONE, and Budoff MJ, respectively. The most frequently cited country, journal, and author are the United States, Journal of the American College of Cardiology, and Floege J, respectively. "Vascular calcification," "atherosclerosis," "chronic kidney disease," and "cardiovascular disease" are the primary keywords. The burst keywords "revascularization," "calciprotein particle," "microRNA," and "microcalcification" are speculated to be the research frontiers. Conclusion: The main research hotspots in the VC field are the molecular mechanisms and prognosis of VC in patients with chronic kidney disease or cardiovascular disease. In addition, endovascular therapy and the development of new drugs targeting signal pathways for VC will become the focus of future research. Moreover, non-coding RNAs related to the diagnosis and treatment of VC are great research prospects.

Clcn3 deficiency ameliorates high-fat diet-induced obesity and adipose tissue macrophage inflammation in mice.

Obesity induces accumulation of adipose tissue macrophages (ATMs) and ATM-driven inflammatory responses that promote the development of glucose and lipid metabolism disorders. ClC-3 chloride channel/antiporter, encoded by the Clcn3, is critical for some basic cellular functions. Our previous work has shown significant alleviation of type 2 diabetes in Clcn3 knockout (Clcn3-/-) mice. In the present study we investigated the role of Clcn3 in high-fat diet (HFD)-induced obesity and ATM inflammation. To establish the mouse obesity model, both Clcn3-/- mice and wild-type mice were fed a HFD for 4 or 16 weeks. The metabolic parameters were assessed and the abdominal total adipose tissue was scanned using computed tomography. Their epididymal fat pad tissue and adipose tissue stromal vascular fraction (SVF) cells were isolated for analyses. We found that the HFD-fed Clcn3-/- mice displayed a significant decrease in obesity-induced body weight gain and abdominal visceral fat accumulation as well as an improvement of glucose and lipid metabolism as compared with HFD-fed wild-type mice. Furthermore, the Clcn3 deficiency significantly attenuated HFD-induced ATM accumulation, HFD-increased F4/80+ CD11c+ CD206- SVF cells as well as HFD-activated TLR-4/NF-κB signaling in epididymal fat tissue. In cultured human THP-1 macrophages, adenovirus-mediated transfer of Clcn3 specific shRNA inhibited, whereas adenovirus-mediated cDNA overexpression of Clcn3 enhanced lipopolysaccharide-induced activation of NF-κB and TLR-4. These results demonstrate a novel role for Clcn3 in HFD-induced obesity and ATM inflammation.

Xyloketal B exerts antihypertensive effect in renovascular hypertensive rats via the NO-sGC-cGMP pathway and calcium signaling.

Xyloketal B (Xyl-B) is a novel marine compound isolated from mangrove fungus Xylaria sp. (No 2508). We previously showed that Xyl-B promoted endothelial NO release and protected against atherosclerosis through the Akt/eNOS pathway. Vascular NO production regulates vasoconstriction in central and peripheral arteries and plays an important role in blood pressure control. In this study, we examined whether Xyl-B exerted an antihypertensive effect in a hypertensive rat model, and further explored the possible mechanisms underlying its antihypertensive action. Administration of Xyl-B (20 mg·kg-1·d-1, ip, for 12 weeks) significantly decreased the systolic and diastolic blood pressure in a two-kidney, two-clip (2K2C) renovascular hypertensive rats. In endothelium-intact and endothelium-denuded thoracic aortic rings, pretreatment with Xyl-B (20 µmol/L) significantly suppressed phenylephrine (Phe)-induced contractions, suggesting that its vasorelaxant effect was attributed to both endothelial-dependent and endothelial-independent mechanisms. We used SNP, methylene blue (MB, guanylate cyclase inhibitor) and indomethacin (IMC, cyclooxygenase inhibitor) to examine which endothelial pathway was involved, and found that MB, but not IMC, reversed the inhibitory effects of Xyl-B on Phe-induced vasocontraction. Moreover, Xyl-B increased the endothelial NO bioactivity and smooth muscle cGMP level, revealing that the NO-sGC-cGMP pathway, rather than PGI2, mediated the anti-hypertensive effect of Xyl-B. We further showed that Xyl-B significantly attenuated KCl-induced Ca2+ entry in smooth muscle cells in vitro, which was supposed to be mediated by voltage-dependent Ca2+ channels (VDCCs), and reduced ryanodine-induced aortic contractions, which may be associated with store-operated Ca2+ entry (SOCE). Taken together, these findings demonstrate that Xyl-B exerts significant antihypertensive effects not only through the endothelial NO-sGC-cGMP pathway but also through smooth muscle calcium signaling, including VDCCs and SOCE.

LNK deficiency aggravates palmitate-induced preadipocyte apoptosis.

LNK (SH2B3) is an intracellular adaptor protein that negatively regulates cellular proliferation or self-renewal of hematopoietic stem cells and some other progenitor cells. LNK is also recognized as a key regulator of insulin resistance and inflammatory responses in several tissues and organs. The function of LNK in adipose tissue is unknown. We previously demonstrated that type 2 diabetes mellitus (T2DM) mouse model had elevated serum free fatty acids (FFAs) levels and increased preadipocyte apoptosis in visceral fat tissue, showing the occurrence of lipotoxicity. Herein, when compared to control mice, the protein expression of LNK decreased in epididymal fat tissue from the high-sucrose/fat diet, low-dose streptozotocin induced T2DM mouse model. We thus investigated whether LNK could regulate palmitate-induced preadipocyte apoptosis in an in vitro apoptotic model in 3T3-L1 preadipocytes. LNK specific siRNA exacerbated palmitate-induced apoptosis and increased pro-apoptotic protein levels of cleaved caspase-3, Bax and cytochrome C; while overexpression of LNK cDNA exhibited significant anti-apoptotic effects. Consistently, LNK specific siRNA further decreased the Akt Ser-473 phosphorylation reduced by palmitate and located on upstream of Bax and cytochrome C. The siRNA-mediated LNK knockdown exacerbated mitochondrial membrane depolarization and mitochondrial-derived reactive oxygen species production induced by palmitate, whereas overexpression of LNK attenuated that. These results indicated that LNK plays a regulatory role in the palmitate-related preadipocyte apoptosis and might be involved in adipose tissue dysfunction.

Cuffed versus uncuffed endotracheal tubes in children: a meta-analysis.

PURPOSE: Cuffed endotracheal tubes (ETTs) have increasingly been used in small children. However, the use of cuffed ETTs in small children is still controversial. The goal of this meta-analysis is to assess the current evidence regarding the postextubation morbidity and tracheal tube (TT) exchange rate of cuffed ETTs compared to uncuffed ETTs in children. METHODS: A systematic literature search in PubMed, Web of Science, Embase, and Cochrane Central Register of Controlled Trials up to November 2014 was conducted to identify randomized controlled trials (RCTs) and prospective cohort studies that compared the use of cuffed and uncuffed ETTs in children. The primary outcome was the incidence of postextubation stridor and the second outcomes were the TT exchange rate, need for re-intubation, and duration of tracheal intubation. All pooled data were estimated using random effects meta-analysis. RESULTS: Two RCTs and two prospective cohort studies including 3782 patients, in which 1979 patients for cuffed tubes and 1803 patients for uncuffed tubes, were included in our analysis. We found that the use of cuffed ETTs did not significantly increase the incidence of postextubation stridor (RR = 0.88; 95 % CI 0.67-1.16, p = 0.36), and the TT exchange rate was lower in patients receiving cuffed tubes intubation (RR, 0.07; 95 % CI 0.05-0.10, p < 0.00001). The need for re-intubation following planned extubations and duration of tracheal intubation did not differ significantly between the cuffed tube group and the uncuffed tube group. CONCLUSIONS: Our study demonstrates that cuffed ETTs reduce the need for TT exchanges and do not increase the risk for postextubation stridor compared with uncuffed ETTs.

Effects of Fentanyl on Emergence Agitation in Children under Sevoflurane Anesthesia: Meta-Analysis of Randomized Controlled Trials.

BACKGROUND AND OBJECTIVES: The goal of this meta-analysis study was to assess the effects of fentanyl on emergence agitation (EA) under sevoflurane anesthesia in children. SUBJECTS AND METHODS: We searched electronic databases (PubMed, Embase, Web of Science and the Cochrane Central Register of Controlled Trials) for articles published until December 2014. Randomized controlled trials (RCTs) that assessed the effects of fentanyl and placebo on EA under sevoflurane anesthesia in children that the outcome were the incidence of EA, postoperative pain, emergence time or adverse effects were included in this meta-analysis. RESULTS: A total of 16 studies, including 1362 patients (737 patients for the fentanyl group and 625 for the placebo group), were evaluated in final analysis. We found that administration of fentanyl decreased the incidences of EA (RR = 0.37, 95% CI 0.27~0.49, P<0.00001) and postoperative pain (RR = 0.59, 95% CI 0.41~0.85, P = 0.004) but increased the incidence of postoperative nausea and vomiting (PONV) (RR = 2.23, 95% CI 1.33~3.77, P = 0.003). The extubation time (WMD = 0.71 min, 95% CI 0.12~1.3, P = 0.02), emergence time (WMD = 4.90 min, 95% CI 2.49~7.30, P<0.0001), and time in the postanesthesia care unit (PACU) (WMD = 2.65 min, 95% CI 0.76~4.53, P = 0.006) were slightly increased. There were no significant differences in the time to discharge of day patients (WMD = 3.72 min, 95% CI -2.80~10.24, P = 0.26). CONCLUSION: Our meta-analysis suggests that fentanyl decreases the incidence of EA under sevoflurane anesthesia in children and postoperative pain, but has a higher incidence of PONV. Considering the inherent limitations of the included studies, more RCTs with extensive follow-up should be performed to validate our findings in the future.

The efficacy of N-methyl-D-aspartate receptor antagonists on improving the postoperative pain intensity and satisfaction after remifentanil-based anesthesia in adults: a meta-analysis.

BACKGROUND: Remifentanil could induce opioid-induced hyperalgesia and tolerance, which would increase pain intensity after the operation. N-methyl-d-aspartate (NMDA) receptor antagonists have been used to prevent these adverse effects while the efficacy is still controversial. We evaluated the effectiveness of NMDA receptor antagonists in reducing postoperative pain and analgesic consumption after remifentanil-based anesthesia. METHODS: Full published reports of randomized controlled trials on adults investigating the effects of intravenous administration of NMDA receptor antagonists compared with placebo for preventing remifentanil-induced postoperative hyperalgesia and tolerance were searched in PubMed, Embase, Springer, and the Cochrane Central Register of Controlled Trials. Postoperative pain scores, analgesic consumption, time to first analgesic request, satisfaction scores, and opioid-related and other adverse effects have been evaluated. Results were combined using fix or random-effects model when appropriate. RESULTS: A total of 14 randomized controlled trials with 729 patients were included in the final analysis. Compared with placebo, NMDA receptor antagonists reduced the pain scores at 0, 4, 6, 8, 12, and 24 hours postoperatively (P < .05), reduced the cumulative analgesic consumption of 0-6, 0-24, and 0-48 hours after the operation (P < .05), prolonged the first time to request analgesic (P < .05), and promoted the satisfaction scores (P < .05). There was no difference in the incidence of postoperative nausea and vomiting, psychological adverse effects, and shivering. Subgroup analysis was conducted on different interventions (ketamine and magnesium); the results are in line with general results. CONCLUSIONS: N-methyl-d-aspartate receptor antagonists can prevent the increase of analgesic consumption and pain intensity induced by remifentanil, and it can improve the postoperative satisfaction of patients.

Elevated preoperative peripheral blood monocyte count predicts poor prognosis for hepatocellular carcinoma after curative resection.

BACKGROUND: Peripheral blood monocyte count is an easily assessable parameter of systemic inflammatory response. The aim of this study was to determine whether monocyte count was prognostic in hepatocellular carcinoma (HCC) following hepatic resection. METHODS: We retrospectively reviewed 351 patients with HCC treated with hepatic resection from 2006 to 2009. Preoperative absolute peripheral monocyte count, demographics, and clinical and pathological data were analyzed. RESULTS: On univariate and multivariate analysis, elevated monocyte counts (≥ 545/mm(3)), tumor size ≥ 5 cm, non-capsulation, and multiple tumors were associated with poor disease-free survival (DFS) and overall survival (OS). The 1-, 3- and 5-year DFS rates were 58%, 41% and 35%, respectively, for patients with monocyte counts <545/mm(3), and 36%, 23% and 21% for patients with monocyte counts ≥ 545/mm(3). Correspondingly, the 1-, 3- and 5-year OS rates were 79%, 53% and 46% for monocyte counts <545/mm(3), and 64%, 36% and 29% for monocyte counts ≥ 545/mm(3). Subgroup analysis indicated that DFS after hepatic resection in hepatitis B virus (HBV)-infected patients was significantly better in those with a peripheral blood monocyte counts <545/mm(3), but it did not differ between patients without HBV infection. In addition, DFS was significantly better for patients with a peripheral blood monocyte count <545/mm(3), whether or not cirrhosis was present. Patients with elevated monocyte counts tended to have larger tumors. CONCLUSIONS: Elevated preoperative monocyte count is an independent predictor of worse prognosis for patients with HCC after hepatic resection, especially for those with HBV infection. Postoperative adjuvant treatment might be considered for patients with elevated preoperative monocyte counts.

Folic acid attenuates hyperhomocysteinemia-induced glomerular damage in rats.

The present study investigated whether lowering plasma homocysteine (Hcy) with folic acid (FA) could attenuate hyperhomocysteinemia (HHcy)-associated glomerular damage and possible mechanisms. The HHcy animal model was established by intragastric administration with l-methionine in rats. FA was also given intragastrically. Plasma Hcy and creatinine and urinary albumin were measured. Histological and ultrastructural changes were observed by light and electron microscopes. The expression of alpha-smooth muscle actin (α-SMA), proliferating cell nuclear antigen (PCNA) and transforming growth factor-beta1 (TGF-ß1) in the kidney was examined by immunohistochemical staining and western blot analysis. The administration of l-methionine induced HHcy in rats. The HHcy rats developed glomerulosclerosis and fibrosis. Plasma creatinine concentration and urinary albumin excretion were also significantly increased in HHcy rats. Effacement and extensively fusion of podocyte foot process was observed in HHcy rats, which was associated with decreased expression of nephrin protein in renal cortex of HHcy rats. Supplementation with FA lowered plasma Hcy significantly. Plasma creatinine concentration and urinary albumin excretion were also significantly attenuated by FA. Morphologically, HHcy-associated glomerulosclerosis, fibrosis, podocyte foot process effacement and loss of podocyte nephrin, were significantly improved by FA. The expressions of α-SMA, PCNA and TGF-ß1 were increased in renal cortex of HHcy rats, and which were also partially reversed by FA. These data suggest that elevated plasma Hcy is an important pathogenic factor for glomerular damage. Lowering plasma Hcy by FA can inhibit TGF-ß1 expression and attenuate HHcy-induced glomerular damage.

Vascular fibrosis in atherosclerosis.

Vascular fibrosis, characterized by reduced lumen diameter and arterial wall thickening attributable to excessive deposition of extracellular matrix (ECM), links with many clinical diseases and pathological progresses including atherosclerosis. It involves proliferation of vascular smooth muscle cell (VSMC), accumulation of ECM and inhibition of matrix degradation. The risk factors associated with cardiovascular disease, including hypertension, hyperglycemia, dyslipidemia and hyperhomocysteinemia (HHcy), are also suggested as initiation and progression factors of vascular fibrosis. Vascular fibrosis has been found to relate to renin-angiotensin-aldosterone system (RAAS), oxidative stress, inflammatory factors, growth factors and imbalance of endothelium-derived cytokine secretion. Angiotensin II (Ang II) and aldosterone, the circulating effector hormones of RAAS, are recognized as responsible for the pathophysiology of vascular fibrosis. Transforming growth factor-beta (TGF-beta) plays a critical role in ECM accumulation and vascular remodeling via up-regulating the production of several agents including connective tissue growth factor (CTGF) and fibroblast growth factor. An imbalance between matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) results in collagen accumulation and adverse matrix remodeling. Aberrant expression or function of peroxisome proliferator-activated receptor gamma (PPAR gamma) is also associated with, and very likely contributes to, the progression of pathological fibrosis and vascular remodeling. In this review, we discuss the pathogenesis of vascular fibrosis in atherosclerosis with focus on the networking among main responsible mediators. The main pathophysiologic factors leading to vascular fibrosis will also be discussed.

Involvement of Kv1.5 protein in oxidative vascular endothelial cell injury.

Endothelial injury related to oxidative stress is a key event in cardiovascular diseases, such as hypertension and atherosclerosis. The activation of the redox-sensitive Kv1.5 potassium channel mediates mitochondrial reactive oxygen species (ROS)-induced apoptosis in vascular smooth muscle cells and some cancer cells. Kv1.5 channel is therefore taken as a new potential therapeutic target for pulmonary hypertension and cancers. Although Kv1.5 is abundantly expressed in vascular endothelium, there is little knowledge of its role in endothelial injury related to oxidative stress. We found that DPO-1, a specific inhibitor of Kv1.5, attenuated H(2)O(2)-evoked endothelial cell apoptosis in an in vivo rat carotid arterial model. In human umbilical vein endothelial cells (HUVECs) and human pulmonary arterial endothelial cells (HPAECs), angiotensin II and oxLDL time- or concentration-dependently enhanced Kv1.5 protein expression in parallel with the production of intracellular ROS and endothelial cell injury. Moreover, siRNA-mediated knockdown of Kv1.5 attenuated, whereas adenovirus-mediated Kv1.5 cDNA overexpression enhanced oxLDL-induced cellular damage, NADPH oxidase and mitochondria-derived ROS production and restored the decrease in protein expression of mitochondria uncoupling protein 2 (UCP2). Collectively, these data suggest that Kv1.5 may play an important role in oxidative vascular endothelial injury.

[Effects of preoperative oral glucose on perioperative insulin resistance and plasma proteins of intestinal surgery].

OBJECTIVE: To investigate the effects of oral intake of glucose solution before surgery on the pH at the lower esophagus, perioperative blood glucose level, and plasmic protein in patients undergoing radical resection for colorectal cancer. METHODS: Between January 2008 and December 2008, 60 patients undergoing radical surgery for colorectal cancer were enrolled and randomized into three groups using the table of random digits. Four patients were withdrawn from the study. Patients in group A (n=19) were given 800 ml of 12.5% glucose solution for oral intake the night before surgery, and 200 ml two hours before surgery. Patients in group B (n=19) were given distilled water instead of glucose. Patients in group C (n=18) were asked to fast for 8-12 hours before operation. Combined general and epidural anesthesia was used. pH at the lower esophagus was monitored during intubation and extubation. Albumin, transferrin, prealbumin, insulin, and fasting blood glucose were measured before surgery and at postoperative day 1, 3, and 7. RESULTS: pH at the lower esophagus was 8.05±0.43 in group A, 7.98±0.41 in group B, and 7.94±0.41 in group C. There were no perioperative acid regurgitations (P>0.05). Serum insulin in group A at postoperative day 1 was (16.32±16.11) µU/L, which was significantly lower than that in group B (30.65±41.74) µU/L and group C (34.01±52.91) µU/L. Log HOMA-IR in group A at postoperative day 1 was significantly lower than that in group B and group C (0.49±0.35 vs. 0.59±0.56 and 0.60±0.63, P<0.05). Transferrin in group C at postoperative day 3 and 7 was significantly lower than that in the other two groups, as was albumin at postoperative day 3 (P<0.05). CONCLUSION: Oral liquid intake 2 hours before surgery is not associated with increased risk of regurgitation or aspiration during intubation and extubation, and may glucose solution intake reduce insulin resistance and protein degradation after colorectal surgery.

Polysaccharide from fuzi (FPS) prevents hypercholesterolemia in rats.

BACKGROUND AND AIM: Polysaccharide from fuzi (FPS), a Chinese herbal medicine extract, has been demonstrated to exert lipid lowering affects. In this study we examined potential mechanisms underlying this affect, specifically alterations in expression of the LDL-receptor (LDL-R), 3-hydroxy-3-methyl glutaryl (HMG)-CoA reductase and cytochrome P450 7alpha-1 (CYP7alpha-1), using a rat model of hypercholesterolemia. METHODS AND RESULTS: Male rats were fed either a normal or high cholesterol (HC) diet for two-weeks. Half of the rats on the HC diet were orally gavaged with FPS (224 mg/kg, 448 mg/kg or 896 mg/kg diet) daily. Serum lipid levels were quantified at end of the study period as were liver levels of LDL-R protein and mRNA expression of CYP7alpha-1 and HMG-CoA. Serum cholesterol and LDL-C concentrations were significantly elevated from control in HC rats, but not in those treated with FPS (P < 0.05). LDL-R expression was significantly decreased in the HC group compared to control (P < 0.05), but significantly increased in the FPS group (P < 0.05). HMG-CoA mRNA levels were significantly increased in the HC group compared both other groups (P < 0.05), while CYP7alpha-1 expression was significantly higher in the FPS group compared to both other groups (P < 0.05). CONCLUSION: These findings suggest that the cholesterol lowering effect of FPS in hypercholesteremic rats is caused at least in part by increased hepatic LDL-R and CYP7alpha-1 expression and decreased HMG-CoA expression. Further study is needed to determine precisely where and how FPS exerts these effects. FPS offers potential as a therapeutic agent for the treatment of hypercholesterolemia.

[Application of remifentanil in neurosurgical anesthesia: a multi-center study].

OBJECTIVE: To observe the hemodynamic changes, recovery profiles, and side effects of propofol and remifentanil anesthesia by target controlled infusion (TCI). At different neurosurgical stages in patients undergoing neurosurgical operations. METHODS: 230 patients were scheduled for elective craniotomy in five hospitals in Beijing, Changsha, and Guangzhou. During the general anesthesia the plasma target-concentration of propofol remained unchangeable and the dose of remifentanil changed at different stages before skin incision, during skull opening, during intracranial procedure, and at skull closing. The hemodynamics changes and anesthetic recovery profiles were recorded. RESULTS: The plasma target-concentrations of remifentanil were set to 3.0, 3.5, 3.6 and 3.4 ng/ml respectively. The time of consciousness loss during induction was (2.0 +/- 0.9) min. The mean arterial pressure (MAP) and heart rate (HR) decreased after induction (both P < 0.05) and increased after intubation. The hemodynamic changes were stable at different surgical stages and the HR was significantly lower than the baseline value (P < 0.01). MAP and HR increased gradually when the spontaneous breathing was recovered. 80, 41, 9, and 12 patients received nicardipine, atropine, esmolol, and ephedrine respectively during the operation. The times of recovery of spontaneous breathing, eye opening, extubation, and orientation were (12 +/- 9) min, (13 +/- 7) min, (16 +/- 8) min, and (21 +/- 8) min respectively. CONCLUSION: When combined with 3 microg/ml propofol, the plasma target-concentrations of remifentanil, 3.0, 3.5, 3.6, and 3.4 ng/ml before skin incision, during skull opening, during intracranial procedure, and at skull closing respectively, can provide rapid induction, faster emergence , and better hemodynamic stability.

Low central venous pressure reduces blood loss in hepatectomy.

AIM: To investigate the effect of low central venous pressure (LCVP) on blood loss during hepatectomy for hepatocellular carcinoma (HCC). METHODS: By the method of sealed envelope, 50 HCC patients were randomized into LCVP group (n=25) and control group (n=25). In LCVP group, CVP was maintained at 2-4 mmHg and systolic blood pressure (SBP) above 90 mmHg by manipulation of the patient's posture and administration of drugs during hepatectomy, while in control group hepatectomy was performed routinely without lowering CVP. The patients' preoperative conditions, volume of blood loss during hepatectomy, volume of blood transfusion, length of hospital stay, changes in hepatic and renal functions were compared between the two groups. RESULTS: There were no significant differences in patients' preoperative conditions, maximal tumor dimension, pattern of hepatectomy, duration of vascular occlusion, operation time, weight of resected liver tissues, incidence of post-operative complications, hepatic and renal functions between the two groups. LCVP group had a markedly lower volume of total intraoperative blood loss and blood loss during hepatectomy than the control group, being 903.9+/-180.8 mL vs 2 329.4+/-2 538.4 (W=495.5, P<0.01) and 672.4+/-429.9 mL vs 1 662.6+/-1 932.1 (W=543.5, P<0.01). There were no remarkable differences in the pre-resection and post-resection blood losses between the two groups. The length of hospital stay was significantly shortened in LCVP group as compared with the control group, being 16.3+/-6.8 d vs 21.5+/-8.6 d (W=532.5, P<0.05). CONCLUSION: LCVP is easily achievable in technique. Maintenance of CVP