Comparison of five extraction methods for evaluating cadmium and zinc immobilization in soil.

The remediation of soil contaminated with heavy metals is an ongoing environmental concern. Paddy soils contaminated with Cd and Zn were collected from around abandoned metals mines in Korea. Limestone and steel slag were mixed with the collected soil, as amendments for Cd and Zn immobilization. Sequential extraction, lettuce cultivation and five single extraction methods were carried out to assess the effects on Cd and Zn immobilization using amendments. The exchangeable fraction of Cd and Zn was decreased and Fe-Mn oxides fraction increased by stabilization using amendments. In addition, the accumulation of Cd and Zn in lettuce decreased in treated soil and indicated the Cd and Zn immobilization effect in soil by the amendments. The extractable Cd and Zn by CaCl2 and Mehlich-3 in the untreated soils were higher than that of treated soils, whereas Cd and Zn extraction by ethylenediaminetetraacetic acid (EDTA), diethylene tetramine penta-acetic acid (DTPA) and toxicity characteristic leaching procedure (TCLP) has a small or no difference between the untreated and treated soils. The extraction results by CaCl2 and Mehlich-3 methods present reasonable results for Cd and Zn immobilization in soil than EDTA, DTPA and TCLP methods. Therefore, the choice of appropriate extraction method is very important when there is the assessment of Cd and Zn immobilization efficiency.

Resveratrol attenuates 4-hydroxy-2-hexenal-induced oxidative stress in mouse cortical collecting duct cells.

Resveratrol (RSV) may provide numerous protective eff ects against chronic inflammatory diseases. Due to local hypoxia and hypertonicity, the renal medulla is subject to extreme oxidative stress, and aldehyde products formed during lipid peroxidation, such as 4-hydroxy-2-hexenal (HHE), might be responsible for tubular injury. This study aimed at investigating the eff ects of RSV on renal and its signaling mechanisms. While HHE treatment resulted in decreased expression of Sirt1, AQP2, and nuclear factor erythroid 2-related factor 2 (Nrf2), mouse cortical collecting duct cells (M1) cells treated with HHE exhibited increased activation of p38 MAPK, extracellular signal regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and increased expression of NOX4, p47(phox), Kelch ECH associating protein 1 (Keap1) and COX2. HHE treatment also induced NF-κB activation by promoting IκB-α degradation. Meanwhile, the observed increases in nuclear NF-κB, NOX4, p47(phox), and COX2 expression were attenuated by treatment with Bay 117082, N-acetyl-l-cysteine (NAC), or RSV. Our findings indicate that RSV inhibits the expression of inflammatory proteins and the production of reactive oxygen species in M1 cells by inhibiting NF-κB activation.

Under general anesthesia arginine vasopressin prevents hypotension but impairs cerebral oxygenation during arthroscopic shoulder surgery in the beach chair position.

BACKGROUND: Patients undergoing surgery in the beach chair position (BCP) are at a risk of cerebral ischemia. We evaluated the effect of arginine vasopressin (AVP) on hemodynamics and cerebral oxygenation during surgery in the BCP. METHODS: Thirty patients undergoing shoulder surgery in BCP under propofol-remifentanil anesthesia were randomly allocated either to receive IV AVP 0.07 U/kg (AVP group, N = 15) or an equal volume of saline (control group, N = 15) 2 minutes before taking BCP. Mean arterial blood pressure (MAP), heart rate (HR), jugular venous bulb oxygen saturation (SjvO2), and regional cerebral tissue oxygen saturation (SctO2) were measured after induction of anesthesia and before (presitting in supine position) and after patients took BCP. RESULTS: AVP itself given before the positioning increased MAP and decreased SjvO2 and SctO2 (P < 0.0001), with HR unaffected. Although MAP was decreased by BCP in both groups, it was higher in the AVP group (P < 0.0001). While in BCP, HR remained unaltered in the control and decreased in the AVP group. SjvO2 in BCP did not differ between the groups. SctO2 was decreased by BCP in both groups, which was more pronounced in the AVP group until the end of study. The incidence of hypotension (13% vs 67%; P = 0.003) was less frequent, and that of cerebral desaturation (>20% SctO2 decrease from presitting value) (80% vs 13%; P = 0.0003) was higher in the AVP group. The incidence of jugular desaturation (SjvO2 <50%) was comparable between the groups. CONCLUSIONS: A prophylactic bolus administration of AVP prevents hypotension associated with BCP in patients undergoing shoulder surgery under general anesthesia. However, it was associated with regional cerebral but not jugular venous oxygen desaturation on upright positioning.

The role of Acidithiobacillus ferrooxidans and Acidithiobacillus thiooxidans in arsenic bioleaching from soil.

Bioleaching of As from the soil in an abandoned Ag-Au mine was carried out using Acidithiobacillus ferrooxidans and Acidithiobacillus thiooxidans. A. ferrooxidans is an iron oxidizer and A. thiooxidans is a sulfur oxidizer. These two microbes are acidophilic and chemoautotrophic microbes. Soil samples were collected from the Myoungbong and Songcheon mines. The main contaminant of the soil was As, with an average concentration of 4,624 mg/kg at Myoungbong and 5,590 mg/kg at Songcheon. A. ferrooxidans and A. thiooxidans generated lower pH conditions during their metabolism process. The bioleaching of As from soil has a higher removal efficiency than chemical leaching. A. ferrooxidans could remove 70 % of the As from the Myoungbong and Songcheon soils; however, A. thiooxidans extracted only 40 % of the As from the Myoungbong soil. This study shows that bioleaching is an effective process for As removal from soil.

Cerebral oxygen saturation measured by near-infrared spectroscopy and jugular venous bulb oxygen saturation during arthroscopic shoulder surgery in beach chair position under sevoflurane-nitrous oxide or propofol-remifentanil anesthesia.

BACKGROUND: We examined the effects of different anesthetics on cerebral oxygenation and systemic hemodynamics in patients undergoing surgery in beach chair position (BCP). Jugular venous bulb oxygen saturation (SjvO2) and regional cerebral tissue oxygen saturation (SctO2) were determined while patients were placed from the supine to BCP. Whether SctO2 and SjvO2 are interchangeable in assessing the cerebral oxygenation was also examined. METHODS: Forty patients undergoing shoulder surgery in BCP were randomly assigned to receive sevoflurane-nitrous oxide (S/N) or propofol-remifentanil (P/R) anesthesia. Four patients taking angiotensin II receptor antagonists were excluded post hoc. Mean arterial pressure and heart rate, as well as SjvO2 and SctO2, were measured before (postinduction baseline in supine position) and after BCP. RESULTS: Mean arterial pressure decreased by BCP in both groups. It was, however, significantly higher in S/N (n = 19) than in P/R group (n = 17) at 7 to 8 min after the positioning. SjvO2 also significantly decreased after BCP in both groups, the magnitude of which was lower in S/N than in P/R group (11 ± 10% vs. 23 ± 9%, P = 0.0006). The incidences of SjvO2 <50% and mean arterial pressure less than 50 mmHg were lower in S/N group, but SctO2and the incidence of cerebral desaturation (more than 20% decrease from baseline) did not significantly differ between the groups. SctO2 and SjvO2 were only weakly correlated (ß = 0.218, r2 = 0.133). Bland-Altman analysis showed a mean difference of -7.2% with 95% limit of agreement between -38.2% and 23.8%. CONCLUSIONS: The margin of safety against impaired cerebral oxygenation is greater and SjvO2 is more preserved with S/N than with P/R anesthesia. SctO2 may not be reliable in detecting a low SjvO2 during the surgery in BCP.

Protective effect of sauchinone against regional myocardial ischemia/reperfusion injury: inhibition of p38 MAPK and JNK death signaling pathways.

Sauchinone has been known to have anti-inflammatory and antioxidant effects. We determined whether sauchinone is beneficial in regional myocardial ischemia/reperfusion (I/R) injury. Rats were subjected to 20 min occlusion of the left anterior descending coronary artery, followed by 2 hr reperfusion. Sauchinone (10 mg/kg) was administered intraperitoneally 30 min before the onset of ischemia. The infarct size was measured 2 hr after resuming the perfusion. The expression of cell death kinases (p38 and JNK) and reperfusion injury salvage kinases (phosphatidylinositol-3-OH kinases-Akt, extra-cellular signal-regulated kinases [ERK1/2])/glycogen synthase kinase (GSK)-3ß was determined 5 min after resuming the perfusion. Sauchinone significantly reduced the infarct size (29.0% ± 5.3% in the sauchinone group vs 44.4% ± 6.1% in the control, P < 0.05). Accordingly, the phosphorylation of JNK and p38 was significantly attenuated, while that of ERK1/2, Akt and GSK-3ß was not affected. It is suggested that sauchinone protects against regional myocardial I/R injury through inhibition of phosphorylation of p38 and JNK death signaling pathways.

Ex-situ field application of electrokinetics for remediation of shooting-range soil.

Electrokinetic process for remediation of a shooting-range site was evaluated in this study. By field operation for 100 days, the newly designed electrokinetic system was evaluated for process stability, performance, and efficiency. The field site of this study was an abandoned military shooting range located in the Civilian Control Line of South Korea. The target area, only, was heavily contaminated by Pb and Cu to a depth of 0.5 m. After dry-sieving of the field soil to separate particulate Pb, two cells in a hexagonal (two-dimensional) arrangement, including ten anodes outside the cell and two cathodes in the middle, were prepared. The pH of each electrolyte was adjusted by use of concentrated HNO(3), resulting in acid-enhanced electrokinetics. The monitoring results indicated that overall removal of heavy metals (Pb, Cu) was achieved, and that both heavy metals were removed from outside the cell. The average final efficiency of removal of Pb and Cu was 39.5 ± 35 and 63.8 ± 12%, respectively. Although the feasibility of this system was confirmed, for commercialization of the process confirmed drawbacks must be improved by further study.

4-Hydroxy-2-hexenal-induced apoptosis in human renal proximal tubular epithelial cells.

BACKGROUND: The aldehyde products of lipid peroxidation such as 4-hydroxy-2-hexenal (HHE) might be responsible for the pathogenesis of kidney injury. The present study was aimed to investigate the effects of HHE on renal tubular epithelial cells and its signaling mechanisms. METHODS: Human proximal tubular epithelial (HK-2) cells were treated with 10 µM of HHE. Cell viability was examined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The fluorescent probe 2',7'-dichlorofluorescein diacetate was used to measure intracellular levels of reactive oxygen species (ROS). The protein expression of NF-κB, mitogen-activated protein kinase (MAPK), pro-apoptoic Bax and anti-apoptotic protein Bcl-2 was determined by semiquantitative immunoblotting. Apoptosis was assessed by flow cytometry analysis after the cells were stained by fluorescein isothiocyanate-conjugated annexin V protein and propidium iodine. RESULTS: Treatment with various doses of HHE resulted in dose-dependent decreases of cell viability and increases of ROS. HHE increased the expression of p38 MAPK, extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK). HHE induced NF-κB activation and IκB-α degradation. Increased nuclear NF-κB activation was blocked by inhibitors of ERK (PD98059) or JNK (SP600125), but not affected by p38 MAPK inhibitor (SB203580). Flow cytometry analysis revealed HHE-induced apoptosis. HHE decreased the expression of Bcl-2, while it increased that of Bax, which was attenuated by the treatment of NF-κB inhibitor (Bay 11-7082) or N-acetyl-L-cysteine (NAC). An inhibition of NF-κB prevented HHE-induced apoptosis. CONCLUSIONS: HHE-induced tubular cell apoptosis is mediated by modulation of Bax and Bcl-2 via ROS generation. HHE-mediated accumulation of ROS may induce redox-sensitive transcription factor, NF-κB, through activation of ERK and JNK, resulting in cellular apoptosis in HK-2 cells.

Layers of Uranium Phosphate Nanorods and Nanoplates Encrusted on Fungus Cladosporium sp. Strain F1 Hyphae.

The hyphae of Cladosporium sp. strain F1 (CFGR 2020-301-00084) were heavily encrusted with pre-synthesized uranium phosphate minerals under a wide range of pH conditions. SEM and TEM images showed that nanorods and nanoplates of uranium phosphate minerals at pH 4 and 5 and at pH 6, 7, and 8, respectively, were tightly adsorbed along the hyphae of Cladosporium sp. strain F1, while only a few uranium phosphate minerals were observed on the hyphae of Aspergillus niger VKMF 1119. Based on the physical mobility and chemical stability of uranium phosphate minerals under in situ oxidizing environmental conditions, the application of Cladosporium sp. strain F1 has potential as a novel strategy for the remediation of uranium contamination in sediments and aquifers under a wide range of pH conditions where larger amounts of phosphate are present in the environment.

Renoprotective effects of paricalcitol on gentamicin-induced kidney injury in rats.

Vitamin D is thought to exert a protective effect on renal disease progression, but the underlying molecular mechanism remains unclear. We investigated whether paricalcitol ameliorates tubular dysfunction and fibrosis in gentamicin (GM)-induced renal injury. Two groups of rats were treated with GM (100 mg x kg(-1) x day(-1)), one of which was cotreated with paricalcitol (0.3 microg x kg(-1) x day(-1)) for 14 days and the other was not. The control group was treated with vehicle only. HK-2 cells were cultured with GM in the absence or presence of paricalcitol. Paricalcitol restored impaired renal function and the downregulated renal sodium transporters and aquaporin-1 expression caused by GM. ED-1-expressing monocyte/macrophage accumulation induced by GM was attenuated by paricalcitol treatment. Paricalcitol prevented upregulated inflammatory cytokines (TNF-alpha, IL-1beta, INF-gamma) and adhesion molecules (monocyte chemoattractant protein-1, ICAM-1, VCAM-1) induced by GM. In addition, paricalcitol effectively reversed TGF-beta1-induced epithelial-to-mesenchymal transition (EMT) process and extracellular matrix accumulation in GM-induced nephropathy. Increased collagen deposition and fibrosis in GM-treated kidney were ameliorated by paricalcitol. Paricalcitol also attenuated the upregulated NF-kappaB and phosphorylated ERK1/2 expression in HK-2 cells cultured with GM. In conclusion, paricalcitol prevents GM-induced renal injury by inhibiting renal inflammation and fibrosis, the mechanism of which is the interruption of NF-kappaB/ERK signaling pathway and preservation of tubular epithelial integrity via inhibiting EMT process.

Paricalcitol attenuates cyclosporine-induced kidney injury in rats.

Despite its benefits, the clinical use of cyclosporine A (CsA) is limited by its nephrotoxic properties. Because paricalcitol (19-nor-1,25-hydroxyvitamin D(2)) has renoprotective effects, we tested whether it can blunt renal dysfunction and fibrosis in a rat model of CsA-induced nephropathy. Treatment with CsA decreased creatinine clearance, increased monocyte/macrophage infiltration, and increased the expression of inflammatory cytokines within the kidney. Paricalcitol reduced the decline in kidney function and pro-fibrotic changes and also blunted the increased transforming growth factor (TGF)-beta1 expression and Smad signaling. Using an in vitro model, we treated HK-2 cells with CsA and found that paricalcitol attenuated the CsA-induced increases in phosphorylated extracellular signal-regulated and c-Jun N-terminal kinases, and also prevented the activation of nuclear factor-kappaB. Paricalcitol effectively prevented TGF-beta1-induced epithelial-to-mesenchymal transitions and extracellular matrix accumulation as evidenced by attenuated collagen deposition and fibrosis in CsA-treated rats. In addition, paricalcitol decreased the number of TUNEL-positive nuclei and reduced the expression of pro-apoptotic markers in CsA-treated HK-2 cells. Thus, paricalcitol appears to attenuate CsA-induced nephropathy by suppression of inflammatory, pro-fibrotic, and apoptotic factors through inhibition of the nuclear factor-kappaB, Smad, and mitogen-activated protein kinase signaling pathways.

alpha-Lipoic acid prevents cisplatin-induced acute kidney injury in rats.

BACKGROUND: Cisplatin-induced nephropathy has been related to increased lipid peroxide formation and decreased activity of antioxidant enzymes in the kidney. The present study aimed to examine whether treatment with alpha-lipoic acid (alpha-LA) prevents the cisplatin-induced nephrotoxicity. METHODS: Two groups of rats were treated with cisplatin, one of which being cotreated with alpha-LA. The control group was treated with vehicle only. Four days later, the expression of aquaporins and sodium transporters was determined in the kidney by immunoblotting and immunohistochemistry. The arginine vasopressin-stimulated generation of cAMP was measured by radioimmunoassay. The expression of nitric oxide synthases (NOS) was determined by immunoblotting. The mRNA expression of endothelin-1 (ET-1) and tumour necrosis factor (TNF)-alpha was measured by real-time PCR. Apoptosis was examined by TUNEL staining. RESULTS: Following the treatment with cisplatin, urinary volume and fractional excretion of sodium increased. Accordingly, the expression of aquaporins 1-3, Na,K-ATPase, NHE3 and NKCC2 was decreased. The expression of adenylyl cyclase VI and vasopressin-stimulated cAMP generation was decreased. The expression of inducible NOS was increased, while that of endothelial NOS decreased. The ET-1 expression was increased. TUNEL-positive cells were increased, in association with an increased expression of TNF-alpha. alpha-LA treatment prevented dysregulation of these parameters and resumed the renal function. CONCLUSION: alpha-LA may prevent the cisplatin-induced nephrotoxicity, possibly through preserving the activities of NO and ET systems and inhibiting the development of apoptosis.

Urinary trypsin inhibitors afford cardioprotective effects through activation of PI3K-Akt and ERK signal transduction and inhibition of p38 MAPK and JNK.

BACKGROUND: We determined the effect of urinary trypsin inhibitors (UTI) in regional myocardial ischemia/reperfusion (I/R) injury and its underlying mechanisms involving the role of prosurvival kinases such as phosphatidylinositol-3-OH kinases (PI3K)-Akt and extracellular signal-regulated kinases (ERK 1/2) and apoptotic kinases such as p38 and JNK. METHODS: The rats were anesthetized and subjected to an I/R insult consisting of 30-min left anterior descending coronary artery (LAD) occlusion followed by reperfusion. Infarct size was measured after 120 min of reperfusion. UTI was given alone or along with wortmannin (inhibitor of PI3K) or PD098059 (inhibitor of ERK1/2) before LAD occlusion. The phosphorylation of Akt, ERK1/2, p38 and JNK was determined by immunoblotting after 5 min of reperfusion. UTI was administered 10 min before LAD occlusion, and wortmannin and PD098059 were administered 20 min before LAD occlusion. RESULTS: UTI significantly reduced the infarct size compared with the control. Wortmannin or PD098059 alone did not affect the infarct size, but they abolished the UTI-induced cardioprotective effect. UTI significantly reduced the phosphorylation of p38 and JNK, while it enhanced that of Akt and ERK1/2. CONCLUSIONS: UTI has a protective effect against regional myocardial I/R injury through activation of survival kinases PI3K-Akt and ERK1/2 and attenuation of p38 and JNK.

Altered renal expression of aquaporin water channels and sodium transporters in rats with two-kidney, one-clip hypertension.

AIMS: To determine whether the renal regulation of aquaporin (AQP) water channels and sodium transporters are altered in 2-kidney, 1-clip (2K1C) hypertension. METHODS: Male Sprague-Dawley rats were used. They were made 2K1C hypertensive for 1 week. The renal expression of AQPs and sodium transporters was determined by semiquantitative immunoblotting and immunohistochemistry. The activity of adenylyl cyclase was measured by stimulated generation of cAMP. RESULTS: Systolic blood pressure was increased in 2K1C rats. Experimental rats revealed impaired urinary concentration in association with increased urine volume. Urinary sodium excretion also increased. The expression of AQP1-3 was decreased in the clipped kidney compared with the control kidney, whereas it was unchanged in the non-clipped kidney. The adenylyl cyclase activity provoked by arginine vasopressin, sodium fluoride or forskolin was blunted in the clipped kidney, but remained unaltered in the contralateral kidney. The expressions of the Na,K-ATPase alpha1-subunit, type 3 Na(+)/H(+) exchanger, Na-K-2Cl cotransporter and epithelial sodium channels were decreased in the clipped kidney, while remaining unchanged in the non-clipped kidney. CONCLUSION: The downregulation of AQPs and major sodium transporters/channels in the clipped kidney may play a role in the urinary concentration defect and impaired sodium reabsorption in 2K1C hypertension.

Increased renal expression of nitric oxide synthase and atrial natriuretic peptide in rats with glycyrrhizic-acid-induced hypertension.

The present study aimed to examine whether there is an altered regulation of local hormonal systems in the kidney following the treatment of glycyrrhizic acid (GA), the active ingredient in licorice. Male Sprague-Dawley rats were treated with GA for 3 weeks. The expression of mineralocorticoid receptor (MR) was determined in the kidney by immunoblotting and real-time polymerase chain reaction (PCR). The protein expression of endothelial nitric oxide synthase (eNOS) and inducible NOS (iNOS) was determined. The expression of atrial natriuretic peptide (ANP), natriuretic peptide receptor (NPR)-A and NPR-C was determined by real-time PCR. The activity of guanylyl cyclase was determined by the amount of cGMP generated in responses to sodium nitroprusside (SNP) or ANP. Following the GA treatment, systolic blood pressure was increased. The mRNA and protein expressions of MR were increased in the kidney. The protein expression of eNOS and iNOS was also increased. The expression of ANP mRNA was increased although that of NPR-A and NPR-C mRNA was not changed. The cGMP production provoked by either SNP or ANP was not changed. The increased expression of MR may contribute to GA-induced hypertension. The enhanced expression of NOS and ANP may play a compensatory role in GA-induced hypertension.

Anaesthetic requirements and stress hormone responses in acute cord-injured patients undergoing surgery of the injured spine.

BACKGROUND AND OBJECTIVE: Neuraxial anaesthesia has been shown to produce a sedative and anaesthetic-sparing effect. The purpose of the present study was to determine the effects of acute spinal cord injury on sevoflurane requirement and stress hormone responses during spinal surgery at the level of the injury. METHODS: Thirty-five patients with traumatic complete spinal cord injury undergoing spinal surgery at the level of the injury were studied. They were grouped into quadriplegics (above C7, n = 20) and paraplegics (below T1, n = 15) according to the level of injury. Patients (n = 35) with spine trauma without neurological impairment undergoing spinal surgery at the respective level served as controls. The bispectral index score was maintained at 40-50 throughout the surgery. Measurements included end-tidal sevoflurane concentrations, mean arterial pressure, heart rate, and plasma concentrations of catecholamines and arginine vasopressin. RESULTS: During the surgery, the mean arterial pressure was significantly lower in both quadriplegics and paraplegics (P < 0.05). The heart rate did not differ significantly in the quadriplegics, but was higher in the paraplegics, compared with their controls. However, end-tidal sevoflurane concentrations and bispectral index score were comparable with controls in both quadriplegics and paraplegics. Throughout the study, the plasma arginine vasopressin concentrations were not altered, although norepinephrine and epinephrine concentrations were lower in the quadriplegics. There were no significant differences in stress hormones between the groups having thoraco-lumbar surgery. CONCLUSION: Spinal cord injury neither alters the anaesthetic requirement regardless of the level of injury during spinal surgery at the level of the injury, nor enhances arginine vasopressin release. However, it blunts catecholamine responses in quadriplegics.

Sevoflurane concentrations required to block autonomic hyperreflexia during transurethral litholapaxy in patients with complete spinal cord injury.

BACKGROUND: Autonomic hyperreflexia (AHR) is a potentially life-threatening hypertensive condition that occurs in patients with high spinal cord injury (SCI). The current study was aimed to determine sevoflurane concentrations that block AHR in SCI patients. METHODS: The study involved 28 patients with chronic, complete SCI scheduled to undergo transurethral litholapaxy during general anesthesia. Nine patients without SCI served as controls post hoc. Anesthesia was induced with thiopental, and sevoflurane concentrations in 50% nitrous oxide were adjusted to maintain a Bispectral Index of 40-50. When a patient developed AHR during bladder distension, the target sevoflurane concentration was maintained for at least 10 min, and then the procedure was resumed. Systolic blood pressure, heart rate, and Bispectral Index as well as plasma concentrations of catecholamines and arginine vasopressin were measured before and during the bladder distension. Each target concentration was determined by the up-and-down method based on changes (15% increase or more) of systolic blood pressure in response to bladder distension. RESULTS: In SCI, systolic pressure increased by 67 +/- 33 mmHg, whereas heart rate decreased by 13 +/- 8 beats/min during the first trial (P < 0.01). The hypertensive event was associated with increases of norepinephrine concentrations, but not of epinephrine or vasopressin concentrations. Systolic pressure, heart rate, and norepinephrine concentrations did not change significantly in the control patients. The end-tidal concentrations of sevoflurane to prevent AHR were EC50 of 3.12% and EC95 of 3.83%. CONCLUSION: The EC95 for sevoflurane in 50% nitrous oxide to block AHR during transurethral litholapaxy in patients with SCI was 3.83%.

Bispectral index values during sevoflurane-nitrous oxide general anesthesia in women undergoing cesarean delivery: a comparison between women with and without prior labor.

BACKGROUND: An end-tidal concentration of 1% sevoflurane (1% ET(SEVO)) in 50% nitrous oxide (N(2)O) during elective cesarean delivery has been associated with bispectral index (BIS) values >60, which are associated with an increased risk of awareness. We hypothesized that BIS values during sevoflurane-N(2)O general anesthesia for cesarean delivery would be lower in women with prior labor compared with women without prior labor. METHODS: Forty patients undergoing cesarean delivery were enrolled in this observational study. One group had urgent surgery after labor (labor group, n = 20) and the other had elective surgery without labor (control group, n = 20). General anesthesia was induced with thiopental 4 mg/kg, followed by succinylcholine 1.5 mg/kg, and maintained with 1% ET(SEVO) and 50% N(2)O in oxygen. BIS values, systolic arterial blood pressure, heart rate, plasma stress hormone concentrations, Apgar scores, and postoperative analgesia variables were assessed and compared between groups. RESULTS: BIS values during the period between intubation and delivery were lower in the labor group than in the control group (P < 0.001). Plasma norepinephrine concentrations increased at delivery compared with baseline in both groups. They were higher in the labor group than in the control group both at baseline and at delivery. Systolic arterial blood pressure, heart rate, Apgar scores, surgical characteristics, and plasma concentrations of vasopressin and cortisol were not different between groups. Postoperative visual analog scale pain scores were similar between groups, while the labor group consumed less analgesics (P < 0.01) during the first 24 h after the operation. CONCLUSIONS: Prior labor was associated with lower intraoperative BIS values during sevoflurane/N(2)O general anesthesia and reduced postoperative analgesic consumption in women undergoing cesarean delivery compared with women without prior labor.

Effects of volume depletion and NaHCO3 loading on the expression of Na+/H+ exchanger isoform 3, Na+: HCO3- cotransporter type 1 and nitric oxide synthase in rat kidney.

1. The effects of volume depletion and NaHCO(3) loading on the expression of Na(+)/H(+) exchanger isoform 3 (NHE3), Na(+) : HCO(3)(-) cotransporter type 1 (NBC1) and neuronal (n) and inducible (i) isoforms of nitric oxide synthase (NOS) were determined in rat kidney. 2. Adult male Sprague-Dawley rats were used. Rats were divided into four groups: (i) euvolaemic (EC); (ii) hypovolaemic (HC); (iii) euvolaemia with NaHCO(3) loading (EB); and (iv) hypovolaemia with NaHCO(3) loading (HB). The expression of NHE3, NBC1, nNOS and iNOS proteins was determined in the cortex of the kidney by immunoblotting and immunohistochemistry. Tissue content of nitric oxide (NO) metabolites (NO(x)) were also determined in the cortex using a colourimetric assay. 3. Compared with the EC group, the expression of NHE3 and NBC1 was increased in the HC group and decreased in the EB group. Comparing the EB and HB groups, the expression of NHE3 and NBC1 was higher in the latter group. The expression of NHE3 was decreased and that of NBC1 was increased in the HB group compared with the HC group. The NO(x) content and nNOS expression were decreased in the hypovolaemic (HC) and NaHCO(3)-loaded (EB and HB) rats. Moreover, the expression of iNOS was decreased in the HB group compared with the other groups. 4. An altered volume status and NaHCO(3) loading may affect the regulation of NHE3 and NBC1 in the kidney and the endogenous NO system may play a role in the observed effects.

Anesthetic requirements and stress hormone responses in spinal cord-injured patients undergoing surgery below the level of injury.

Neuraxial anesthesia decreases the minimum alveolar concentration. We determined the effects of spinal cord injury (SCI) on sevoflurane requirements and stress hormone response. Twenty-two chronic SCI patients undergoing surgery below the level of the injury were enrolled in the study, and 15 patients without cord injury served as control patients. Bispectral index score was maintained at 40-50. Measurements included end-tidal sevoflurane concentrations, systolic arterial blood pressure, heart rate, and plasma catecholamine and cortisol concentrations. During surgery, systolic arterial blood pressure, heart rate, and Bispectral index were comparable between SCI and control groups. However, end-tidal sevoflurane concentration was significantly smaller in the SCI (0.81%-1.06%) versus control (1.28%-1.31%) patients. In the control group, plasma norepinephrine and cortisol concentrations were significantly increased during and 1 h after surgery compared with awake baseline values. In the SCI group, the sympathoadrenal and cortisol responses were virtually abolished. We conclude that SCI reduces the anesthetic requirement by 20%-39% during surgery below the level of injury, in association with blunted sympathoadrenal and cortisol responses.