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Fluid Loss (fluid + loss)
Selected AbstractsProstaglandin I2 sensory input into the enteric nervous system during distension-induced colonic chloride secretion in rat colonACTA PHYSIOLOGICA, Issue 3 2010J. D. Schulzke Abstract Aim:, Intestinal pressure differences or experimental distension induce ion secretion via the enteric nervous system, the sensorial origin of which is only poorly understood. This study aimed to investigate sensorial inputs and the role of afferent and interneurones in mechanically activated submucosal secretory reflex circuits. Methods:, Distension-induced rheogenic chloride secretion was measured as increase in short-circuit current 10 min after distension (,ISC10; distension parameters ± 100 ,L, 2 Hz, 20 s) in partially stripped rat distal colon in the Ussing-chamber in vitro. PGE2 and PGI2 were measured by radioimmunoassay. Results:, ,ISC10 was 2.0 ± 0.2 ,mol h,1 cm,2 and could be attenuated by lobeline, mecamylamine and dimethylphenylpiperazine, indicating an influence of nicotinergic interneurones. Additionally, a contribution of afferent neurones was indicated from the short-term potentiation of ,ISC10 by capsaicin (1 ,m). As evidence for its initial event, indomethacin (1 ,m) inhibited distension-induced secretion and the release of PGI2 was directly detected after distension. Furthermore, serotoninergic mediation was confirmed by granisetron (100 ,m) which was functionally localized distally to PGI2 in this reflex circuit, as granisetron inhibited an iloprost-induced ISC, while indomethacin did not affect serotonin-activated ion secretion. Conclusions:, Distension-induced active electrogenic chloride secretion in rat colon is mediated by a neuronal reflex circuit which includes afferent neurones and nicotinergic interneurones. It is initiated by distension-induced PGI2 release from subepithelial cells triggering this reflex via serotoninergic 5-HT3 receptor transmission. Functionally, this mechanism may help to protect against intestinal stasis but could also contribute to luminal fluid loss, e.g. during intestinal obstruction. [source] The use of near infrared interactance in hemodialysisHEMODIALYSIS INTERNATIONAL, Issue 1 2005N. Sarhill Forty-one consecutive admissions to a hemodialysis center were evaluated. Demographic information including age, gender, race, and diagnosis was collected. Patients, >18 years old, with end stage renal disease and on hemodialysis for at least one year were included. Those with edema or known ascites were excluded. Weight was measured before and after hemodialysis (HD) using a standard scale and by considering the amount of fluid loss by the hemodialysis machine. Body composition including total body water (TBW) was calculated before and after HD using near infrared interactance (NIR). All measurements were completed during half hour before and after HD. Forty-one patients included: men (n = 26), women (n = 15); median age 58 (range 28,88 years). Twenty-eight were African American and the rest Caucasians. The amount of intravascular fluid taken after HD (assessed by weight reduction) ranged 0,5 L with median 2.2 L. NIR analysis for the same patients at the same time showed different total body water measurements in 91% of cases (P > 0.05). Moreover, NIR analysis showed increase in total body water in 24% of patients even though the hemodialysis machine showed a loss of total body water; median of 1.3 (range: 0,3L). The error in measuring body composition with NIR was both large and varied (random and not systematic error). We conclude that NIR analysis cannot be considered as a reliable method to evaluate body composition, especially total body water, amongst patients with end stage renal disease undergoing hemodialysis. [source] Effect of Hot Water Surface Pasteurization of Whole Fruit on Shelf Life and Quality of Fresh-Cut CantaloupeJOURNAL OF FOOD SCIENCE, Issue 3 2008X. Fan ABSTRACT:, Cantaloupes are associated with recent outbreaks of foodborne illnesses and recalls. Therefore, new approaches are needed for sanitization of whole and cut fruit. In the present study, whole cantaloupes were submerged into water in the following 3 conditions: 10 °C water for 20 min (control), 20 ppm chlorine at 10 °C for 20 min, and 76 °C water for 3 min. Populations of microflora were measured on the rinds of the whole cantaloupes. Quality and microbial populations of fresh-cut cantaloupes prepared from whole fruit were analyzed after 1, 6, 8, 10, 13, 16, and 20 d of storage at 4 °C. The hot water significantly reduced both total plate count (TPC) and yeast and mold count on rind of whole fruits while chlorine or cold water wash did not result in a significant reduction of microbial population. Fresh-cut pieces prepared from hot water-treated cantaloupes had lower TPC than the other 2 treatments in the later storage periods (days 13 to 20) in 2 of 3 trials. The hot water treatment of whole fruits was inconsistent in reducing yeast and mold count of fresh-cut pieces. Soluble solids content, ascorbic acid content, fluid loss, and aroma and appearance scores were not consistently affected by either hot water or chlorine treatment. Our results suggested that hot water pasteurization of whole cantaloupes frequently resulted in lower TPCs of fresh-cut fruit during storage and did not negatively affect quality of fresh-cut cantaloupes. [source] MicroCommentary: Smarter than the average phageMOLECULAR MICROBIOLOGY, Issue 4 2004Garry W. Blakely Summary The seventh cholera pandemic emerged in the poorer nations of the world towards the end of the 20th century and continues to kill thousands of people per year. The causative agent of cholera, the Gram-negative bacterium Vibrio cholera, is only pathogenic when it contains a lysogenic bacteriophage, CTX,, that encodes the toxin responsible for inducing massive fluid loss from the human host. Site-specific integration of CTX, into chromosome I of V. cholera occurs at a site, dif, that is normally required for resolution of chromosome dimers generated by homologous recombination. An article in this issue of Molecular Microbiology reports the analysis of interactions between two host encoded recombinases, XerC and XerD, and the recombination sites involved in lysogeny. Surprisingly, recombination between the CTX,attP site and the chromosomal dif site requires additional recombinase binding sites, downstream from the positions of strand exchange, which might play an architectural role. The positions of strand cleavage also differ significantly between the two sites, suggesting a novel recombination mechanism that implicates additional host factors in resolution of the Holliday junction intermediate. [source] The oral mucosa as a therapeutic target for xerostomiaORAL DISEASES, Issue 8 2008WR Thelin Autoimmune disorders, medical interventions, and aging are all known to be associated with salivary gland hypofunction, which results in the uncomfortable feeling of dry mouth (xerostomia) and significantly diminished oral health. The current therapeutic regimen includes increasing oral hydration using over-the-counter oral comfort agents and the use of systemic cholinergic drugs to stimulate salivary output. However, these approaches produce very transient relief or are associated with uncomfortable side-effects. Thus, new treatments that provide long-lasting relief from discomfort and improve oral health with minimal side-effects would benefit the therapy of this disease. The processes that mediate fluid loss from the oral cavity, such as the absorption of fluid from the oral mucosa, represent novel therapeutic targets for xerostomia. Preventing fluid absorption from the oral cavity is predicted to improve oral hydration and alleviate the clinical symptoms and discomfort associated with dry mouth. Furthermore, therapeutic strategies that prevent fluid absorption should complement current approaches that increase salivary output. This review discusses the current understanding of oral fluid balance and how these processes may be manipulated to provide relief for those suffering from dry mouth. [source] A new method to determine the feto-placental volume based on dilution of fetal haemoglobin and an estimation of plasma fluid loss after intrauterine intravascular transfusionBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 10 2002M. Hoogeveen Objectives (1) To calculate the feto-placental volume (FPV), using the haematocrit (Ht) values and the percentages of fetal haemoglobin (HbF), before and after red blood cell transfusion. (2) To estimate the transfusion-induced loss of plasma fluid. Design Retrospective analysis of data of 42 anaemic fetuses at the first transfusion [gestational age (GA) 19,36 weeks]. Setting Department of Obstetrics, Leiden University Medical Centre, The Netherlands. Sample Fifteen hydropic and 27 non-hydropic fetuses. Methods Donor blood volume (Vdonor) and Ht (Htdonor), fetal pre- and post-transfusion Ht values (Htinitial, Htfinal) and percentages of HbF (HbFinitial and HbFfinal) were used to calculate the FPV. The total red cell volume after transfusion (RCVfinal) and Htfinal were used to estimate the plasma fluid loss. Main outcome measures Feto-placental blood volume and loss of plasma fluid. Results The equations that use Htfinal over-estimate the FPV when the formula does not account for the difference between donor and post-transfusion Ht (FPVHt= 21.36 * GA , 390; r= 0.89). FPV is under-estimated (FPVHt= 9.90 * GA , 172; r= 0.84) when the blood volume increases with a volume less than the added donor blood volume. The calculation of FPV, using HbF percentages and the initial fetal RCV, is independent of volume changes (FPVHbF= 15.10 * GA , 279; r= 0.85). Comparing RCVfinal and Htfinal values showed that 31.1 ± 14.5% of the transfused volume was lost. Results of the hydropic fetuses did not differ from those of the non-hydropic fetuses. Conclusions FPV values based on Ht values are less reliable than those based on RCV and HbF findings. When, for practical reasons, Ht values have to be used, we propose an adapted equation for the calculation of the necessary volume of donor blood: Vdonor= FPVHbF* (Htfinal, Htinitial) / (Htdonor, 0.70 * Htfinal). [source] Acute renal failure in patients with cirrhosis: Perspectives in the age of MELDHEPATOLOGY, Issue 2 2003Richard Moreau In patients with cirrhosis, acute renal failure is mainly due to prerenal failure (caused by renal hypoperfusion) and tubular necrosis. The main causes of prerenal failure are "true hypovolemia" (induced by hemorrhage or gastrointestinal or renal fluid losses), sepsis, or type 1 hepatorenal syndrome (HRS). The frequency of prerenal failure due to the administration of nonsteroidal anti-inflammatory drugs or intravascular radiocontrast agents is unknown. Prerenal failure is rapidly reversible after restoration of renal blood flow. Treatment is directed to the cause of hypoperfusion, and fluid replacement is used to treat most cases of "non-HRS" prerenal failure. In patients with type 1 HRS with very low short-term survival rate, liver transplantation is the ideal treatment. Systemic vasoconstrictor therapy (with terlipressin, noradrenaline, or midodrine [combined with octreotide]) may improve renal function in patients with type 1 HRS waiting for liver transplantation. MARS (for molecular adsorbent recirculating system) and the transjugular intrahepatic portosystemic shunt may also improve renal function in these patients. In patients with cirrhosis, acute tubular necrosis is mainly due to an ischemic insult to the renal tubules. The most common condition leading to ischemic acute tubular necrosis is severe and sustained prerenal failure. Little is known about the natural course and treatment (i.e., renal replacement therapy) of cirrhosis-associated acute tubular necrosis. [source] Estimation of Acute Fluid Shifts Using Bioelectrical Impedance Analysis in HorsesJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 1 2007C. Langdon Fielding Background: Multi-frequency bioelectrical impedance analysis (MF-BIA) has been used to evaluate extracellular fluid volume (ECFV), but not fluid fluxes associated with fluid or furosemide administration in horses. If able to detect acute changes in ECFV, MF-BIA would be useful in monitoring fluid therapy in horses. Hypothesis: The purpose of this study was to evaluate the ability of MF-BIA to detect acute fluid compartment changes in horses. We hypothesized that MF-BIA would detect clinically relevant (10,20%) changes in ECFV. Animals: Six healthy mares were used in the study. Methods: This is an original experimental study. Mares were studied in 3 experiments: (1) crystalloid expansion of normally hydrated subjects, (2) furosemide-induced dehydration followed by crystalloid administration, and (3) acute blood loss followed by readministration of lost blood. MF-BIA measurements were made before, during, and after each fluid shift and compared to known changes in volume calculated based on the intravenous fluids that were administered in addition to urinary fluid losses. Mean errors between MF-BIA estimated change and known volume change were compared using nonparametric analysis of variance. Estimated ECFV pre- and post-fluid administration similarly were compared. The level of statistical significance was set at P < .05. Results: Results of the study revealed a statistically significant change in ECFV and total body water during crystalloid expansion and dehydration. Statistically significant changes were not observed during blood loss and administration. Mean errors between MF-BIA results and measured net changes were small. Conclusions and Clinical Importance: MF-BIA represents a practical and accurate means of assessing acute fluid changes during dehydration and expansion of ECFV using isotonic crystalloids with potential clinical applications in equine critical care. [source] | |||||||||||||