ones of our study. The possible causes of differences in the results may be interpreted that in their study, the level of Sodium Dialysis fluid was specified for each patient based on their PlasmaSodium level. In the current research, however, both patients were treated through a gradual reduction of Sodium Dialysis fluid and fixed Sodium, which had no relationship with the pre-Dialysis PlasmaSodium. It should be noted that the use of crossover method is one of the strengths of this paper. The restrictions of the patient evaluation sessions (three sessions per intervention) and the low number of patients were considered as some limitations of this study. No correlation was found between the PlasmaSodium and blood pressure. This result is different from the results of the Zahed et al. (2015). Their paper is discussed about the relationship between the Sodium Dialysis fluid concentration and blood pressure in chronic renal failure patients. Their study was carried out on 266 hemodialysis patients suffering from ESRD for various reasons. They were on Loghman Hakim, Ashrafi Isfahani and West of Tehran. In this study, the systolic blood pressure was measured before and after Dialysis and Sodium Dialysis fluid for one month. It is worth noting that the systolic blood pressure changes before and after Dialysis are significantly correlated with changes in dialysis fluid Sodium, based on which this relationship is independent of all other factors affecting on the blood pressure and direction. This study was contrary to the results of the study by Zahid (2015). 29 The
sympathetic stimulation in man. [Na] in the venous return from the forearm of each of 21 normal subjects was reduced (to an average of 118 mEq/liter), increased (147 mEq/liter), and maintained within the normal range (140 mEq/liter) by means of infusions into the brachial artery of three solutions containing different [Na]. Mannitol or sucrose and disodium sulfate were substituted for sodium chloride to produce the desired changes in [Na] without changing blood osmolarity.
Material and Methods: From all intertrochanteric fracture admissions between January 2007 and May 2012, 160 patients were included in this study. The variables studied were age, gender, length of hospital stay, and analytical data such as hemoglobin, total leucocyte count, platelets, urea, creatinin and plasmasodium. Follow-up data on mortality were obtained from the civil registry and, considering 6 months as the cut-off point, patients were divided into 2 groups based on their survival. Mann-Whitney and Chi square statistics were used to study the association between our variables and patients survival.
Knechtle B, Knechtle P, Kohler G, Rosemann T. Does a 24-hour ultra-swim lead to dehydration? J. Hum. Sport Exerc. Vol. 6, No. 1, pp. 68-79, 2011. We investigated the change in body composition and hydration status in one male ultra-endurance swimmer during a 24-hour swim. Body mass, percent body fat and skeletal muscle mass using the anthropometric method as well as total body water using bioelectrical impedance analysis were determined pre race, every 6 hours and after the race. Parameters of hydration status (urinary specific gravity, haematocrit, plasmasodium) and skeletal muscle damage (plasma urea) were measured at the same time. The swimmer achieved a total distance of 41.1 km. Body mass decreased by 1.6 kg, skeletal muscle mass by 1.5 kg, body fat by 2.4 kg and total body water by 3.9 l. Urinary specific gravity remained unchanged at 1.015 g/ml. Haematocrit increased from 46 to 47, plasma volume decreased by 4 % and plasmasodium by 4.0 mmol/l. We found in this ultra-swimmer a decrease in body mass of 1.7 % and a consistent urinary specific gravity of 1.015 g/ml. According to the general concept of dehydration, this corresponds to minimal dehydration. Key words: ULTRA-ENDURANCE, BODY MASS, FAT MASS, SKELETAL MUSCLE MASS.
The measured serum sodium concentration in uncontrolled diabetes mellitus is variable because of the interaction of multiple factors. The increase in plasma osmolality created by hyperglycemia pulls water out of the cells, and reduces the plasmasodium concentration. Physiologic calculations suggest that, in the absence of urine losses, the serum sodium concentration should fall by about 1.6 mEq/L for each 100 mg/100 mL (5.5 mmol/L) increase in glucose concentration. So, the "corrected" sodium concentration can be approximated by adding 2.0 mEq/L to the plasmasodium concentration for each 100 mg/100 mL increase above normal glucose concentration . 89
of burn patients. Additionally, daily weights could not be included in our analysis because they were variably collected in the patient charts. All maintenance fluid rates were based on the patients’ weight and evapora- tive loss due to the burn injury; however, the treating clinical team adjusted these rates based on their clin- ical decisions and thus cannot be normalized in a way that is comparable. A prospective study would add greatly to the influence of intravenous fluid amounts and sodium variability. Fourth, our current study does not directly aid clinicians about dysnatre- mia or sodium variability. Sodium variability would be difficult for a clinician to determine in a patient given the need to analyze and calculate the variability over a given time period (e.g., 7 days). It is likely that two things are needed in order for sodium variability to become a clinically useful marker. One, a prospective study needs to be completed that established the rela- tionship between sodium variability over different time periods with current and future physiologic con- ditions. Two, once established, sodium variability limits can then be presented with laboratory analysis or through clinical calculators that will provide clini- cians with established parameters to aid in their as- sessments of a patient’s clinical condition. Despite these limitations, our analysis indicates that hyperna- tremia is more prevalent in burn patients who die and that increased plasmasodium variability may be a risk factor for death.
tract, is partially removed from the plasma by glomerular filtration and nearly completely reabsorbed in the proximal tubule. Unlike sodium, it is effectively re-excreted by the distal tubules of the kidneys. Our findings suggest a major elevation in plasmasodium level with administration of artemisinin-lumefantrine combination and also with prolonged use of calcium supplements. This suggests that continuous use of these medications can alter renal function. The findings are comparable to previous studies on artemisinin 8,9 . Currently there are no major reported cases of
enhance nimodipine bioavailability. The relative bioavailability (RB) of nimodipine when compared with the control are 1.6, 2.4, 2.0 and 3.4-fold increase for glycerol-water mixture, propylene glycol-water mixture, polysorbate-80- water mixture and sodium lauryl sulfate-water mixture respectively. Since nimodipine has excellent gastrointestinal tract absorption and very low systemic bioavailability due to extensive first-pass hepatic metabolism, the increase in the oral bioavailability by the studied vehicles, could be attributed to reduction in first-pass metabolism of nimodipine involving the inhibition of the cytochrome P450 (CYP3A subfamily) in the liver and reduction of the total body clearance. The findings agreed with previous studies [9, 10, 11] reporting cosolvents (including propylene glycol) and surfactants (including polysorbate 80) to be enhancers of pharmacokinetic features of drugs by inhibiting cytochrome P450 or P-glycoprotein efflux transporter. P-glycoprotein efflux transporter inhibition is considered not to be involved because nimodipine is not a substrate for this transporter.
It was observed that the corrosion of the coated sample initiated from localized pitting. Then it developed into ﬁliform corrosion or general corrosion. The results of salt spray testing are in agreement with the corrosion resistance of potentiodynamic polarization tests. Severe ﬁliform corro- sion is observed on the thin oxide layer of AZ91 Mg alloy without sodium stannate. However, the sample of the electrolyte containing sodium stannate shows localized pitting corrosion. It is clear that tin ions have a good inﬂuence on the corrosion resistance. Also, the thickness of the coatings plays an important role in the corrosion resistance of the coatings in the AZ91 Mg alloy as previous shown in Fig. 1(c), (d).
(a) net movement of potassium into the cell. (b) net movement of sodium into the cell. (c) iodine uptake by thyroid gland cells. (d) transport of hydrogen ion into the stomach lumen in association with hydrochloric acid secretion during digestion of a meal. (e) both (b) and (d) above.
Whi l e o the r samp l e s may give a better ind ica t ion o f th e actual status of an e l ement or compound in the anima l e . g . sal iva for sodium and bone biopsy for pho spha t e , the ba s i s o f a prof i le i nvo lve s a blood s ampl e because of i t s ease of co l l ec t ion and e a s e of s tandard i s at ion o f co l lection and handl ing procedur e s . It i s there fore import ant to devi s e methods whi c h wi l l y i e ld i n fo rmation that i s u s e ful for the parameters that are inc luded . Central l aboratory fa c i l ities may be neces s ary to e l iminate betwe en- l abora tory d i fferences and regular mon i toring may be e s senti a l to provide adequate . information on whi ch to - base a dec i s ion .