Intravenous Sodium Administration Research Articles

Скрытые опасности периоперационного периода: фокус на гипофосфатемии

Гипофосфатемия (ГФЕ) — одно из частых электролитных расстройств, для развития которого в периоперационном периоде существует много причин. Мы проанализировали базу данных Medline за последние 20 лет с целью идентификации статей, которые содержали бы в качестве одного из ключевых слово «гипофосфатемия». В поиск включили клинические и экспериментальные исследования, обзоры и сообщения о клинических случаях при наличии англоязычного резюме. Этот поиск дал 1754 публикации. На основе изученных статей нами были суммированы сведения о метаболизме фосфатов, основных клинических проявлениях ГФЕ, влиянии ГФЕ на течение периоперационного периода. Авторами представлен собственный опыт выявления и лечения ГФЕ. Определение уровней фосфатов проведено у 328 больных, перенесших хирургические вмешательства в операционных различного хирургического профиля. Наиболее высокая частота ГФЕ наблюдалась у ожоговых больных (23,08 %), после нейрохирургических (17,94 %) и абдоминальных (17,64 %) оперативных вмешательств. Установлено, что коррекцию ГФЕ тяжелой степени целесообразно проводить введением препарата D-фруктозо-1,6-дифосфата натрия — Эзафосфины. После проведенной коррекции препаратом уровень фосфатемии стабилизировался до референтных значений, что совпало с клиническим улучшением состояния пациентов. Больные в целом хорошо перенесли терапию Эзафосфиной, ни у одного из них не было зарегистрировано побочных эффектов.

HIDDEN COMPLICATIONS OF THE POSTOPERATIVE PERIOD: DIAGNOSIS AND TREATMENT

One of the hidden complications of the postoperative period is hypophosphatemia (HPE), which often develops imperceptibly, but can worsen the overall results of treatment. The objective of the work: to investigate the frequency of development of disorders of phosphate exchange in the postoperative period and to establish the possibility and effectiveness of correction of such violations. Materials and methods. The determination of phosphate levels was carried out in 328 patients undergoing surgical treatment in surgical operations of various surgical status. Results. The highest rate of HPE was observed in patients with burns (23.08 %), after neurosurgical (17.94 %) and abdominal (17.64 %) surgical interventions. It is established that the correction of severe HPE is advisable by intravenous administration of sodium D-fructose-1,6-diphosphate. Conclusion. In the postoperative period, HPE is common, but is successfully corrected to abstract values, which coincides with the clinical improvement of patients.

Factors regulating renal angiotensin-converting enzyme activity in the rat.

Changes in angiotensin-converting enzyme (ACE) activity appear to be important in mediating the natriuresis which ensues after administration of an oral or gastric sodium load. In this study, we sought to determine the time course of the changes in ACE activity in the kidney which occur after sodium ingestion. In addition, we sought to investigate mechanisms which might underlie these changes. Angiotensin-converting enzyme activity was measured by generation of histidyl-leucine in homogenates of kidneys harvested at varying time-points after gastric sodium administration. The effects of intravenous sodium loading, solution osmolality and of changes in renal nerve activity were also investigated. Intragastric instillation of both the sodium-containing solution and its iso-osmotic urea control solution resulted in significant increases in renal ACE activity (NaCl: P < 0.0005; Urea: P < 0.01). The increase in renal ACE activity after gastric sodium loading was more prolonged than after the urea control (P < 0.025, NaCl vs. urea at 90 min). This prolonged increase in renal ACE activity appeared to reflect a response to absorbed sodium as intravenous sodium administration caused a significant increase in renal ACE activity at 90 min (P < 0.0005). In contrast to these stimuli which increased renal ACE activity, renal denervation caused a significant decrease in ACE activity in the kidney (P < 0.05). We conclude that gastric sodium loading increases renal ACE activity. This effect appears to be due initially to a response to an increase in gastric lumenal osmolality and later to absorbed sodium. These changes in renal ACE activity are not mediated by a decrease in renal nerve activity.

Angiotensin II: a humoral mediator for the gastric sodium monitor.

Natriuresis in direct response to a gastric sodium stimulus (upper-gut sodium monitor) has paradoxically only been demonstrated in humans and animals on a low-sodium diet preceding each study. It is possible that the low-sodium diet itself induces or suppresses systems that mediate or oppose the ensuing natriuresis. In this study, we sought to determine whether a system activated by this diet, the renin-angiotensin system, mediates the natriuretic response. Specifically, we sought to show whether changes in the circulating concentration of angiotensin II (ANG II) may mediate the renal response to stimulation of the gastric sodium monitor. Male New Zealand White rabbits were randomly assigned to low- (0.008%) or normal (2.2%) sodium diets. After 1 wk on the experimental diet, they received a sodium load intragastrically or intravenously, and plasma ANG II was measured at 0, 5, 10, 30, 60, and 120 min. Urine was collected for 4 h after the sodium load, and plasma sodium was measured at 0, 2, and 4 h. Urinary sodium excretion was greater in the 4 h after gastric than after intravenous sodium administration (P < 0.025) in the rabbits on the low-sodium diet. No significant difference was noted in the rabbits on the normal sodium. In rabbits on the low-sodium diet, there was an immediate and significant decline in plasma ANG II after sodium was administered both intragastrically (P < 0.025) and intravenously (P < 0.05). This decrease was greater after intragastric than intravenous sodium (P < 0.0025), and the difference was still evident at 120 min (P < 0.05). No significant difference in plasma ANG II was found in the normal diet group. We conclude, therefore, that a prolonged decrease in ANG II concentration may play a role in mediating the natriuretic response to the gastric sodium monitor.

Systemic Fluoride Poisoning Following Dermal Hydrofluoric ACID Exposure: Development of an Intravenous Sodium Fluoride Infusion Model in Rats

AbstractThe effect of dermal exposure to concentrated (48% w/v) hydrofluoric acid (HF) on survival and plasma fluoride concentration was investigated in rats. Results of dermal exposure to abdominal and back skin were compared with intravenous administration of sodium fluoride.Dermal HF exposure on 6 cm2 for 5 min resulted in toxic plasma fluoride concentrations. The location of application on the body influenced both the survival time of the rats and the kinetics of plasma fluoride concentrations.After abdominal application of 0.25 or 0.5 ml HF, a 50% mortality rate within 300 min (time of death between 75 and 270 min) was observed. After application of 0.25 ml HF on the back all rats survived the 315 min observational period while after application of 0.5 ml HF an LD50 was reached (time of death between 280 and 314 min).Abdominal exposure caused a gradually increasing plasma fluoride concentration while after exposure on the back a rapid increase of the plasma fluoride concentration was observed, follow...

Quantification of menstrual and diurnal periodicities in rates of cholesterol and fat synthesis in humans.

The mass isotopomer distribution analysis (MIDA) technique is applied here in men and menstruating women to quantify periodicities in the biosynthesis of serum cholesterol and very low density lipoprotein (VLDL)-palmitate. The isotopic enrichment of the true biosynthetic precursor (intracellular acetyl-CoA) during oral or intravenous administration of sodium[1-13C]- or [2-13C]acetate was calculated from mass isotopomer fractional abundances in free cholesterol and VLDL-palmitate, determined by gas chromatography-mass spectrometry (GC-MS). To convert fractional into absolute cholesterol synthesis rates, decay rate constants of plasma cholesterol were determined from the die-away curves of endogenously labeled high-mass isotopomers. Oral [13C]acetate was a 3-4 times more efficient means of labeling the precursor pool for VLDL-palmitate than was intravenous [13C]acetate, consistent with a splanchnic site of VLDL-fatty acid synthesis, whereas the precursor for free cholesterol had an intermediate enrichment, suggesting a contribution from extra-splanchnic tissues as well. Endogenous synthesis of serum cholesterol was 8-11 mg/kg per day (an estimated 65-75% of input into serum cholesterol); it was 1.5- to 3-fold higher at night than during the day (37-49 mg/h at night compared to 9-23 mg/h during the day) and did not vary over the menstrual cycle (608-697 mg/day). In contrast, endogenous synthesis of fatty acids made a relatively minor contribution to body fat pools (1/10-1/20) of input into VLDL-palmitate) compared to dietary fat intake; it was greater in the day-time, and was influenced by menstrual cycle (3-fold elevated in the follicular phase compared to the luteal phase), and body composition (higher in obese men than normal weight men, r2 = 0.59 for lipogenesis vs. body mass index). Factors responsible for periodicities in endogenous lipid synthesis can be studied in humans using this approach.

The Effect of the Intrapancreatic Calcium and Glucagon Administration on the Somatostain-Induced Inhibition of Insulin and Glucagon Secretion in Dogs

We made a study to determine if calcium and glucagon have an effect on insulin secretion, which is inhibited by somatostatin in normal dogs.After an over-night fast, six mongrel dogs weighing 15 to 32 kg were anesthetized with an intravenous administration of sodium pentobarbital.Calcium (0.8 mg/kg.b.w. of CaCl2) and glucagon (10-1 mg) were injected into the superior pancreaticoduodenal artery under the infusion of saline (1 ml/min) or cyclic somatostatin (50 μg bolus plus 5 μg/ml/min) through the pancreatic artery in 6 normal anesthetized dogs. Levels of plasma immunoreactive insulin (IRI) and glucagon (IRG) were estimated in the pancreatic vein and femoral artery by using the double antibody method and canine insulin standard and by employing anti-glucagon antibody AJ 15 (which crossreacted with glucagon-like immunoreactivity) and the method of dextran-coated charcoal. The saline and somatostatin infusions were conducted on the same dog at 20 minute intervals. Blood samples were collected from the pancreatic vein every 5 seconds for 2 minutes and thereafter every 1 min until 5 minutes had elapsed and from the femoral artery every 1 min.The results were the following : 1. The calcium levels of the pancreatic vein increased from 4 to more than 8 mEq/L within one minute, whereas those of the femoral artery did not change significantly. 2. Under the saline infusion, CaCl2 evoked a sharp rise in the pancreatic venous IRI levels which started 25 seconds after the injection, rose to a peak of thirteen folds from baseline at 40 seconds and lasted for almost 2 minutes, whereas under the somatostatin infusion, the peak level was reached at 55 seconds and affected only one third of those under the saline infusion. 3. IRG levels in the pancreatic vein under the saline infusion did not show any significant changes after the CaCl2 injection and were higher than those under the somatostatin infusion at all points. 4. Under the somatostatin infusion, 10-1 mg of glucagon did not induce any rise at all in IRI concentrations of the pancreatic vein. But when CaCl2 was given just before the glucagon administration, a slight but significant rise in IRI was observed.It is concluded that, in vivo, calcium has an insulin secretory effect under a normoglycemic state, and that somatostatin has an inhibitory action on both calcium- and cyclic-AMP-mediated insulin release.

Evanescent enlargement of salivary glands following tri-iodinated contrast media.

Three cases of acute and transient salivary gland enlargement after intravenous administration of sodium and methylglucamine diatrizoate as Renografin 60 are presented. The evanescent nature of the sialadenopathy is stressed.

Sulphur metabolism in sheep. I. Preliminary investigations on the movement of sulphur in the sheep's body

In a series of experiments with sheep maintained on high sulphur rations, measurements were made on the levels of 35S in urine, faeces, and various body fluids following single intravenous infusions of sodium [3%]sulphate and single infusions of sodium [35S]sulphate or sodium [353]sulphide into the gastrointestinal tract. Sulphide was rapidly absorbed from the duodenum and post-duodenal intestinal tract, an estimated 40–90% of the dose being absorbed within 60 min. Absorption of sulphate from the same region was much slower, 25% or less being absorbed over a 60-min interval. An attempt to use antibiotics to eliminate the effects of the intestinal bacteria on the metabolism of [35S]sulphate before absorption was not conclusive. Following intravenous administration of sodium [35S]sulphate, 12–19% of the dose was recovered in the faeces within 6 days. This activity appeared to be due to secretion into the post-ruminal tract rather than to return of 35S by salivary secretion or by passage across the rumen wall. Sodium [35S]sulphate was reduced to sulphide in the rumen and appreciable amounts appeared to be absorbed from this organ. The variations in total sulphur and sulphide of rumen digesta, urinary total sulphur, and blood inorganic sulphate levels during the day appeared to be related. Whole blood inorganic sulphate sulphur levels varied between 2 and 6 mg%. Urinary excretion following intravenous administration of 35S was extremely rapid, at least 70% of the dose being collected within 24 hr.

EFFECT OF INTESTINAL RESECTION ON BILE SALT ABSORPTION IN DOGS.

The efficiency of intestinal absorption of bile salts was evaluated by studying the rate of disappearance of radioactivity from the bile of dogs after the intravenous administration of sodium taurocholate-24-C14. Bile was sampled through an indwelling tube in the gall bladder. One day after a high-fat meal normal dogs retained 48% of the radioactivity; dogs with resection of the jejunum retained 48%, whereas those with resection of the ileum retained only 3% in the bile. This is consistent with previous observations that the ileum is the site of bile salt absorption in vitro and in anesthetized animals. Animals with resection of the ileum exhibited significant steatorrhea; however, three-fourths of the ingested fat was absorbed in spite of almost complete failure to absorb bile salts. This indicates that fat and bile salts are not normally absorbed together. Elimination of enterohepatic circulation of bile salts by resection of the ileum contributes to the observed steatorrhea.

Augmented Natriuretic Response to Acute Sodium Infusion Following Blood Pressure Elevation with Metaraminol in Normotensive Subjects.

Excerpt It is well-established that patients with essential hypertension have an exaggerated natriuresis in response to acute intravenous administration of sodium. While the mechanism for this rema...

Acute renal conservation of sodium in hypertension.

It is well established that patients with essential hypertension have an exaggerated natriuretic response to the rapid intravenous administration of sodium. 1-4 While the mechanisms responsible for the enhanced natriuresis of essential hypertension remain unknown, a defect in the renal tubular capacity to conserve sodium has been proposed as a possible explanation. 5 Most of the available literature relating to salt conservation in patients with hypertension is concerned with the response to chronic salt restriction. The experiments of Black 6 and Renwick 7 seem to offer conclusive proof that the hypertensive patient conserves sodium normally under these conditions. However, these chronic experiments may not be applicable to the problem of exaggerated natriuresis, because the latter occurs only in response to an acute stimulus for sodium excretion. The enhanced natriuretic response is a transient one and is followed by a rate of sodium excretion comparable to that of the normotensive subject.