Third-Day Oxygenation Index is an Excellent Predictor of Survival in Children Mechanically Ventilated for Acute Respiratory Distress Syndrome.

PURPOSE: The aim of this study was to assess the association between oxygenation index (OI) and outcome in children with acute respiratory distress syndrome (ARDS). PATIENTS AND METHODS: Patients (age, >30 days) in the pediatric intensive care unit from April 2011 to March 2016 with ARDS and who were mechanically ventilated were included. Patients were divided into two age groups: infants (<12month) and older children. Lowest PaO2/FiO2 and SpO2/FiO2 ratios and highest mean airway pressure (MAP) were recorded on the first day of ARDS and after 72 h. OI was calculated on the first and third days of mechanical ventilation (MV) and its association with OI (first and third days) and short-term mortality evaluated at 28 days. RESULTS: MV was initiated a mean of 2.3 days after admission (median, 1.0 day; maximum 14 days). The average MV duration for all patients was 11.8 (median, 7.0) days. Mean (95% confidence interval (CI)) OI values on the first day of MV were 14.17 (11.94-16.41), 12.72 (10.68-14.75), and 13.24 (11.73-14.74) for infants, older children, and all participants, respectively. In survivors (n=39) mean OI was 11.66 (9.64-13.68) compared with 15.22 (13.03-17.40) in non-survivors (n=31). Logistic regression analysis revealed that OI on day 3 had highly significant prognostic value for mortality (odds ratio, 256.5, 95% CI 27.1-2424, p<0.001), with an AUC of 0.919 (cut-off value, 17; positive predictive value, 0.905; negative predictive value, 0.964; p=0.0001). In contrast, OI on day 1 did not have significant prognostic value (AUC, 0.634; p=0.056) for short-term mortality. Different modes of MV were not significantly associated with outcome (p>0.05). CONCLUSION: OI is a simple, highly accurate, and sensitive predictor of the survival (short-term mortality) of children mechanically ventilated for ARDS.

Effects of subchronic methionine stimulation on oxidative status and morphological changes in the rat ileum.

This study was conducted to explore the effects of sulfur containing amino acids on redox status and morphological parameters in the rat ileum tissue. Male Wistar albino rats were randomly divided into the following groups: Group K (saline (1 ml/day, i.p.)), Group M (methionine (0.8 mmol/kg/day, i.p.)), Group C (methionine (0.8 mmol/kg/day) + L-cysteine (7 mg/kg/day), i.p.) and Group N (methionine (0.8 mmol/kg/day) + N-acetyl-L-cysteine (50 mg/kg/day), i.p.). Activities of antioxidant enzymes in the ileum were analyzed to profile oxidative status. Morphometric analysis included measurement of villus height (µm), tunica mucosa thickness (µm), tunica muscularis thickness (µm), the total thickness of the ileal wall (µm) and the number of cells in the lamina propria (per 0.1 mm2 of tissue). Results showed that methionine treatment reduced the activity of antioxidant enzymes (SOD, GPx, CAT) and the GSH content compared to the control group (p > 0.05). The application of methionine reduced the following parameters statistically significant compared to the control group: length of the ileal villi (p < 0.01), tunica mucosa thickness (p < 0.01), and ileal wall thickness (p < 0.01). We concluded that methionine induced the changes in the gut redox status, which implied oxidative stress occurrence. L-cysteine and N-acetyl-L-cysteine both exhibited antioxidant properties.

Suppression of methionine-induced colon injury of young rats by cysteine and N-acetyl-L-cysteine.

Changes in the methionine metabolism can cause a state called hyperhomocysteinemia, inducing oxidative stress in the gut. The production of free radicals is important in the colon damage caused by methionine. This study aimed at evaluating the effect of the use of L-cysteine and N-acetyl-L-cysteine on the colon morphometry of young rats treated with methionine. A total number of 32 male rats were distributed in a randomized experimental design in 4 groups: control group treated with saline; methionine group; cysteine + methionine group, and N-acetyl-L-cysteine + methionine group. After 21 days of treatment, rats were sacrificed and the colon samples were taken for histological and biochemical analysis. Methionine load increased depth of crypts, the lamina muscularis mucosae thickness, the mucosal height, and the number of cells in lamina propria (p < 0.01). Combination of methionine with L-cysteine (C group) and with N-acetyl-L-cysteine (N group) reversed methionine effects. Methionine treatment increased the GPx activity and MDA concentration, while L-cysteine and N-acetyl-L-cysteine increased the catalase activity compared to methionine group. It was concluded that the use of L-cysteine and N-acetyl-L-cysteine was beneficial to decrease intestinal mucosal height and oxidative damage when methionine was used in combination with them.

Overweight in trained subjects - are we looking at wrong numbers? (Body mass index compared with body fat percentage in estimating overweight in athletes.).

Body mass index (BMI) is widely used as an index of obesity in adults. In trained population, individual with low body fat could be classified as overweight by BMI. To evaluate this problem, the purposes of this study were to determine the BMI and body fat percentage (BF%) of trained and untrained subjects and to evaluate the accuracy of BMI classification (> or =25 kg.m(-2)) as a prediction of overweight/obesity in trained subjects. The total number of 299 trained (basketball players) and 179 untrained male subjects participated in this study. Body height and body mass were measured; BMI was calculated for all subjects. BF% was determined via Tanita bioimpedance body composition analyzer. BMI >or = 25 kg.m(-2) and BF% > 20% were used to define overweight. There was no significant age differences. Body mass, height (p < 0.01) and BMI (p < 0.05) were significantly higher, although BF% was significantly lower (p < 0.01) in trained group when compared to untrained. Eighty-five trained subjects had a BMI of 25 or higher, indicating overweight. Of these, only three individuls had excess BF%. The results of the present study suggest that a BMI > or = 25 kg.m(-2) is not an accurate predictor of overweight in trained subjects.

[Possible inhibitory effect of nitric oxide donor, dipropylenetriamine nonoate (DPTA/NO), on oxygen consumption of isolated rats' testis interstitial cells].

INTRODUCTION: The understanding of testicular physiology, pathology, and male fertility issues requires knowledge of male germ cell death, energy production and oxygen consumption. The aim of this study was to examine the effect of a new donor of exogenous nitric oxide, di-propylen-three amin-NONOate (DPTA/NO), on the oxygen consumption by freshly isolated rats' testis interstitial cells. MATERIAL AND METHODS: Rats' testis interstitial cells (ISC) were isolated according to Anakwe method and oxygen consumption was measured in an ex vivo bath. The ISC were stimulated with glutamate (0.5 M, 20 microl). DPTA (10(-3) - 10(-6) M) was added and its effect was tested in the absence of ADP (state 4 of respiration) and after that in the presence of ADP (state 3). The reaction was followed for 10 minutes and for each concentration the measurement was done in duplicate. The same measurements without treatment of DPTA/NO were done for control group. RESULTS: DPTA/NO (10(-4) - 10(-6) M) reduced the oxygen consumption rate compared with the control group. The inhibition of respiration was not noticed in concentration of 10(-3) M. In V3 respiratory phase, all tested concentrations of DPTA/NO (10(-3) - l0(-6) M) decreased the oxygen consumption rate in comparison with the control group. CONCLUSION: Our results demonstrate that a NO donor, DPTA/NO (10(-3) - 10(-6) M) inhibits oxygen consumption in isolated rat testis interstitial cells in a manner that could be concentration dependent. Because of limited number of measurements this was not fully proved and additional experiments are needed.

Dose-dependent anticonvulsive effect of ethanol on lindane-induced seizures in rats.

Chronic ethanol consumption is a major risk factor for epilepsy, and seizures frequently occur during the withdrawal period. The aim of our study was to investigate effects of ethanol on lindane-induced seizures in rats. Male Wistar rats were injected i.p. with one of the following 5 treatments: (i) saline, (ii) dimethylsulfoxide, (iii) lindane (8 mg/kg) (L), (iv) ethanol in doses of 0.5 g/kg (E(0.5)), 1 g/kg (E(1)), and 2 g/kg (E(2)), and (v) groups that received ethanol 30 min before lindane (LE(0.5), LE(1), and LE(2)). Behavioral changes were described by using a descriptive scale as follows: 0, no response; 1, head nodding, lower jaw twitching; 2, myoclonic body jerks, bilateral forelimb clonus; 3, generalized tonic-clonic convulsions; 4, status epilepticus. The incidence of convulsions in the LE(2) group was significantly lower than the incidence in the L (p < 0.01) and LE(0.5) groups (p < 0.05). The median grade of convulsive behavior was significantly lower in the LE(2) (p < 0.01) and LE(1) groups (p < 0.05) compared with the L group. Latencies to the first seizure response were not significantly different among groups. ED50 of ethanol was 1.40 (1.19-1.65). Our findings suggest that ethanol decreased severity and incidence of lindane-induced seizures in a dose-dependent manner.

Properties of thiamine transport in isolated perfused hearts of chronically alcoholic guinea pigs.

The aim of this study was to determine the mechanism of transport of (14)C-thiamine in the hearts of healthy (nonalcoholic) and chronically alcoholic guinea pigs. We used the single-pass, paired-tracer dilution method on isolated and retrogradely perfused guinea pig hearts. The maximal cellular uptake (U(max)) and total cellular uptake (U(tot)) of (14)C-thiamine were determined under control conditions and under influence of possible modifiers. We tested how the presence of unlabeled thiamine, metabolic inhibitors, or absence of sodium ions influence the transport of (14)C-thiamine. The results of our experiments show that the transport of (14)C-thiamine is specific and energy-dependent and that its properties are significantly changed under the influence of chronic alcoholism. The latter effect occurs by increase in both U(max) and U(tot), as a manifestation of a compensatory mechanism in thiamine deficiency.

[Distinguishing the athlete's heart syndrome from some pathological conditions].

The response of the body to vigorous physical activity is a multiorgan system phenomenon. As a result, the body undergoes profound morphologic and functional alterations, but as there are different kinds of physical activities, the degree of these changes is highly variable as well. Considering many sudden cardiac deaths in sport, it is needless to say how important it is to know where the border of normal changes of the body due to physical activity is and when these changes become unhealthy. Also it is very important to distinguish physiological changes of the body due to physical activity and pathological changes due to some cardiac diseases. In order to prevent sudden cardiac deaths in sport, it is very important to distinguish athletes heart syndrome and hypertrophic cardiomiopathy, dilatative cardiomiopathy, aritmogenic cardiomiopathy of the right ventricle and myocarditis. More frequent physical examinations of athletes are recommended.

[Causes of sudden cardiac death in athletes].

INTRODUCTION: Sudden cardiac death in athletes is a growing problem, despite the huge existing knowledge in medicine and sports. EFFECTS OF VIGOROUS PHYSICAL ACTIVITY: In response to vigorous physical activity, the body undergoes profound morphologic and functional changes. These changes are usually healthy, but sometimes may gravitate to some cardiac diseases. But still, most saudden cardiac deaths are due to previous unknown diseases. CAUSES OF SUDDEN CARDIAC DEATH: The most common cause of sudden cardiac death in athletes is hypertrophic cardiomyopathy. Other reasons are congenital coronary artery anomalies, nivocarditis, dilatative cardiomyopathy, arrhythmogenic cardiomyopathy of the right ventricle, sarcoidosis, mitral valve prolapse, aortic valve stenosis, atherosclerosis, long QT syndrome, and blunt impact to the chest. CONCLUSION: Bearing in mind the above mentioned, more frequent physical examinations of athletes are recommended.

[Electrophysiological characteristics of the athlete's heart].

INTRODUCTION: The athletic heart syndrome is characterized by morphological, functional and electrophysiological alterations as an adaptive response to vigorous physical activity. Athletes heart is predominantly associated with a programmed, intensive training. But as there are different kinds of physical activities, the degree of these changes is highly variable. ELECTROPHYSIOLOGICAL CHARACTERISTICS OF THE ATHLETE'S HEART: The response of the body to vigorous physical activity is a multiorgan system phenomenon. The integrated functioning of each of these organ systems is very important, but the cardiovascular system plays a critical role in mediating the activity. Because of that, most changes in the neurohumoral regulation predominantly affect the cardiovascular system. These changes include: depression of sympathetic activity and stimulation of parasympathetic activity, so electrophysiological characteristics of the athlete's heart must differ from the sedentary Although these facts, are well known, the athlete's heart is not a precisely defined concept. It is a gray zone between physiology, and pathology. CONCLUSION: Considering the number of sudden cardiac deaths in athletes, it is needless to say how important it is to distinguish physiological changes of the heart due to physical activity, and pathological changes due to some cardiac diseases.

[Athlete's heart syndrome].

Performing vigorous physical activity means a multiorgan system engagement, but the cardiovascular system plays a critical role. In order to provide enough oxygen to activate muscles during repeated physical activity of high intensity, the heart undergoes profound morphologic, functional and electrophysiological alterations, which have been identified as the "athlete's heart syndrome". "The athlete's heart" is a complex, but not precisely defined concept, anatomically and functionally and in relation to health and disease. It means the whole heart enlargement and/or hypertrophy of the cardiac muscle, also increasing economy of cardiac performance at rest and during physical activity with higher maximal functional capacities, all that having an adaptive response to vigorous physical activity. For morphological changes called the "athlete's heart, full-time, programed and intensive physical activity at maximal levels is primarily responsible. But as there are different kinds of physical activities, the degree of those morphological changes is highly variable. Considering many sudden cardiac deaths in sports, it is needless to say how important it is to know where the borderline is between normal changes of the heart due to physical activity and pathological changes due to some cardiac diseases. As sport has a growing socio-economic significance, sudden cardiac death events have to be reduced.

[Labor pain--physiologal basis and regulatory mechanisms].

Clinically, labor (visceral) pain is extremely prevalent in general population, yet its mechanisms have been poorly understood. With development of new electrophysiological techniques and molecular biology technologies, our understanding of physiological bases of labor pain has been markedly improved; in that way possibilities for therapeutic modulation of labor pain are expanded. The aim of this study was to describe the new insight into this topic. In this paper, the theory was exposed that the reason for labor pain had been found in sensitization at the levels of the uterus, dorsal root neurones and phychologic factors. Peripheral sensitization occurs due to cervical inflammatory reaction, associated with cervical ripening and remodeling. Chemical inflammatory mediators (notably prostaglandins, cytokines, granulocytes, enzymes such as metalloproteinases, integrines) activate nociceptive nerve fibers. Nociceptive threshold is reduced (resulting in primary hyperalgesia) and because of that there occurs the total number of action potentials generated and propagated by nociceptive peripheral nerves (visceral hypersensitivity). Central sensitization arises due to phosphorylation of N-methyl-D-aspartate (NMDA) receptors of dorsal root neurones. Numerous receptors, ion channels and signaling molecules, which, together with opioid peptides participate in spinal pain control, represent, at the level of central sensitization, possible therapeutic goals for labor pain modulation. Some of them are: DREAM which constitututively suppresses transcription of mRNA for opioid peptides, oncostatin M, COX-2 inhibitors, cFOS protein, tachykinins, gamma-butyric acid agonist, L-type Ca++ channels. Fear, as one of the most frequent phychologic factors, does (not) provide good control in transmision of pain sensitization by descendent nerve fibers. Some of the candidates for objective pain marker are also described. This article outlines the factors that, based on the contemporary viewpoint, could reduce transmission of pain signals, and thus broaden therapeutic possibilities for modulation of labor pain.

[The incidence of sudden cardiac death in athletes].

INTRODUCTION: Despite remarkable advances in medicine and sports, sudden cardiac death remains a significant problem. INCIDENCE OF SUDDEN CARDIAC DEATH: The incidence of sudden cardiac death varies in different studies and there are no systematic data about it. It varies in different types of sports, with age and sex. SUDDEN CARDIAC DEATH AND PHYSICAL ACTIVITY: Many changes in cardiac morphology and function represent an adaptive response to physical activity. As a result, the heart undergoes profound morphologic, functional and electrophysiological alterations. But as there are different kinds of physical activities, the degree of these morphological changes is highly variable. It is needless to say how important it is to know which changes in the heart due to physical activity are normal, and when they are pathological. Considering the results of many studies, the main cause of sudden cardiac death is hypertrophic cardiomiopathy. CONCLUSION It is very important to distinguish physiological changes of the heart due to physical activity, and pathological changes due to some cardiac diseases. That is why, clear recommendations on intensity, type, duration and frequency of physical training in every sports discipline are necessary. That is the only way to decrease the incidence of sudden cardiac death in athletes.