Effects of magnesium sulfate on spinal cord tissue lactate and malondialdehyde levels after spinal cord trauma.

OBJECTIVE: In the present study, the effects of magnesium sulfate (MgSO4) on tissue lactate and malondialdehyde (MDA) levels after spinal cord trauma (SCT) in rabbits were studied. SUBJECTS: Thirty New Zeland rabbits. Interventions. The rabbits were divided equally into three groups: group I was the sham- operated group, group II suffered from SCT but received no treatment, group III was given a dose of 100 mg/kg of magnesium sulfate intravenously at 5th minute after SCT. MEASUREMENTS. The lactate and MDA levels were measured in contused spinal cord tissue at 60 minutes after SCT. There was a significant increase of lactate and MDA levels in group II (p < 0.05) when compared with groups I and III, and a significant increase in the level of MDA in group III compared with group I, and also a significant decrease compared with group II, which was the trauma group without treatment (p < 0.05). CONCLUSION: The findings of this study showed that magnesium sulfate can attenuate the increase of tissue MDA and supply a normalization of lactate levels following SCT which may be related to the neuroprotective effects of (MgSO4).

Effects of magnesium sulfate on tissue lactate and malondialdehyde levels in experimental head trauma.

OBJECTIVE: To determine the effects of magnesium sulfate (MgSO4) on tissue lactate and malondialdehyde (MDA) levels in rabbit brain after experimental head trauma. DESIGN: Prospective, randomized trial. SUBJECTS: Thirty New Zealand rabbits. INTERVENTIONS: Group 1 (n = 10) was the sham operated group. Group 2 (n = 10) (untreated group) and group 3 (n = 10) received head trauma with the weight drop method. MgSO4 was administered 100 mg/kg (15 %) i. v. immediately after the head trauma to group 3. Trauma was applied to one side. The non-contused side was named as "a" and the contused side as "b". MEASUREMENTS: One hour after trauma, brain cortices were resected and the concentrations of lactate and MDA were determined using the spectrophotometric enzymatic and thiobarbituric acid methods. One-way ANOVA and Tukey's HSD tests were used for the evaluation of the results. P < 0.05 was considered as significant. Pearson's correlation test was used between lactate and MDA levels (P < 0.001). RESULTS: There were significant differences between MDA and lactate levels of group 1 and all other groups; non-contused (a) and contused (b) sides of groups 2 and 3; groups 2b-3a, 2b-3b (P < 0.05). The difference in MDA levels was significant between groups 2a-3b (P < 0.05). Correlation between lactate and MDA was very good in group 1, and excellent in groups 2a, 2b, 3a, and 3b. CONCLUSIONS: These results demonstrate that head trauma leads to an increase in brain tissue lactate and MDA levels, and MgSO4 suppresses the rise in contused tissue when given after head trauma.

Effects of deferoxamine on tissue lactate and malondialdehyde levels in cerebral ischemia.

In the present study, the effects of deferoxamine on tissue lactate and malondialdehyde (MDA) levels after cerebral ischemia in rabbits was studied. Rabbits were divided equally into three groups: group 1: sham-operated group; group 2: cerebral ischemia produced by clamping bilateral common carotid arteries for 60 min; and group 3: deferoxamine 100 mg/kg i.v. administered within 5 min after opening the clamps. EEG recordings were obtained in all groups before clamping and in group 2 and 3 60 min after clamping and 60 min after opening the clamps. One hour after opening the clamps and taking EEG recordings, brain cortices were resected and the concentrations of lactate and MDA were determined using the spectrophotometric enzymatic and thiobarbituric acid methods, respectively. There were significant differences between group 1 and the other groups in MDA and lactate levels (p < 0.05). There were no significant differences in lactate levels between groups 2 and 3. Preischemic EEG grades were the same in all groups. Preischemic and postischemic EEG values were significantly different (p < 0.05), but there were no significant differences between postischemic EEG grades in groups 2 and 3. There was also a correlation between postischemic EEG grades and lactate levels, but no correlation between postischemic EEG grades and MDA levels. These results demonstrate that cerebral ischemia leads to an increase in brain tissue lactate and MDA levels and deferoxamine suppresses the increase of MDA, but not lactate. Deferoxamine treatment caused no significant EEG changes. EEG grades correlated well with lactate levels.

Effects of nitric oxide synthase inhibition on intestinal damage in rats with experimental necrotizing enterocolitis.

In the inflamed intestinal mucosa of necrotizing enterocolitis (NEC), nitric oxide (NO) generated by inducible nitric oxide synthase (iNOS) may contribute to the pathogenesis of local intestinal damage. To study the importance of iNOS for the pathogenesis of NEC, the effects of selective (aminoguanidine, AG) and nonselective (L-nitroarginine methyl ester, L-NAME) iNOS inhibitors on intestinal morphologic changes were assessed in neonatal rats with experimental NEC. The neonatal rats were randomized into one of the five treatment groups. The control group consisted of rats that were breast-fed. The NEC group, consisting of neonates separated from their mothers, were gavaged with a special rodent formula to produce NEC. Rats in the sham, the AG, and the L-NAME groups were gavaged in a similar fashion to those in the NEC group; in addition, they were treated with 0.9 % saline, 10 mg/kg/day AG, and 10 mg/kg/day L-NAME, respectively. The rats were sacrificed on day 4, and the last 4 cm of terminal ileum was harvested for morphological studies and detection of nitrite and nitrate levels in tissue. The animals in the NEC and sham groups showed various degrees of intestinal inflammatory changes and increased tissue levels of nitrite and nitrate compared to those in the control group. Both AG and L-NAME treatment decreased the tissue levels of these nitrogen oxides, but the inflammatory changes of the intestine appeared to be attenuated only in the AG treated animals. L-NAME treatment did not improve the intestinal damage and increased mortality. These results may indicate that NO synthesized by iNOS plays a pathogenic role in formula-fed induced NEC and that inhibition of iNOS improves intestinal inflammatory damage.

Serum cardiac troponin-I in active rheumatic carditis.

OBJECTIVE: The study was performed to investigate the level of serum cardiac troponin I (cTnI), a specific marker for myocardial cell damage, in the acute rheumatic carditis (RC). METHODS: Twenty seven consecutive patients with acute RC and 23 healthy children were enrolled. RESULT: cTnI level in both groups showed no statistical difference (p > 0.05). CONCLUSION: Serum cTnI level did not gain clinical use.

[Serum and tissue silver levels after burns treated with silver compounds]. / Niveaux d'argent du sérum sanguin et du tissu après brûlure traitée par les compositions à l'argent.

This study was performed in order to investigate serum and tissue silver levels in burns which were used 10 percent silver nitrate as a topical agent. We formed four groups of animals and pulverized 10 percent silver nitrate solution to the first group (GI) that included ten rabbits of which backs were burned by boiling water and silver sulphadiazine cream to second group (GII) with nine rabbits. We carried out 10 percent silver nitrate solution to the first control group (GIII) and silver sulphadiazine cream to the second control group (GIV) each of which had seven animals with unburned skin. We obtained blood samples from every animal before and after application of topical agent on the 1st, 3rd, 7th, 15th, 21st and 28th. We determined serum and tissue silver levels by atomic absorption spectrophotometer in kidney and liver of the animals which were sacrificed on the 28th day. In first and second groups we found that serum silver values reached on 3rd day to the maximum level and then the values decreased gradually. We also determined that diminution of the serum silver levels were prominent following on 15th day. It was shown that there was no silver in the serum on 28th day except four animals. The silver deposition in the liver was much more than in the kidney. Between these two groups there was significant difference neither in the serum on the same days nor the tissue silver levels. According to these data it was concluded that serum and tissue silver levels with 10 percent silver nitrate used in burns produced no difference from that of 1 percent silver sulphadiazine cream.

Effectiveness of corticosteroids in otitis media with effusion: an experimental study.

OBJECTIVE: The aim of the present study was to investigate the dose-related effectiveness of corticosteroids in the management of otitis media with effusion, by using the objective assessment techniques of tympanometry and cytokine measurement. MATERIALS AND METHODS: The eustachian tubes of 42 male rats were obstructed. Thirty-six subjects with effusion were randomly divided into three equal groups: controls; 0.5 mg/kg/day corticosteroid; and 1 mg/kg/day corticosteroid. Concentrations of interleukin-1beta and tumour necrosis factor alpha in the middle-ear effusions were analysed using enzyme-linked immunosorbent assay. RESULTS: An effusion occurred on the 14th post-operative day and was present on the 30th post-operative day in the control group. Otomicroscopic examination and tympanometric measurement showed an improvement in the intervention groups. There was a significant difference between both intervention groups and the control group for both interleukin-1beta and tumour necrosis factor alpha concentrations (p 0.05). CONCLUSION: The study confirmed a short term beneficial effect of systemic steroids on resolution of otitis media with effusion in a rat model. Our results support the theory that corticosteroids significantly decrease concentrations of both interleukin-1beta and tumour necrosis factor alpha. In our model, the 0.5 mg/kg corticosteroid dose was as effective as the 1 mg/kg corticosteroid dose. Further studies should be carried out to determine the optimal dose and duration of corticosteroids in the treatment of otitis media with effusion.

Effect of gamma-hydroxybutyric acid on tissue Na+,K- ATPase levels after experimental head trauma.

BACKGROUND: A failure of the Na(+),K(+)-ATPase activity (which is essential for ion flux across the cell membranes) occurs in many pathological conditions and may lead to cell dysfunction or even cell death. By altering the concentration of specific opioid peptides, gamma-hydroxybutyric acid (GHB) may change ion flux across cell membranes and produce the 'channel arrest' which we assumed will inhibit the failure of Na+,K(+)-ATPase activity and therefore lead to energy conservation and cell protection. Therefore we planned this study to see the effects of GHB at two different doses on Na(+),K(+)-ATPase activity in an experimental head trauma model. METHODS: Forty New Zealand rabbits were divided equally into four groups: group I was the sham-operated group, group II (untreated group), group III received head trauma and intravenous (i.v.) 500 mg/kg GHB and group IV received head trauma and i.v. 50 mg/kg GHB. Head trauma was delivered by performing a craniectomy over the right hemisphere and dropping a weight of 10 g from a height of 80 cm. The non-traumatized (left) side was named as 'a' and the traumatized (right) side as 'b'. One hour after the trauma in groups II and III and craniotomy in group I, brain cortices were resected from both sides and in group I only from the right side was the tissue Na-K-ATPase activity determined. RESULTS: The mean +/- SD of Na(+),K(+)-ATPase levels of each group are as follows: group I - 5.97 +/- 0.55; group IIa - 3.90 +/- 1.08; group IIb - 3.58 +/- 0.90; group IIIa - 5.53 +/- 0.60; group IIIb - 5.33 +/- 0.88; group IVa - 5.05 +/- 0.72; group IVb - 4.93 +/- 0.67. The Na(+),K(+)-ATPase levels of group IIa, IIb, IVa and IVb were significantly different from group S (P < 0.05). There were also significant differences between group IIa and groups IIIa and IVa; group IIb and groups IIIb and IVb (P < 0.05). CONCLUSIONS: We conclude that GHB is effective in suppressing the decrease in Na(+),K(+)-ATPase levels in brain tissue at two different dose schedules after head trauma.

Effect of 1,25 (OH)2D3 treatment on glucose intolerance in uraemia.

The aim of this study was to evaluate the effect of calcitriol treatment on glucose intolerance in uraemia. Thirty one patients on haemodialysis who had never been treated with vitamin D or related drugs, and 12 healthy control subjects with normal renal functions were studied. Uraemic patients were randomly divided into two groups; 16 patients were treated with oral calcitriol (0.5 micrograms/day) for 8 weeks, and 15 uraemic patients and 12 healthy subjects were given a placebo. In all these cases, before and 8 weeks after treatment, baseline serum glucose, insulin, calcium, parathormone (PTH), and 1,25 (OH)2D3 were measured. After an oral load of 75 g glucose, blood glucose and insulin were determined at 30, 60, 90, and 120 min. The same measurements were repeated after 8 weeks. HbA1c and fructosamine were also measured at 0 and 8 weeks. Baseline serum insulin was significantly elevated after calcitriol treatment (7.81 versus 11.63 microIU/ml) there was also a significant increase in insulin following calcitriol treatment at 30, 60, 90, and 120 min. On the other hand, glycosylated haemoglobin (HbA1c) and fructosamine decreased after calcitriol treatment (HbA1c 7.09% versus 5.22% P < 0.01 and fructosamine 2.92 versus 2.50 mmol/l P < 0.01). Blood glucose significantly decreased after calcitriol treatment at 0, 30, 60, 90, and 120 min. In the other two groups there were no significant changes in any parameters. These results seem to confirm that vitamin D influences pancreatic beta (beta) cell secretion and suggest that calcitriol may improve glucose intolerance in uraemic haemodialysis patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of oral glucose loading on serum gastrin level in pregnant and non-pregnant women.

AIM: To evaluate the relationship between the changes in gastrin and insulin serum concentrations after oral glucose loading in pregnant and non-pregnant women. METHODS: Thirty women, 12 pregnant and 18 non-pregnant, with normal fasting glucose values were included in the study. Serum concentrations of gastrin, glucose, insulin, and glucagon were analyzed at 0 (t1), 30 (t2) and 60 (t3) minutes after 75 g oral glucose loading. Gastrin, insulin, and glucagon levels were determined by means of radioimmunoassay kits. RESULTS: Serum gastrin concentration in pregnant women increased insignificantly (gastrin median values 57.91, 70.62, and 68.70 for t1, t2, and t3, respectively; Friedman's test, p = 0.264). In non-pregnant women gastrin levels insignificantly increased from t1 to t2, but reduced significantly from t2 to t3 (gastrin median values 62.91, 86.92, and 62.25 for t1, t2 and t3, respectively; Bonferroni adjusted Wilcoxon test, p = 0.002). Unlike in pregnant women, the changes in gastrin release in non-pregnant women were associated with changes in blood glucose concentrations at t2 and t3, which were induced by oral glucose loading. Glucose median values were 7.48 and 6.43 for t2 and t3, respectively. The insulin release due to the oral glucose loading markedly increased at t2 and t3 (Friedman's test, p < 0.001), whereas glucagon release decreased irrespective of pregnancy. CONCLUSION: Changes in blood glucose concentrations induced by oral glucose loading could influence gastrin release, especially in non-pregnant women. Changes in insulin and glucagon levels induced by oral glucose loading, particularly after 60 minutes, could not be associated with changes in gastrin release.

Effects of deferoxamine on tissue superoxide dismutase and glutathione peroxidase levels in experimental head trauma.

BACKGROUND: This study aims to evaluate the effects of deferoxamine on tissue superoxide dismutase (SOD) and glutathione peroxidase (GPx) brain levels after head trauma. METHODS: Thirty rabbits were divided equally into three groups: group 1 was the sham-operated group, group 2 suffered head trauma (no treatment was given), and group 3 received deferoxamine 50 mg/kg after the trauma. Head trauma was applied unilaterally. One hour after trauma, brain cortices were resected and SOD and GPx levels were determined. One-way analysis of variance and Tukey-HSD tests were used for analysis. Significance was defined as p < 0.05. RESULTS: Baseline SOD levels are preserved in the traumatized side of the deferoxamine-treated group. Although GPx level of the traumatized side of the deferoxamine-treated group decreased significantly, the decrease was significantly less than the nontreated group. CONCLUSION: Trauma leads to a decrease in brain tissue SOD and GPx levels. Deferoxamine suppresses this decrease completely in SOD level and partially in GPx level when given after trauma.

Effects of magnesium sulfate on tissue lactate and malondialdehyde levels after cerebral ischemia.

In the present study, the effects of magnesium sulfate on tissue lactate and malondialdehyde (MDA) levels after cerebral ischemia in rabbits were studied. The rabbits were divided equally into three groups. Group 1 (n = 8) was the sham-operated control group, in group 2 (n = 8) only cerebral ischemia was induced by clamping bilaterally the common carotid arteries for 60 min, and in group 3 (n = 8) magnesium sulfate was administered at a dose of 100 mg/kg i.v. within 5 min after opening the clamps. In group 1 EEG recordings were obtained immediately and 60 and 120 min after craniectomy. In groups 2 and 3 EEG recordings were obtained immediately after craniectomy but before clamping and 60 min after clamping. One hour after opening the clamps and taking EEG recordings, brain cortices were resected, and the concentrations of lactate and MDA were determined using spectrophotometric/enzymatic and thiobarbituric acid methods, respectively. In all groups, there were significant differences between MDA and lactate levels (p < 0.05). There were no significant differences in lactate levels between groups 2 and 3 (p > 0.05), and also the preischemic EEG grades were the same in all groups. Preischemic and postischemic EEG values were significantly different (p < 0.05), and there were also significant differences between postischemic EEG grades in groups 2 and 3 (p < 0.05). There was a correlation between postischemic EEG grades and MDA and lactate levels. These results demonstrate that cerebral ischemia-reperfusion injury leads to an increase in brain tissue lactate and MDA levels, that magnesium sulfate suppresses the increase of MDA and lactate concentrations, and that magnesium sulfate treatment improves the EEG changes. The EEG grades correlated well with MDA and lactate levels.