BNP shows myocardial injury earlier than Troponin-I in experimental carbon monoxide poisoning.

OBJECTIVE: In this study, our purpose was to determine whether plasma BNP level can be useful or not in determining the severity of myocardial injury formed by CO poisoning and to compare plasma BNP level with serum cTnI level. MATERIALS AND METHODS: In the study, 46 female Wistar Albino rats were used. Rats were divided into four groups, one control group and three poisoning groups. The mixture of pure CO and air was injected for 60 minutes to provide 3000 ppm CO concentration. Blood samples of groups were collected to measure COHb, BNP and cTnI levels. Blood samples of poisoning groups were collected at the 1st, 6th and 12th hours after poisoning. After biochemical procedures, findings were analysed statistically and compared with each other. RESULTS: Eight rats which died in poisoning groups were excluded and 38 rats were evaluated. BNP levels were high in all poisoning groups compared to control group and the difference between them was statistically significant (p < 0.05). cTnI levels were high in 6th and 12th hours poisoning groups compared to control and 1st hour group but only 12th hour group had statistically significant difference (p < 0.05). A statistically positive relation was established between BNP and cTnI levels in 6th and 12th hour groups (R: 0.76 - p < 0.05 - n:38). CONCLUSIONS: It was found that BNP levels increased earlier than cTnI levels in acute severe CO poisoning. BNP levels of the cases which were determined to have increased cTnI levels showing myocardial injury increased as well. BNP can show myocardial injury and its severity in acute CO poisoning.

Is the Behcet's disease a risk factor for osteoporosis and is relation to cytokines?

BACKGROUND AND OBJECTIVES: To determine if the Behcet's disease poses a risk for a lower bone mineral density (BMD), and the relation to cytokines. Behcet's disease is a complex, multisystemic, chronic inflammatory disorder. METHODS: This study was carried out on 60 patients and 24 sex- and age-matched healthy controls. Serum osteocalcin (OK) and bone specific alkaline phosphatase (BALP), which are bone formation markers and urine deoxipyridinolin (DOP) levels that is bone resorption marker were evaluated in patient and controls groups. Serum IL-1 and TNF-alpha levels were measured in both groups. BMD was measured with dual X-ray absorptiometry (DEXA) at the lumbar spine and left femur. RESULTS: There were no significant differences in OK and DOP levels between BD and control groups. BALP levels were significantly higher in BD than control groups (p = 0.002). Although there were no statistically significant differences in IL-1 levels between BD and control groups, TNF-alpha levels were significantly higher in BD than control groups. There were significant differences in BMD values of lumbar spine (p < 0.05). No significant differences in BMD values of the left femur were detected in the groups (p > 0.05). CONCLUSIONS: Behcet's disease can be a risk for osteoporosis especially in the lumbar spine. We determined a negative correlation between IL-1 and femur neck BMD (Tab. 4, Fig. 2, Ref. 23).

The association of serum total sialic acid/total protein ratio with diabetic parameters in young type 1 diabetic patients.

Sialic acid is a terminal component of the non-reducing end of carbohydrate chains of glycoproteins and glycolipids. The purpose of this study was to estimate serum total sialic acid (TSA) concentrations and serum TSA/serum total protein (TP) ratios in young type 1 diabetic subjects and to investigate their association with diabetes-related parameters in that population. Twentyfour young type 1 diabetic patients and 20 healthy controls were enrolled in this study. Serum TSA and serum TSA/TP ratio were measured in both groups. Moreover, we looked for correlation among serum TSA, serum TSA/TP ratio and clinically relevant parameters such as urinary albumin excretion, blood pressure, diabetes duration, HbA1c, daily insulin dose, serum lipids and magnesium in type 1 diabetic patients. Serum TSA concentrations and serum TSA/TP ratio showed no statistical difference between patients and controls (p>0.05). While serum TSA concentrations only correlated with urinary albumin excretion (r=0.44, p=0.028), serum TSA/TP ratio correlated with diastolic blood pressure (r=0.48, p=0.015), diabetes duration (r=0.46, p=0.022) and urinary albumin excretion (r=0.53, p=0.007) in the diabetic subjects. We concluded that serum TSA/TP ratio might be a better indicator than serum TSA as an index of diabetic complications.

Effect of interleukin-10 on pancreatic damage caused by organophosphate poisoning.

Organophosphate poisoning is a common cause of severe morbidity and mortality in emergency departments. Acute pancreatitis is a frequently reported consequence of organophosphate poisoning, but preventing this potentially severe complication has not been the subject of much research. We tested whether interleukin-10, a cytoprotective agent, could prevent or diminish pathological signs of acute pancreatitis caused by organophosphate poisoning. Thirty rats were divided into three equal groups. Group 1 did not receive any agent during the experiment. Group 2 received 0.8 g/kg fenthion intraperitoneally, followed by 6 ml/kg intraperitoneal normal saline 30 min and 3 h later. Group 3 received 0.8 g/kg fenthion intraperitoneally, followed by 2 microg/kg of interleukin-10 intraperitoneally 30 min and 3 h later. All rats underwent laparotomy and thoracotomy while still under anesthesia at 6 h, and tissue samples were obtained from the pancreas. After blood samples were taken by cardiac puncture, the animals were sacrificed. Organophosphate poisoning resulted in significant elevations of serum amylase and glucose. Interleukin-10 significantly reduced pancreatic damage as determined by pathologic scoring, but not by enzyme elevations. Interleukin-10 should be considered for larger studies in other animal models to confirm its ability to decrease pancreatic damage after organophosphate poisoning treatment with interleukin-10.

Promotion of fracture healing by vitamin E in rats.

We investigated the effects of the antioxidant alphae-tocopherol on early- and late-phase fracture healing in a rat model. Sixty male Sprague-Dawley rats were randomized into two groups. The right tibia of each rat was fractured manually under anaesthesia, and fracture sites fixed with intramedullary Kirschner wires. The alpha-tocopherol group received 20 mg/kg alpha-tocopherol intraperitoneally; the control group received intraperitoneal saline injections. Ten rats from each group were sacrificed on day 15, day 45 and day 60. In the alpha-tocopherol group, malondialdehyde concentrations, a measure of lipid peroxidation associated with oxygen free radicals, were significantly decreased on day 15 and day 45 compared with the control group, but had regained the 15-day value on day 60. On histopathological and radiological assessment, fracture healing on day 60 was significantly more advanced in the alpha-tocopherol group. We conclude that alpha-tocopherol has a positive effect on both early and late-phase fracture healing, and may be beneficial in clinical fracture

Portosystemic shunt prevents apoptosis in rat intestinal mucosa caused by total hepatic ischemia.

BACKGROUND: Prolonged splanchnic congestion due to total hepatic ischemia (THI) has been shown to induce damage to the intestinal mucosa. The present study was conducted to examine whether the protective effect of portosystemic shunt (PSS) can be seen on apoptosis of intestinal mucosa in a rat model of THI. METHODS: Adult male Wistar rats were divided into the following 3 groups: control group; the THI group underwent THI for 30 min, and the PSS group was subjected to THI for 30 min with PSS. Rats were killed after 1, 2, and 6 h of reperfusion. For each time point, levels of serum liver enzymes, intestinal morphology, malondialdehyde (MDA) contents and DNA fragmentation in intestinal tissue were determined. In addition, the 7-day survival rate was measured. RESULTS: The 7-day survival rate of THI group remained at 50%, whereas that of PSS group was significantly higher at 90% (p < 0.01). Serum AST and ALT levels of the THI and PSS groups rapidly increased after reperfusion, reaching peak values at 2 h. MDA levels after 1 and 2 h of reperfusion in the THI group were significantly increased as compared with the control group (p < 0.001). Increases in the percentage of fragmented DNA peaked 1 h after reperfusion in the THI group. PSS resulted in the reduction of DNA fragmentation and preserved the macroscopic and microscopic appearance of the intestinal mucosa. CONCLUSIONS: Splanchnic congestion due to portal occlusion increased apoptosis in the rat intestinal mucosa. PSS is very effective in counteracting the principal negative effects of total hepatic ischemia.

The effects of dimethylsulfoxide in experimental obstructive jaundice.

MATERIAL AND METHODS: Thirty rats were divided into three groups, as sham, control and DMSO groups. Laparatomy was performed on each animal in the control and DMSO groups and common bile ducts were ligated. Common bile duct was observed but was not ligated for the rats in the sham group. Saline solution injection (1.5 mg/kg/intraperitoneally (i.p.)) was begun on the first day of surgical procedure and repeated once a day for the next 5 days. The same procedure was performed with DMSO (1.5 mg/kg/i.p.) instead of saline in the DMSO group. The rats were sacrificed on the postoperative seventh day, at which time venous blood and liver tissue specimens were taken. MAIN OUTCOME MEASUREMENTS: On the 7th postoperative day, the bilirubin, AST, ALT, ALP and GGT levels of the control and DMSO groups were significantly higher in comparison with the sham group (p < 0.01). On the 7th postoperative day, the erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels of the control and DMSO groups were significantly lower than those of the sham group (p < 0.01), but there was no statistical difference between the two groups (p > 0.05). Erythrocyte and liver malondialdehyde (MDA) levels in the control and DMSO groups were significantly higher compared with the sham group (p < 0.01). However, the MDA levels were significantly lower in the DMSO group compared to the control group (p < 0.01). CONCLUSION: It is stated that free oxygen radicals seem to play a role in the liver tissue injury, secondary to obstructive jaundice. In our experimental study, exogenic DMSO seems to have decreased lipid peroxidation and to have improved some of the parameters of liver tissue injury due to the obstructive jaundice in rats.

Role of granulocyte-macrophage colony-stimulating factor on apoptosis induced by ischemia-reperfusion in the intestinal epithelium.

BACKGROUND: To evaluate the effect of granulocyte-macrophage colony-stimulating factor (GM-CSF) on ischemia-reperfusion-induced apoptosis in the intestinal epithelium. METHODS: In this study, 50 male Wistar albino rats were used. After midline laparotomy superior mesenteric artery (SMA) was identified only in the sham group, while 60 min of ischemia and 2 h of reperfusion were performed in the control group. In the treatment groups, after 15, 30 and 60 min of ischemia, respectively, 1 microg/kg GM-CSF was administered subcutaneously, followed by 2 h of reperfusion. Malondialdehyde (MDA), campothecin (CAM), an indicator of DNA fragmentation, and histopathology were evaluated in the intestinal mucosa. RESULTS: Tissue MDA levels were found significantly high in all groups at various times of ischemia and 2 h of reperfusion compared with the sham group (p < 0.001). Administration of GM-CSF following 60 min of ischemia caused a significant increase in the MDA levels compared with the control group (6430 +/- 725 vs. 4174 +/- 565 nmol/g protein for jejunum. 7576 +/- 618 vs. 4938 +/- 809 nmol/g protein for ileum, p < 0.05). Intestinal ischemia and reperfusion resulted in a significant increase in tissue CAM levels (p < 0.05). The highest CAM value was found in the group in which 60 min of ischemia and 2 h of reperfusion were performed (50 +/- 3.2 ng/ml for jejunum, 52.8 +/- 2.7 ng/mg for ileum). Compared with the control group, GM-CSF administration following 1 h of ischemia aggravated the tissue injury. CONCLUSIONS: Apoptosis was induced in the small intestine by ischemia-reperfusion. GM-CSF increased the apoptosis of intestinal epithelial cells and exacerbated mucosal injury due to ischemia-reperfusion.

Role of oxygen free radical scavengers in acute renal failure complicating obstructive jaundice.

Obstructive jaundice is associated with high morbidity and mortality. Major complications such as pulmonary dysfunction, renal failure and sepsis are frequently encountered. Recent studies and observations suggest that the free oxygen radicals (FORs) produced in obstructive jaundice may play a significant role in the etiopathogenesis of acute renal failure (ARF). Thirty rats were divided into three groups, as sham, control and treatment groups containing 10 rats each. Laparatomy was performed on each animal in the control and treatment groups and common bile ducts were ligated. Common bile duct was observed but was not ligated for the rats in the sham group. Saline solution injection was begun on the first day of surgical procedure and repeated once a day during the following 5 days. The same procedure was performed with oxygen radical scavenger dimethyl sulfoxide (1.5 mg/kg/day i.p.) instead of saline in the treatment group. The rats were sacrificed on the 7th postoperative day. On the 7th postoperative day, the bilirubin, urea and creatinine levels of the control and treatment groups were significantly higher in comparison with the sham group (p < 0.01). Although there was no statistically significant difference between the bilirubin levels of the control and treatment groups (p > 0.05), the urea and creatinine levels in the treatment group were significantly lower (p < 0.01). On the 7th postoperative day, the erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels of the control and treatment groups were significantly lower than those of the sham group (p < 0.01), whereas renal and erythrocyte malondialdehyde (MDA) levels were significantly higher (p < 0.01). Although SOD and GSH-Px levels did not differ significantly between the treatment and control groups (p > 0.05), renal and erythrocyte MDA levels of the treatment group were significantly lower than those of the control group (p < 0.01). The histopathological scores were significantly higher in the control and treatment groups (p < 0.01); there was no significant difference between the control and treatment groups (p > 0.05). FORs seem to play a significant role in the etiopathogenesis of renal failure in obstructive jaundice. Antioxidant treatment may decrease oxidative damage due to FORs and may prevent renal failure.

Evaluation of contralateral testicular damage after unilateral testicular torsion by serum inhibin B levels.

BACKGROUND/PURPOSE: It is still controversial whether unilateral testicular torsion (TT) affects contralateral testis. The authors wanted to evaluate contralateral testicular damage in a rat model by the serum inhibin B levels, which is suggested as a marker of Sertoli cell function and spermatogenesis. METHODS: Fifty peripubertal male Wistar Albino rats were divided into 5 groups each containing 10 rats. Surgery was conducted under intraperitoneal 1-shot ketamine (50 mg/kg) anesthesia. Torsion-detorsion, torsion-detorsion-orchiectomies, orchiectomies, and sham operations were performed on the right testicle through a midline incision. Torsions were created by rotating the right testes 720 degrees in a clockwise direction and maintained by fixing the testes to the scrotum with a silk suture. Torsion duration was 4 hours. After each surgical intervention the incisions were closed. In group 1, 3-mL blood samples were taken to determine basal values of inhibin B in serum, and bilateral orchiectomies were performed. In group 2, 4 hours of torsion and detorsion was created and 1 month later, 3-mL blood samples were taken, and bilateral orchiectomies were performed. In group 3, 4 hours of torsion-4 hours of detorsion was created, and right orchiectomies were performed and 1 month later, 3-mL blood samples were taken and contralateral orchiectomies were added. In group 4, unilateral orchiectomies were performed, and 1 month later, 3-mL blood samples were taken, and contralateral orchiectomies were added. After the measurement of the serum inhibin B levels and histopathologic examinations, results are expressed as mean +/- SD. RESULTS: Serum inhibin B levels expressed as mean +/- SD were 108.233 +/- 21.296 pg/mL for group 1, 54.065 +/- 16.910 pg/mL for group 2, 74.195 +/- 2.779 pg/mL for group 3, 108.335 +/- 26.078 pg/mL for group 4, and 107.645 +/- 4.705 pg/mL for group 5. Inhibin B levels in group 2 and group 3 were different from group 1, group 4, and group 5 (P <.05). In histologic examination, Johnsen's scores expressed as mean +/- SD of right testes were 9.74 +/- 0.08 for group 1, 3.64 +/- 3.36 for group 2, and 9.86 +/- 0.05 for group 5. Histologic findings in group 2 were different from group 1 and group 5 (P <.05). Johnsen's scores expressed as mean +/- SD of left testes were 9.78 +/- 0.09 for group 1, 9.75 +/- 0.14 for group 2, 9.76 +/- 0.15 for group 3, 9.79 +/- 0.07 for group 4, and 9.82 +/- 0.08 for group 5, and there was no difference between groups (P >.05). CONCLUSIONS: The serum inhibin B levels decrease after unilateral TT reflecting contralateral testicular damage. Orchiectomy to prevent contralateral testicular damage after TT may not be effective after critical period. Measurement of inhibin B levels to evaluate contralateral testicular damage after unilateral TT is more effective than histopathologic examination.

The effects of dimethylsulfoxide on experimental hepatic ischemia.

AIMS: The aim of the study is to investigate the effects of dimethylsulfoxide (DMSO), a non-enzymatic free oxygen radical detoxifier, on the alterations observed during hepatic ischemia. METHODS: Twenty four albino rabbits were entered into the study. DMSO (500 mg/kg) was administered through inferior vena cava following dissection of the portal triad and immediately prior to clamping. The alterations on liver glycogen, blood glucose, ALT, AST, LDH, intracellular ATP, GSH-px, SOD, MDA within the erythrocyte and hepatic tissue MDA were investigated. RESULTS: In the control group, following ischemia, a reduction in blood glucose, hepatic glycogen and ATP levels within the cell and an increase in AST and LDH levels, MDA, GSH-px and SOD levels within the erythrocyte and hepatic tissue MDA level were observed (p < 0.01). In the study group, the blood glucose values increased at 30th minute following ischemia. The increase in LDH level was not statistically significant (p > 0.05). The increase in AST level was significantly lower when compared to the control group (p < 0.05). No effect was observed on ALT and ALP levels. DMSO lowered the reduction in hepatic glycogen level (p < 0.05), GSH-px (p < 0.01), MDA (p < 0.05) and ATP (p < 0.05) levels within the erythrocyte and hepatic tissue MDA level (p < 0.01) that were increased following ischemia. The increase in blood SOD level was not statistically significant (p > 0.05). CONCLUSION: DMSO can be administered in attempt to prolong the duration of ischemia or to reduce the adverse effects of ischemia on the hepatic tissue during the existing ischemic period.

The role of nitric oxide in testicular ischemia-reperfusion injury.

PURPOSE: This study was designed to determine the role of nitric oxide (NO) in the ischemia-reperfusion (I/R) injury process in testes. METHODS: Fifty prepubertal male rats were divided into 5 groups each containing 10 rats. After 4-hour torsion and 4-hour detorsion, bilateral orchiectomies were performed for measurement of tissue malondialdehyde (MDA) level and histopathologic examination. The results were compared statistically. The groups were labeled as group 1, basal values of biochemical parameters in testes; group 2 (control group), torsion plus detorsion; group 3, torsion plus N-monomethyl-L-arginine (L-NMMA) plus detorsion; group 4, torsion plus L-arginine plus detorsion; group 5, sham operation. RESULTS: The highest MDA values were determined in the L-arginin group in ipsilateral testes. Group 3 and group 4 were statistically different from control group. Histological examination showed that specimens from group 4 had a significantly (P < .05) greater histological injury than group 3, and contralateral testes showed normal testicular architecture in all groups. CONCLUSIONS: These results suggest that NO plays an important role in damaging the testis with I/R. Although inhibition of NO synthesis with L-NMMA significantly improves I/R injury in testes, enhancing NO production by providing excess of L-arginine increases such damage. In the early periods of detorsion, there is no damage to contralateral testes after unilateral testicular torsion.

The role of oxygen free radicals and nitric oxide in organ injury following hemorrhagic shock and reinfusion.

BACKGROUND: Vital organ injury due to tissue hypoperfusion is a major complication of hemorrhagic shock. Nitric oxide (NO) has been implicated in the pathophysiology of hemorrhagic shock. AIMS: To determine the effects of L-arginine on the central organ injury due to severe hemorrhagic shock and reinfusion and the relationship among endogenous antioxidants, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) in dogs. METHODS: After induction of anesthesia, twenty six mongrel dogs were hemorrhaged to a mean arterial pressure (MAP) of 35 +/- 3.3 mmHg where they were held for 1 hr. Five minutes prior to the end of the shock period, either saline (5 mL/kg), L-arginine (250 mg/kg), or NG-nitro-L-arginine-methyl-ester (L-NAME) (25 mg/kg) was administered i.v., being followed by reinfusion of shed blood. MAP was monitored. Blood samples were taken for the measurement of blood urea nitrogen (BUN), creatinine, aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), intraerythrocytic SOD, CAT, GSH-Px, and serum nitrite and nitrate levels. Tissue samples from liver, kidney and small intestines were taken for histological studies and liver samples were also taken for the mesurement of SOD, CAT, GSH-Px tissue levels. RESULTS: L-arginine treatment reduced MAP. In contrast, L-NAME treatment significantly increased MAP. L-arginine treatment increased BUN and creatinine. L-NAME treatment significantly increased the activity of hepatic enzymes. L-arginine decreased the reinfusion injury in the liver and the small intestine histopathologically. In addition, L-arginine caused significant decreases in the intraerythrocytic and the liver SOD, CAT and GSH-Px levels from the shock levels. CONCLUSION: L-arginine has a preventive role in liver and intestine following hemorrhagic shock and reinfusion. Inhibition of NO synthesis aggravates reinfusion injury.

Twenty two weeks of transdermal estradiol increases sex hormone-binding globulin in surgical menopausal women.

OBJECTIVE: To compare the effects of continuous noncombined transdermal estradiol versus oral conjugated estrogen on serum sex hormone-binding globulin (SHBG) levels prior to and during the 10th and 22nd weeks of therapy in patients with surgical menopause. STUDY DESIGN: Open, comparative trial. Patients were consecutively assigned to three groups: group 1 (n = 18) received continuous transdermal estradiol (0.050 mg/day), group 2 (n = 18) continuous oral conjugated estrogens (0.625 mg/day), whereas group 3 (n = 15) received no treatment. Serum SHBG levels were determined before treatment and after 10 and 22 weeks of treatment. RESULTS: Serum SHBG increased significantly with oral conjugated estrogens at 10 (p < 0.01) and 22 weeks (p < 0.01) compared with baseline. With transdermal estrogens there was a much smaller increase of SHBG. At 22 weeks, this increase was significant compared with baseline (p < 0.05), but not compared with the control group (p > 0.05). CONCLUSION: Transdermal estrogen has no effect on SHBG, whereas oral conjugated estrogens causes considerable increase.

The role of the oxidative state of glutathione and glutathione-related enzymes in anemia of hemodialysis patients.

OBJECTIVE: To investigate the oxidative state of glutathione and glutathione peroxidase (GSH-Px), glutathione reductase (GSSG-R), and glucose-6-phosphate dehydrogenase (G-6-PD) levels in patients with chronic renal failure (CRF) and controls. RESULTS: Erythrocyte GSH levels of patients were decreased, but GSSG was not significantly different from that of controls. Also, plasma GSH levels were not different, although GSSG was increased. GSSG/GSH ratios in erythrocyte and plasma were significantly higher in CRF patients. Erythrocyte GSSG-R activity was high, but G-6-PD and GPX were low. CONCLUSIONS: The findings suggest that: 1. Low GSH is related to decreased G-6-PD activities. 2. The reduction of peroxides with GPX are decreased by low GSH and low GPX activity. 3. GSSG may react with hemoglobin and causes protein aggregation in erythrocytes. These alterations cause hemolysis and could play a role in the pathogenesis of anemia in hemodialyzed patients.

Effects of naloxone on beta-endorphin and cortisol release in sepsis.

We investigated the effects of the opiate antagonist naloxone on the release of beta-endorphin and cortisol in rats subjected to sepsis. Sepsis was induced in weanling male Wistar albino rats (3-4 weeks old, 75-90 g) by cecal ligation and double perforation (CLP). Forty animals were randomly allocated to four groups. Group 1 was given naloxone hydrochloride 0.5 mg/kg subcutaneously after CLP and this treatment was repeated at 2-h intervals until the rats were killed. Group 2 rats underwent a sham operation. Group 3 (control group) rats had CLP. Group 4 consisted of nonoperated animals used to establish normal reference values. Eighteen hours after CLP or sham operation, the rats were killed by cervical dislocation and a blood sample was drawn via cardiac puncture to determine the beta-endorphin and cortisol levels. The beta-endorphin levels were significantly higher in the control group than in the sham-operated, naloxone-treated (NT), and nonoperated rats (P < 0.05). However, there were no significant differences in plasma beta-endorphin levels between sham-operated, NT and nonoperated rats (P > 0.05). Plasma cortisol levels were significantly higher in the control group compared with the other three groups and this difference was more significant in sham-operated and nonoperated rats (P < 0.01). However, no difference existed between sham-operated, NT, and nonoperated rats (P > 0.05). This study demonstrates that the endogenous opioid system may play a role in the activation of the pituitary-adrenal axis following sepsis, and shows that the increase in beta-endorphin and cortisol could be blocked by naloxone.

Effects of bupivacaine infiltration on beta-endorphin and cortisol release and postoperative pain following inguinal herniorrhaphy in children.

This study was undertaken to investigate the effects of bupivacaine on beta-endorphin (BE) and cortisol (C) release and postoperative pain in children. Thirty children aged 1 month to 2 years undergoing outpatient inguinal hernia under general anesthesia were randomized into three groups. Wound infiltration in group 1 patients (precisional group) was performed with 0.5 ml/ kg 0.25% bupivacaine following anesthesia induction but prior to surgery. Group 2 patients (postincisional group) had wound infiltration with bupivacaine following repair of the hernia but before skin closure. Group 3 patients (control group) did not receive any local anesthetic. In the post-anesthesia care unit (PACU) objective pain assessments were performed every 5 min using a standardized ten-point objective pain scale. Plasma C concentrations increased at the end of the operation in all groups, but this increase was significant only in the control group (P < 0.001). There was no significant difference between the pre- and postincisional groups with regard to pre- and postoperative C alterations (P > 0.05). Although plasma BE concentrations increased significantly at the end of the operation in the control group (P < 0.001), no significant difference was found between pre- and postoperative values in the infiltration groups. There was a more marked difference in BE release between the preincisional and control groups (P < 0.001) than the postincisional group (P < 0.05). Although the objective pain scores were not statistically different upon PACU arrival, the patients in the infiltration groups achieved a pain score of 0 much more quickly than those in the control group (P < 0.05). These findings suggest that wound infiltration with bupivacaine decreases the stress response to surgery and postoperative pain.

Analyses of serum vitamin D-binding protein, ceruloplasmin and copper levels in preterm infants.

The cord blood specimens of 12 preterm and 20 term babies were investigated. We determined serum calcium (Ca), phosphorus (P), magnesium (Mg), vitamin-D binding protein (DBP), ceruloplasmin (Cp) and copper (Cu) levels in two groups. We found that Ca, P, and MG levels of cord sera did not differ between the groups (p > 0.05), but DBP, Cp and Cu values showed a significant decrease in the preterm group (p < 0.05). The Cu and Cp values of the preterm infants correlated with those of the term infants.