Loss of capsaicin-induced meningeal neurogenic sensory vasodilatation in diabetic rats.

Neuropathic alterations of sensory nerves involved in the mediation of neurogenic inflammation of the meninges may contribute to the increased incidence of headaches in diabetics. In the rat, activation of capsaicin-sensitive nociceptors, which express the transient receptor potential vanilloid type 1 (TRPV1) receptor, induces meningeal vasodilatation, a significant component of neurogenic inflammation, through the release of calcitonin gene-related peptide (CGRP). This study examines the effects of streptozotocin-induced diabetes on TRPV1 receptor-mediated neurogenic sensory vasodilatation, CGRP release and nerve fiber density in the rat dura mater. In a cranial window preparation, epidural application of capsaicin (10(-7) M) produced distinct vasodilatory responses in control animals as measured by laser Doppler flowmetry. In diabetic rats, capsaicin-induced vasodilatation was reduced or even abolished 6, but not 2 or 4 weeks after diabetes induction. In contrast, vasoconstriction, a non-neurogenic response to capsaicin at a higher concentration (10(-5) M), was not altered in diabetic rats. The vasodilatory effects of histamine (10(-5) M), acetylcholine (10(-4) M) and CGRP (10(-5) M) were similar in control, diabetic and insulin-treated diabetic animals. In diabetic rats, a significant decrease in the capsaicin-evoked release of CGRP and reduction in the density of TRPV1-immunoreactive (IR) nerves were demonstrated. Treatment of the diabetic rats with insulin restored both the vasodilatory response and the capsaicin-induced CGRP release toward control values. In conclusion, this study revealed a marked impairment of meningeal TRPV1-IR nerves in streptozotocin diabetic rats by showing reduced neurogenic sensory vasodilatation, decreased capsaicin-evoked CGRP release and reduction in the number of TRPV1-IR nerve fibers of the dura mater. The findings suggest that capsaicin-sensitive afferents may play an important role in meningeal nociceptor function and their dysfunction, e.g. due to a limited removal of inflammatory mediators and/or tissue metabolites from the meningeal tissue, may contribute to the enhanced incidence of headaches in diabetics.

Delayed riluzole treatment is able to rescue injured rat spinal motoneurons.

The effect of delayed 2-amino-6-trifluoromethoxy-benzothiazole (riluzole) treatment on injured motoneurons was studied. The L4 ventral root of adult rats was avulsed and reimplanted into the spinal cord. Immediately after the operation or with a delay of 5, 10, 14 or 16 days animals were treated with riluzole (n=5 in each group) while another four animals remained untreated. Three months after the operation the fluorescent dye Fast Blue was applied to the proximal end of the cut ventral ramus of the L4 spinal nerve to retrogradely label reinnervating neurons. Three days later the spinal cords were processed for counting the retrogradely labeled cells and choline acetyltransferase immunohistochemistry was performed to reveal the cholinergic cells in the spinal cords. In untreated animals there were 20.4+/-1.6 (+/-S.E.M.) retrogradely labeled neurons while in animals treated with riluzole immediately or 5 and 10 days after ventral root avulsion the number of labeled motoneurons ranged between 763+/-36 and 815+/-50 (S.E.M.). Riluzole treatment starting at 14 and 16 days after injury resulted in significantly lower number of reinnervating motoneurons (67+/-4 and 52+/-3 S.E.M., respectively). Thus, riluzole dramatically enhanced the survival and reinnervating capacity of injured motoneurons not only when treatment started immediately after injury but also in cases when riluzole treatment was delayed for up to 10 days. These results suggest that motoneurons destined to die after ventral root avulsion are programmed to survive for some time after injury and riluzole is able to rescue them during this period of time.

Vascular changes play a role in the pathogenesis of necrotizing enterocolitis in asphyxiated newborn pigs.

Necrotizing enterocolitis (NEC) is the most common acquired gastrointestinal emergency in neonates. We have developed an animal model of NEC in asphyxiated newborn pigs and investigated the effects of asphyxia on blood flow in superior mesenteric artery and abdominal aorta, cardiovascular data, arterial acid-base and blood gas parameters, and endothelial cytoskeletal structure in mesenteric microvasculature. Anesthetized, mechanically ventilated newborn pigs were included in two groups: piglets underwent severe asphyxia, and sham-operated control animals. A cardiovascular and metabolic failure developed in asphyxiated piglets approximately 1 h after the induction: severe hypotension and bradyarrhythmia were seen and significant reductions of the blood flow were measured in the superior mesenteric artery and abdominal aorta during the critical phase. Rearrangement of cytoskeletal actin structure corresponding to enhanced vascular permeability was seen with bodipy phallacidin in mesenterial endothelium of asphyxiated piglets after a 24-h recovery period. In conclusion, severe vasomotor changes during asphyxia may result in mesenteric endothelial dysfunction implicated in increased vascular permeability, edema formation, and development of NEC in asphyxiated piglets.

Improving reproductive performance in lactating dairy cows by synchronizing ovulation or inducing oestrus.

Lactating crossbred Holstein-Friesian dairy cows (n = 331) were started on an Ovsynch regimen 68 +/- 8.2 days after calving; 200 micrograms GnRH intramuscularly (i.m.) on Days 0 and 9, and 35 mg prostaglandin F2 alpha i.m. on Day 7. Thirty-eight and 31 cows (11.5 and 9.4%, respectively) were in oestrus on Days 0 to 6 and 7 to 8, respectively, and inseminated, and the remainder were fixed-time inseminated (on Day 10). For these three groups, pregnancy rates (60-65 days after breeding) were 31.6, 38.7 and 34.0%, respectively (P = 0.82) and calving rates were 100, 100 and 89.9% (P = 0.23). In a preliminary trial, twelve lactating cows (45 to 60 days postpartum) with inactive ovaries were given 1500 IU eCG i.m.; 10 were in oestrus within 10 days after treatment (and inseminated) and eight of these were pregnant (30 days after breeding). The Ovsynch program resulted in acceptable reproductive performance in cyclic cows and eCG treatment has considerable promise for inducing oestrus in anoestrous cows.

Inhibitory effects of methylxanthines on the pre-eclamptic-like symptoms in ewes.

OBJECTIVE: Our objective was to determine whether two methylxanthines, pentoxifylline (PTX) and allopurinol, would have beneficial effects on experimental pregnancy-induced pre-eclampsia- like disease in ewes. STUDY DESIGN: 20 animals at the gestational age of 130-135 days were divided into four groups (control; fasting; fasting, pentoxifylline-treated; and fasting, allopurinol-treated). The illness was provoked with a 4-day fasting period. Electrolytes, glucose, conventional parameters, plasma haem content, indirect bilirubin concentration and free thiol levels were measured. RESULTS: Unlike in the fasting group, conventional signs of the disease, such as hypertension, kidney and liver injury and platelet count decrease, were all mitigated in the fasting, drug-treated animals. In the treated animals plasma haem content increased by a less significant level, while indirect bilirubin concentration showed a more rapid rise. CONCLUSIONS: Both methylxanthines partly inhibited the pre-eclamptic-like symptoms in ewes. We speculate that the better induction of haem oxygenase might play an important role in this inhibitory effect on this particular animal model.

Impaired early neurologic outcome in newborn piglets reoxygenated with 100% oxygen compared with room air after pneumothorax-induced asphyxia.

Birth asphyxia is a serious problem worldwide, resulting in 1 million deaths and an equal number of neurologic sequelae annually. It is therefore important to develop new and better ways to treat asphyxia. In the present study we tested the effects of reoxygenation with room air or with 100% oxygen (O2) after experimental pneumothorax-induced asphyxia on the blood oxidative stress indicators, early neurologic outcome, and cerebral histopathology of newborn piglets. Twenty-six animals were studied in three experimental groups: 1) sham-operated animals (SHAM, n = 6), 2) animals reoxygenated with room air after pneumothorax (R21, n = 10), and 3) animals reoxygenated with 100% O2 after pneumothorax (R100, n = 10). In groups R21 and R100, asphyxia was induced under anesthesia with bilateral intrapleural room air insufflation. Gasping, bradyarrhythmia, arterial hypotension, hypoxemia, hypercarbia, and combined acidosis occurred 62 +/- 6 min (R21) or 65 +/- 7 min (R100; mean +/- SD) after the start of the experiments; then pneumothorax was relieved, and a 10-min reoxygenation period was started with mechanical ventilation with room air (R21) or with 100% O2 (R100). The newborn piglets then breathed room air spontaneously during the next 3 h. Blood oxidative stress indicators (oxidized and reduced glutathione, plasma Hb, and malondialdehyde concentrations) were measured at different stages of the experiments. Early neurologic outcome examinations (neurologic score of 20 indicates normal, 5 indicates brain-dead) were performed at the end of the study. The brains were next fixed, and various regions were stained for cerebral histopathology. In the SHAM group, the blood gas and acid-base status differed significantly from those measured in groups R21 and R100. In group R100, arterial PO2 was significantly higher after 5 (13.8 +/- 5.6 kPa) and 10 min (13.2 +/- 6.3 kPa) of reoxygenation than in group R21 (8.7 +/- 2.8 kPa and 9.2 +/- 3.1 kPa). The levels of all oxidative stress indicators remained unchanged in the study groups (SHAM, R21, and R100). The neurologic examination score in the SHAM group was 18 +/- 0, in group R21 it was 13.5 +/- 3.1, and in group R100 it was 9.5 +/- 4.1 (significant differences between SHAM and R21 or R100, and between R21 and R100). Cerebral histopathology revealed marked damage of similar severity in both asphyxiated groups. We conclude that the blood oxidative stress indicators and cerebral histopathology did not differ significantly after a 10-min period of reoxygenation with room air or with 100% O2 after pneumothorax-induced asphyxia, but reoxygenation with 100% O2 might impair the early neurologic outcome of newborn piglets.

Sodium azide treatment decreases striatal and cortical concentrations of alpha-tocopherol in rats.

Sodium azide (20mg/kgsc), given for a maximum of 3 days to rats, significantly decreased the alpha-tocopherol concentrations in the cortex on day 2 and in the striatum on day 3. In these brain regions the oxidized glutathione values showed 30 to 36% (statistically not significant) elevation on day 3. Reduced glutathione levels were not altered. The observations suggest an important role for alpha-tocopherol in the defense against azide induced free radicals probably including NO and lipid peroxide radicals.

Diminished blood levels of reduced glutathione and alpha-tocopherol in two triosephosphate isomerase-deficient brothers.

The glutathione redox system and alpha-tocopherol, both of which are essential for maintaining the normal structure of biological membranes, some other lipid-soluble antioxidants (lycopene, beta-carotene, retinol), and lipid peroxidation, were investigated in the blood from two triosephosphate isomerase (TPI)-deficient brothers. Both of the genetically identical compound heterozygote brothers have congenital hemolytic anemia, but only one of them has a neurological defect, the second cardinal symptom of TPI deficiency. Whole blood reduced glutathione levels were markedly decreased in both brothers. The glutathione reductase activities as well as the NADPH contents of their erythrocytes were in the normal range or slightly enhanced. Increased ratio of oxidized/reduced glutathione, elevated glutathione S-transferase activity, and increased d-lactate level, a metabolite of the glyoxalase pathway, were detected only in the neurologically affected propositus. The plasma carotenoids (lycopene + beta-carotene), alpha-tocopherol/cholesterol + triglyceride ratios, and the erythrocyte alpha-tocopherol levels were significantly decreased in both patients. It seems conceivable that membrane alterations due to the low level of these reducing agents may contribute to the shortened life span of erythrocytes. The imbalance of the prooxidant/antioxidant homeostasis as well as the increased rate of methylglyoxal formation may also have been involved in the development of the neurological manifestations in the propositus.

[Reoxigenation after neonatal asphyxia with 21% or 100% oxygen in piglets]. / Ujszülöttkori asphyxiát követö reoxigenizáció sertéseken 21% vagy 100% oxigénnel.

Birth asphyxia represents a serious problem worldwide, resulting in 1 million deaths and an equal number of neurologic sequelae annually. It is therefore important to develop new and better ways to treat asphyxia. In the present study we tested the effect of reoxygenation with room air or 100% oxygen following experimental pneumothorax induced asphyxia on blood oxidative stress indicators, early neurologic outcome and cerebral histopathology of newborn piglets. 26 animals were studied in three experimental groups: sham-operated (SHAM, n = 6), reoxygenation with room air after pneumothorax (RORA, n = 10) and reoxygenation with 100% oxygen after pneumothorax (RO100, n = 10). In RORA and RO100 asphyxia was induced under anesthesia with bilateral intrapleural room air insufflation. Gasping, bradyarrhythmia, arterial hypotension, hypoxemia, hypercarbia and severe combined acidosis occurred 62 +/- 6 (RORA) and 65 +/- 7 min (RO100) after the start of the experiments, when the pneumothorax was relieved and ten min of reoxygenation period was started with mechanical ventilation with room air (RORA) or 100% oxygen (RO100). Then the spontaneously breathing animals were followed on room air during the next three hours. Blood oxidative stress indicators--as oxidized and reduced glutathione, plasma hemoglobin and malondialdehyde concentrations--were also measured at different stages of the experiments and early neurologic examinations (neurological score: 20 = normal, 5 = brain dead) were performed at the end of the study. Then the brains were fixed and stained. In SHAM blood gases and acid/base status differed significantly from values measured in RORA and RO100. In RO100 PaO2 was significantly higher at 5 (13.8 +/- 1.8 kPa) and 10 min (13.2 +/- 2.0 kPa) than in RORA (8.7 +/- 0.9, 9.2 +/- 1.0 kPa), respectively. All the measures of oxidative stress indicators remained unchanged in the study groups (SHAM, RORA, RO100). Neurologic examination scores from SHAM were 18 +/- 0, from RORA 13.5 +/- 1.0 and from RO100 9.5 +/- 1.3 (significant differences between SHAM and RORA and RO100, significant difference between RORA and RO100). Cerebral histopathology showed marked damage with similar severity in both asphyxiated groups. We conclude that blood oxidative stress indicators and cerebral histopathology did not differ significantly after 10 min reoxygenation either with room air or with 100% oxygen following pneumothorax induced asphyxia, but reoxygenation with 100% oxygen might impair the early neurologic outcome of newborn pigs.

Nonenzymatic antioxidants of blood in multiple sclerosis.

Free radical action has been suggested as a causal factor in multiple sclerosis. We investigated the plasma level of lipid peroxides expressed in terms of malone dialdehyde and changes in blood nonenzymatic antioxidants (glutathione, alpha-tocopherol, retinol, plasma sulfhydryl groups, and uric acid) in multiple sclerosis patients with exacerbation or in remission, including a group treated with beta-interferon. The malone dialdehyde level was increased by 38% (n.s.) during exacerbations. The blood concentration of oxidized glutathione was likewise elevated (P<0.05), while the ratio of plasma alpha-tocopherol to cholesterol plus triglyceride was decreased (P<0.001). These changes suggest increased free radical production and consumption of the scavenger molecules during the active phase of the disease. Blood reduced glutathione level was increased (P<0.01) during exacerbation and remission as well. The rise in this thiol is likely to be a compensatory mechanism defending the cells from further oxidant injuries. Beta-interferon increased plasma alpha-tocopherol levels (P<0.001) but not the lipid corrected alpha-tocopherol value. Other parameters were not influenced by the drug.

Differential regulation of vasopressin gene expression in the hypothalamus of endotoxin-treated 14-day-old rat.

The E. coli endotoxin 0111 B4, a lipopolysaccharide (LPS), in a dose of 200 ng/kg body weight/50 microl artificial cerebrospinal fluid (CSF) was given intracisternally to 14-day-old rats. Four hours later CSF, blood and urine were sampled, and consecutive brain sections from the hypothalamic area of the brain were prepared for in situ hybridization. The LPS treatment resulted in a significant (p<0.001) pleocytosis and an elevation of the protein content of the CSF. There were no changes observed in the chemical parameters of the CSF, plasma, blood or urine, i.e. vasopressin (VP) levels, osmolality, Na+ and K+ concentrations, glucose level, pH, bicarbonate or PaCO2, PaO2 values. LPS injection, however, resulted in a significantly (p<0.01) increased VP mRNA level (121% of the control value) in the supraoptic nuclei (SON), but not in the paraventricular nuclei (PVN), as compared to controls. Our findings suggest an early effect of LPS on VP gene expression selectively in the SON of 14-days-old rats. This animal model might be suitable for studying the regulation of VP gene expression and the role of this peptide in the pathogenesis of bacterial meningitis in pediatric patients.

Phacoemulsification in eyes with past pars plana vitrectomy: case-control study.

PURPOSE: To determine intraoperative and postoperative complications and outcomes of phacoemulsification of cataract in eyes that had previous pars plana vitrectomy. SETTING: University-based anterior segment disease referral practice. METHODS: This was a retrospective case-control study of a surgical series of 52 consecutive postvitrectomy cataract extractions statistically compared with control eyes from the same practice. RESULTS: Cataract extraction followed vitrectomy by 2 months to 6 years (mean 19 months). Cataracts with a posterior subcapsular component were seen more frequently in postvitrectomy eyes (58% versus 25% in control eyes). Cataract extraction after pars plana vitrectomy was often more challenging than in control eyes. Challenges included unstable posterior capsules, loose zonules, and posterior capsule plaque. Postoperative posterior capsule opacification (PCO) was more common in study than in control eyes (51% versus 21%; P = .002), especially if expandable gas or silicone oil had been used at vitrectomy. Visual acuity improved in 87% of study eyes, with 46% achieving a visual acuity of 20/40 or better. In study eyes in which the indication for vitrectomy was macular hole or epiretinal membrane, nuclear sclerosis was the most common cataract type, no intraoperative complications occurred, the PCO rate was low (13%), and visual acuity was better (73% 20/40 or better) than in the other study eyes. CONCLUSION: Phacoemulsification after pars plana vitrectomy can be performed with a low complication rate and with good visual results, although limited by underlying retinal disease. Posterior capsule opacification requiring neodymium: YAG capsulotomy was common in this series.

Postasphyxial reoxygenation reduces the activity of Na+/K+-ATPase in the erythrocytes of newborn piglets.

The aim of our study was to determine whether the impairment of Na+/K+ pump is detectable in erythrocytes during hypoxia and reoxygenation. Acute asphyxia was induced in 10 newborn piglets for 1 h by bilateral pneumothorax. The Na+/K+-ATPase activity, Na+, K+ and ATP content of RBCs were determined in baseline condition (paO2: 60.4 +/- 9.3 mm Hg), at the end of the hypoxic period (1 h) (paO2: 30.2 +/- 10.3 mm Hg), then hourly during the reoxygenation phase (2, 3, 4 h) (paO2: 54.8 +/- 9.0, 56.1 +/- 8.7, 57.2 +/- 9.6 mm Hg). The Na+/K+-ATPase activity was constant during the first 3 h. However, it decreased at 4 h (676 +/- 168 versus baseline 833 +/- 141 U, p < 0.05). The highest ATP content was measured also at this point (4.32 +/- 0.57 versus baseline 3.27 +/- 0.45 mmol/l RBC, p < 0.01). The Na+ content was lower at 1 and 2 h (14.0 +/- 1.8; 13.8 +/- 1.2 versus baseline 15.7 +/- 1.2 mmol/100 g Hb, p < 0.05), but later it became normal. Plasma monovalent cationic levels and intracellular K+ content did not alter during the experiment. Our results indicate that the deterioration of enzyme activity occurs within the same time-frame that previously described morphological alterations in brain tissue develop, so the RBC Na+/K+-ATPase activity might reflect the progress of posthypoxial brain damage.

Surface tension, glutathione content and redox ratio of the tracheal aspirate fluid of premature infants with IRDS.

OBJECTIVE: Determination of the surface tension (ST), the total glutathione (GL) content and the ratio of oxidized glutathione (GSSG) to reduced glutathione (GSH) in the tracheal aspirate (TA) of newborn infants with IRDS. METHODS: The ST of the TA was determined by monitoring the fluid level pulsated in a capillary glass tube by means of a digitalized videocomputerized picture analysis program, a technique developed in our laboratory. The concentrations of GSSG and total GL in the TA were determined enzymatically with glutathione reductase. All results of laboratory tests were referred to the total phospholipid (PL) concentration. Patients, Experimental Material: TA samples were collected from 32 intubated premature and newborn infants admitted to the NICU with IRDS during the first 2 weeks of their lives. Control samples were obtained from 11 children prior to elective surgery. RESULTS: The ST relative to the PL content (surface tension index, STI) was significantly lower in the newborns with IRDS than in the control group, and the concentration of GSH in the TA was also markedly decreased in all IRDS infants studied. The concentration of GSSG and the ratio of GSSG to GSH were significantly higher in the severe cases and in those with an unfavourable prognosis. Surfactant treatment had a protective effect against oxidative stress, it induced a decrease in both the GSSG concentration and in the GL redox ratio (GSSG/GSH) in the TA. There was a close correlation between the GSH content and the STI value of the samples studied. CONCLUSION: Oxidation and consequent depletion of GSH in the TA may be an aggravating factor in the development of the insufficient surface activity in intubated newborns with IRDS.

[Possible pitfalls in giving expert opinion in legal actions against medical services]. / Szakmai tévedések lehetösége orvosi perek szakértöi véleményezésében.

The authors report their experience in cases under legal action against medical service needing expert opinion. By the rapid development and differentiation of medical science in the recent years the possibility of making mistake in every day practice increased, on the other hand this circumstance includes also occurrence of the pitfalls in giving expert opinion in legal actions against medical service.

Fetal renal hyperechogenicity in pathological pregnancies.

A relationship was sought between renal hyperechogenicity and the hypoxic state of fetuses. 120 pathological pregnancies were examined between the 28th and 36th week. All of these women exhibited moderately increased levels of hepatic enzymes, 3 of them had a pathological kidney function, and 4 of them displayed hyperuricemia during the examination period. The echogenicity of the fetal kidneys was examined with Hitachi EUB-450 ultrasound equipment with a 3.5 MHz transducer. The kidney (creatinine, urea-N, uric acid, triglyceride, cholsterin) and liver (SGOT, SGPT, GGT, bilirubin) functions and plasma electrolytes (Na, K, Ca, Cl) of the mothers were also examined and blood was collected from the pulsating umbilical artery for determination of the same parameters. After delivery, the physical condition of the neonates was followed and their kidneys were examined with the same ultrasound equipment within the first 5 days. There was a significant correlation between a pathological neonatal clinical outcome and the frequency of fetal and hyperechogenicity (chi-square test with Yates correction, p < 0.01). The results demonstrate that fetuses exhibiting renal hyperechogenicity in pathological pregnancies require particularly careful obstetric control and neonatological consultation. It is important that hyperechogenic cases be admitted to a perinatal intensive care unit. Fetal renal hyperechogenicity is considered to be associated with an enhanced risk of an adverse perinatal outcome.

The pathogenetic role of heme in pregnancy-induced hypertension-like disease in ewes.

Toxicosis syndrome of fasting pregnant ewes has a close similarity to human preeclampsia (hypertension, albuminuria). The common etiological factor might be oxidative hemolysis and heme-induced endothelial damage. Ewes (5 starving, 5 control) at 130-135 gestational days with a 96-h fasting period followed by refeeding were used. Blood pressure, platelet count, electrolytes, kidney and liver function parameters, as well as plasma glucose, hemoglobin/heme, free thiol groups and Trolox equivalent antioxidant capacity, and plasma iron and ferritin levels were measured. Statistical significance was assessed using Student's t test (P < 0.05). Besides hypertension and renal disturbances, hemolysis, elevated liver enzymes and low platelet count, characteristic of human HELLP syndrome, were also present. In the first 24 h of glucose deprivation there was a significant rise in both the plasma hemoglobin/heme and indirect bilirubin concentrations. The antioxidant free thiol levels decreased significantly the next day, without any change in the total antioxidant capacity of the plasma. While the loss of calcium and magnesium levels related to the similarity to preeclampsia, reduced plasma iron concentrations referred to species differences in iron homeostasis. An oxidative stress causing hemolysis in a glucose-6-phosphate dehydrogenase-deficient animal model was proven by the loss of free thiols after glucose deprivation. The activation of the oxidative stress protein heme oxygenase was a signal of endothelial cell injury, the primary cause of pregnancy-induced hypertension.

Oxidative stress induced by bloodless limb surgery on humans.

Measure of oxidative stress were studied in blood samples from 10 patients undergoing bloodless lower limb surgery. Ischaemia induced a significant increase in plasma hypoxanthine concentration and xanthine oxidase activity both in the operated leg and in the systemic circulation. Five minutes after reperfusion, ratio of xanthine oxidase/total xanthine oxidase and dehydrogenase activities rose moderately, whereas at 20 min xanthine oxidase accounted for all xanthine oxidoreductase activity in the systemic circulation. A significant increase in blood glutathione redox ratio, enhanced oxidation of haemoglobin to methaemoglobin and rise in plasma haemoglobin concentration were present only in the operated limb. Thus, although the level of the potential free radical generators rose significantly both locally and in the systemic circulation, oxidative stress, as indicated by blood glutathione and erythrocyte injuries, remained limited to the reperfused leg.

[Resuscitation of neonates in the delivery room. Recommendations by the American Heart Association and American Academy of Pediatrics]. / Ujszülöttek szülöszobai resuscitatiója.

According to the recommendation of the American Heart Association and the American Academy of Pediatrics 43 newborn babies with mean birth weight 3300 g (range 610-5100 g) were resuscitated. One-minute Apgar score was 0:1, 1:22, 2:11, 3:7, 4:2 cases. Mask and bag ventilation were needed in 43, heart compression in 7, tracheal intubation in 2, drugs in 2 cases. Five-minute Apgar values were 8:39, 5:1, 7:1 case. All resuscitations were successful. The resuscitation program is a great advance in the field of neonatology. Nationwide application of it might be helpful to decrease neonatal mortality in Hungary.

The possible role of uric acid in renal hyper-echogenicity in neonatal hypoxic acute shock.

Sonographic examinations as well as blood and urine chemistry tests were carried out in 4 neonates (3 mature, 1 premature) with transient renal failure, who were suffering from the effects of neonatal asphyxia of varying etiology. The first ultrasound examinations of the kidneys were performed within 24 hours after the hypoxic event. Simultaneously, blood and urine tests for parameters of renal function and purine metabolites were also carried out. Transient insufficiency of renal function could be detected in all cases with hyper-uricemia and hyper-uricosuria with no hypercalciuria. Ultrasonographic examinations showed hyper-echogenicity of the renal pyramids in all of the cases and hyper-reflectivity of the renal cortex in cases 2 and 4. In 3 cases, hyper-echogenicity appeared within 24 hours and disappeared in a short time, while in case 3 it could be detected from day 4 until day 14. These findings demonstrate, that the neonatal kidney is very sensitive to hypoxia and that hypoxic renal failure is accompanied by hyper-echogenicity of the kidneys. Uric acid is a possible cause of the renal hyper-echogenicity.