PubMed Health⌕ Search

Biomedical subjects

P Temesvári

Publications and source records attributed to P Temesvári.

At least 19 recordsLinked to original sources
PubMed2003

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.

Animals↗
PubMed2003

The role of HLA-DRB1*04 alleles and their association with HLA-DQB genes in genetic susceptibility to rheumatoid arthritis in Hungarian patients.

We investigated the HLA-DRB, and DQB polymorphism and haplotypes in RA subjects of Hungarian origin by PCR typing using sequence-specific primers. Molecular subtyping of HLA-DRB1*04 alleles in RA patients showed strongest association with highest relative risk with DRB1*0404. A significantly decreased frequency of DRB1*0403 was observed in patients compared to controls. A significant number of patients carried DR4 haplotypes on DQB1*0302 (54%) relative to DQB1*0301 which was present on 36% of the haplotypes. When compared to controls, the frequency was higher in the latter allele only. Few unique DRB-DQB haplotypes were observed in Hungarian RA patients. In spite of the fact, that the Hungarian population has been isolated linguistically over centuries, a considerable racial admixture has occurred following immigration and invasions, thus the present study confirms in Hungarian patients with RA, previous findings for RA and HLA in European countries.

Alleles↗
PubMed2002

Unaltered cerebral Na+,K+-ATPase activity after hypoxic/ischemic injury in piglets.

We examined whether hypoxic/ischemic (H/I) stress decreased the cerebral Na(+),K(+)-ATPase enzyme activity (NEA) of newborn pigs. The effects of global ischemia (10 min), asphyxia (10 min), and incomplete forebrain ischemia (45 min) were analyzed in ten different brain regions. The lengths of the reperfusion periods varied between 15 min and 3 h. NEA was determined as the ouabain-sensitive fraction of the total ATPase activity of the sample. Marked regional differences in NEA were observed in all experimental groups, whereas NEA was not significantly affected in any of the brain structures investigated. The present results suggest that damaged brain Na(+),K(+)-ATPase may not be the cause of the neuronal-vascular impairment following H/I stress.

Animals↗
PubMed2002

Neonatal pneumonia caused by Trichomonas vaginalis.

The authors present two cases of newborn babies infected by Trichomonas vaginalis (hereafter referred to as T. vaginalis) and suffering from severe congenital breathing difficulties and needing artificial respiration. Microscopic examination of the tracheal discharge revealed characteristically moving, flagellated, pear-shaped unicellular organisms. Cultures on CPLM medium proved the presence of T. vaginalis. During pregnancy the mothers' clinical status was negative and both of them mentioned leukorrhoea of changing intensity. They were regularly involved in antenatal care. The infection caused by T. vaginalis could be detected in the two mothers later by culture procedures.

Animals↗
PubMed2001

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.

Acid-Base Equilibrium↗
PubMed2000

[Reoxigenation after neonatal asphyxia with 21% or 100% oxygen in piglets].

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.

Animals↗
PubMed1999

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.

Animals↗
PubMed1998

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.

Adenosine Triphosphate↗
PubMed1996

Plasma and cerebrospinal fluid hyperinsulinism in asphyxiated piglets.

Insulin (I) plays a crucial role in the maturation of the perinatal brain, and it may also be involved in the pathogenesis of neonatal brain injuries. The aim of the present study was to reveal the effect of neonatal asphyxia on the regulation of I and glucose (G) metabolism in plasma and cerebrospinal fluid (CSF) in newborn piglets. The I concentrations were measured by radioimmunoassay, while the G levels were analyzed by the G oxidase method during three phases (basal, critical, recovery) of bilateral pneumothorax in newborn piglets. We observed a significant hyperinsulinism (p < 0.001) both in plasma and CSF and a mild hypoglycemia (p < 0.05) during the recovery period. Postasphyxial G infusion (1.1 M, 10 ml.kg-1) amplified the hyperinsulinism. The ICSF/plasma ratio (mean +/- SEM; n = 16) was decreasing during cardiovascular failure (0.09 +/- 0.02; NS) as compared with the initial value (0.12 +/- 0.04), then it returned to basal values by 60 min (0.14 +/- 0.04; NS), and increased significantly 180 min (0.40 +/- 0.14; p < 0.05) after resuscitation of the piglets. There was a similar increase in GCSF/plasma ratio in asphyxiated animals at the end of experiments (0.99 +/- 0.15 vs. initial 0.76 +/- 0.05; p < 0.05). In conclusion, neonatal asphyxia resulted in plasma and CSF hyperinsulinism which may alter hypoxic-ischemic cerebral damages.

Acid-Base Equilibrium↗
PubMed1995

The role of cerebral microvessels in the elimination of histamine released during postasphyxial reperfusion in newborn piglets.

Histamine, released from intracerebral sources during hypoxic-ischemic conditions, may take part in the pathogenesis of neonatal brain injuries. In order to elucidate the possible role of cerebral microvessels in the elimination of histamine from the extracellular space, we determined the concentration of histamine using a modified radioenzymatic method in plasma taken from the internal jugular vein, in cerebrospinal fluid, and in capillary-rich fraction of cerebral microvessels prepared from cortex in 12 sham-operated piglets. Then, bilateral pneumothorax was induced in 20 piglets, samples were taken from the same compartments as from the controls before and during asphyxia, as well as 15 and 180 min thereafter, respectively. Plasma histamine level was significantly (P < 0.05) elevated in animals during hypoxic cardiovascular and metabolic failure (13.5 +/- 1.9 nM l-1) compared to value measured in the control group (2.2 +/- 0.5 nM l-1), preceding any detectable change of histamine concentration in cerebrospinal fluid (5.2 +/- 1.9 versus 3.8 +/- 1.1 nM l-1, respectively) or in cerebral microvessels (8.4 +/- 0.8 versus 7.1 +/- 0.6 pM (mg protein)-1). After resuscitation, histamine levels in plasma samples remained high during the early (15 min, 16.2 +/- 4.3 nM x l-1) and late (180 min, 15.3 +/- 2.9 nM l-1) reperfusion period. By contrast, histamine concentration was increased considerably (P < 0.05) in cerebrospinal fluid samples obtained 15 min (12.8 +/- 6.5 nM l-1), but not 180 min (5.2 +/- 1.9 nM l-1) after resuscitation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗