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F Bari

Publications and source records attributed to F Bari.

At least 19 recordsLinked to original sources

Novel calretinin and reelin expressing neuronal population includes Cajal-Retzius-type cells in the neocortex of adult pigs.

Cajal-Retzius cells and their secreted product reelin are essential for the lamination of the cerebral cortex. In all species studied to date Cajal-Retzius cells form a transient neuronal population that almost completely disappears from the neocortex postnatally. Recently, in the hippocampal formation of adult domestic pig, we have found a large calretinin- and reelin-immunoreactive cell population that morphologically corresponded to Cajal-Retzius cells. In the present study, we examined calretinin- and reelin-immunoreactive neurons in layer I of the prefrontal, temporal, parietal and occipital neocortical areas of newborn, young adult and adult domestic pigs. Large numbers of bipolar or fusiform calretinin-positive cells were found in the upper half of layer I in all examined age groups. The morphology of these neurons resembled that of the Cajal-Retzius cells. Layer I was occupied by a dense calretinin-positive axonal plexus that was similar to the previously described axons of Cajal-Retzius cells in other species. In a similar location, where calretinin-positive cells occurred in layer I, large numbers of reelin-immunoreactive cells were found in all examined age groups. In addition, reelin colocalized with calretinin in layer I neurons. The number of calretinin and reelin-positive neurons decreased from 1 day to one year, but calretinin-positive Cajal-Retzius-type cells still comprised a remarkable large population in 12-month-old animals. Correlated light and electron microscopic examination of calretinin-labeled Cajal-Retzius-type cells indicated that these cells are integrated in the synaptic circuitry of the neocortex. Our results suggest that Cajal-Retzius cells do not disappear inevitably from the mature neocortex in all mammalian species. The function of this cell type is not known, but late persisting Cajal-Retzius-type cells in the domestic pig provide an opportunity to study their neuronal connections and the possible role of reelin in plasticity and regeneration of neocortex.

Aging↗

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↗

Factors affecting the survival of sheep embryos after transfer within a MOET program.

Multiple ovulation and embryo transfer (MOET) has the potential to increase the rate of genetic improvement in sheep. However, better realization of this potential requires maximum survival rates of transferred embryos of high genetic merit after transfer into recipient ewes. These studies were therefore conducted to investigate the effect of both embryonic and recipient ewe factors on the survival rate of transferred embryos. Survival rate was similar after transfer of morula or blastocyst stage embryos, and these were higher (P<0.05) than for very early morulae and early morulae. Advanced embryos (Day 5 blastocyst) had an advantage (P<0.05) in survival rate over retarded embryos (Day 6 morula). Grades 1 and 2 embryos survived significantly (P<0.05) better than Grades 3 or 4 embryos. There was no difference in embryo survival rate following transfer to recipients with different numbers of corpora lutea. In general, age or parity of recipient ewes did not affect embryo survival rate, although a higher (P<0.05) embryo survival rate was observed for yearling recipients. Buserelin (GnRH agonist) treatment of recipient ewes 5 or 6 days after transfer of embryos (Day 12 of the cycle) did not improve embryo survival rate. These results confirm that both embryonic and recipient factors can play an important role in the success of a MOET program in sheep.

Age Factors↗

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↗

Effect of axillary brachial plexus blockade on baroreflex-induced skin vasomotor responses: assessing the effectiveness of sympathetic blockade.

BACKGROUND: The combination of laser Doppler flowmetry and non-invasive blood pressure monitoring allows the continuous observation of cutaneous vascular resistance (CVR). Continuous recording of unmodulated skin blood flow (SBF) is very sensitive to artefacts, rendering the method unreliable. In contrast, intermittent short lasting challenges of the CVR by cardiovascular autonomic reflexes may provide information about the responsiveness of the sympathetic nervous system in the skin. METHODS: Eleven patients with below-wrist hand surgery (six males and five females; aged 35.2+/-7.1 years) performed Valsalva maneuver following axillary blockade. Skin blood flow was continuously monitored on the forearm of the side axillary blockade, as well as on the contra-lateral forearm, which was used as the control. The responses were expressed as changes compared with the baseline level derived from a resting period of 30 s. The maximal change in CVR was determined during the late strain phase of the Valsalva maneuver on both sides. For numerical comparison the change in CVR on the axillary blockade and control sides were simultaneously calculated. RESULTS: During the Valsalva maneuver a significant increase in CVR was observed on the control side with a maximum value during the late strain phase (baseline 0.18+/-0.1 and late strain phase 0.42+/-0.2 relative units; P<0.01). In contrast, only minimal changes were detected on the side of axillary blockade in CVR (baseline 0.17+/-0.8 and late strain 0.16+/-0.2 relative units; P=NS). CONCLUSIONS: Our findings support the disputed hypothesis that the human skin microvasculature is involved in baroreflex regulation under thermoneutral conditions. The determination of baroreflex stimulus-induced microvascular responses may serve as a feasible method for monitoring the effectiveness of sympathetic blockade.

Adult↗

Cyclooxygenase-2 inhibitor NS398 preserves neuronal function after hypoxia/ischemia in piglets.

Anoxic stress attenuates NMDA-induced pial arteriolar dilation via a mechanism involving actions of cyclooxygenase (COX)-derived reactive oxygen species (ROS). We examined whether the selective COX-2 inhibitor NS398 would protect neuronal function after global hypoxia/ischemia (H/I) in piglets. Pial arteriolar responses to NMDA (10-100 micromol/l) were determined using intravital microscopy in anesthetized piglets before and 1 h after H/I. Study groups received vehicle, 0.3, 1, or 5 mg/kg NS398, or 0.3 mg/kg indomethacin (n = 7, 6, 6, 5 and 8, respectively) i.v. 20 min prior to H/I. H/I reduced NMDA- induced dilation to 44 +/- 6% (100 micromol/l NMDA, mean +/- s.e.m.) of the pre-ischemic response in vehicle animals (p < 0.05). However, NS398 dose-dependently protected arteriolar dilation to NMDA (77 +/- 8, 81 +/- 16, and 102 +/- 10% preservation at 0.3, 1 and 5 mg/kg, respectively). Indomethacin caused similar preservation. However, indomethacin but not NS398 reduced serum thromboxane B(2) levels to undetectable values. In conclusion, COX-2 appears to be a major source of ROS in the piglet cerebral cortex after H/I.

Animals↗

The repeatability of superovulatory response and embryo recovery in sheep.

Over an 8-year period, a total of 328 Scottish Blackface donor ewes were involved in a MOET program. They were synchronized with fluorogestone acetate sponges and superovulated with ovine FSH. After the onset of estrus, ewes were hand-mated and laparoscopic artificial insemination was performed with fresh semen 44-46 h after sponge removal. Embryos were recovered semi-laparoscopically on either Day 5 or Day 6 after insemination. Of the 328 donor ewes used, 222 ewes were supervoulated only once, while the remaining ewes were superovulated either twice (73 ewes), 3 times (26 ewes) or 4 times (7 ewes) at yearly intervals to generate a maximum of 474 records for subsequent analysis. There was no significant change in either mean ovulation rate or the mean number of embryos recovered per donor ewe at successive treatments. However, significant (P < 0.05 at least) effects of both year and donor ewe age existed for superovulatory response and number of embryos recovered, though only the effect of year was significant (P < 0.001) for percentage embryo recovery. Repeatability was significant (P < 0.05 at least) for both superovulatory response (r = 0.55, s.e. 0.055) and number of embryos recovered (r = 0.38, SE 0.074), but not for percentage embryo recovery (r = 0.04, SE 0.102).

Age Factors↗

Ischemia increases prostaglandin H synthase-2 levels in retina and visual cortex in piglets.

BACKGROUND: Ischemia increases levels of prostaglandin H synthase-2 (PGHS-2) in neonatal brain and cerebral vasculature, but effects on the developing visual system are unknown. We examined the effects of ischemia on PGHS-2 mRNA and protein levels in the retina and visual cortex in anesthetized piglets. METHODS: Ten minutes of complete retinal and brain ischemia was induced by increasing intracranial pressure. After 2-12 h of reperfusion, samples of retina and visual cortex were collected for determinations of levels of PGHS-2 mRNA (RNase protection assay) or protein (immunohistochemistry and western blotting). Tissues also were obtained from control animals. RESULTS: Levels of PGHS-2 mRNA were undetectable in control animals but showed a dramatic increase at 2-4 h in the cortex and retina in animals exposed to ischemia. Detectable but limited PGHS-2 immunoreactivity (IR) was present in the retina and visual cortex from control animals. In piglets not subjected to ischemia, PGHS-2 IR was localized mainly to the outer limiting membrane and to the Muller cells. Ischemia induced a marked increase in PGHS-2 IR in the neural retina, with the greatest increase in the photoreceptor layer. PGHS-2 levels in whole retina also increased at 8 h after ischemia. In the intact visual cortex PGHS-2 IR was evident in layers II and V. Ischemia increased the intensity of IR in layers II/III as well as layer V. CONCLUSIONS: Detectable amounts of PGHS-2 protein are present in the piglet retina and visual cortex under normal conditions, but levels are markedly increased 8-12 h after ischemic stress. Enhanced PGHS-2 levels after ischemic stress may contribute to delayed pathological changes of the visual system in the neonate.

Animals↗

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↗

Prostanoid synthesis in the cerebral blood vessels of asphyxiated piglets.

The aim of this study was to examine the effects of asphyxia-reventilation and hyperoxia on the cerebral blood perfusion and prostanoid production of the brain arteries and microvessels in piglets. After 10 min of asphyxia, animals were ventilated with room air, or with 100% O2. Following 4 hours of recovery, the brains were perfused, cerebral arteries were removed and microvessels were isolated from the cortex. The microvessels and the arteries were incubated with 1-14C-arachidonic acid, and the 1-14C-prostanoids were then separated by means of overpressure thin-layer chromatography and were quantitatively determined. Under control conditions, the synthesis of dilatory prostanoids dominated the arachidonate cascade both in the microvessels and in the arteries. Asphyxia and reventilation with room air did not modify the prostanoid production. O2 ventilation greatly affected the prostanoid synthesis of the microvessels, with an enhancement of PGD2 up to 247 +/- 27%. In the arteries, the production of PGI2 and of PGE2 was elevated to 272 +/- 15% and to 148 +/- 13%, respectively. These findings indicate that O2 ventilation after asphyxia substantially increases the extent of prostanoid synthesis in the cerebral blood vessels.

Animals↗

[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↗

Kainic acid rapidly induces cyclooxygenase (COX)-2 in piglet cerebral cortex.

Ischemia/reperfusion (I/R) results in a robust induction of cyclooxygenase (COX)-2 in the newborn brain via unknown mechanisms, but glutamate release and activation of KA receptors may be involved. We examined effects of local KA (3-300 micromol/l for 10 min) treatment on cortical COX-2 expression in anesthetized piglets using a closed cranial window. Treated and corresponding control tissue samples were collected 0.5-10 h after treatment. COX-2 mRNA and protein levels were assessed using RNase protection assay and immunohistochemistry, respectively. KA elicited reproducible dose-dependent increases in cortical COX-2 mRNA unaffected by indomethacin or N(G)-nitro-L-arginine methyl ester pretreatment. COX-2 mRNA levels were elevated at 30 min, peaked at 2 h, but remained enhanced for up to 10 h after KA. Neuronal COX-2 immunoreactivity was also enhanced compared with the control side in all cortical layers 8h after KA. In summary, activation of KA receptors may be involved in the neuronal induction of COX-2 after I/R in the newborn.

Animals↗

Capsaicin-sensitive mechanisms are involved in cortical spreading depression-associated cerebral blood flow changes in rats.

We tested the hypothesis that capsaicin-sensitive mechanisms play a role in the cortical spreading depression (CSD)-related changes in cortical blood flow (CBF). CBF was measured with laser Doppler flowmetry in anesthetized rats. The animals were treated with capsaicin before (48 h-2 weeks) or during the experiments. This agent is thought to stimulate small-diameter sensory nerve fibers selectively and to deplete stored peptides. In the vehicle-treated group (n=8), the peak value of the CSD-associated hyperperfusion was 257+/-12% above the baseline (mean+/-SEM, P<0.05). In the groups treated with 20 and 40 microg/kg or 20 mg/kg capsaicin, there were only small decreases in CBF. In the groups treated with 100 mg/kg capsaicin, the CSD-associated hyperemia was reduced at 48 h (158+/-7%, P<0.05). However, at 96 h a transient hyperresponsiveness (390+/-38%, P<0.05) was observed, which had disappeared by 2 weeks. These results indicate that the manipulation of sensory neuropeptide stores results in a biphasic effect on CSD-induced CBF responses.

Animals↗

Glibenclamide enhances cortical spreading depression-associated hyperemia in the rat.

We investigated the contribution of ATP-sensitive potassium channels (K(ATP)) and calcium-activated potassium channels (Kca2+) to cortical spreading depression (CSD)-associated hyperemia using the rat closed cranial window model. The peak CBF response was enhanced by 12 +/- 5, 13 +/- 4, and 28 +/- 8% (p<0.01) of the control with 10(-6), 10(-5) and 10(-4) mol/l glibenclamide (glyb), a K(ATP) antagonist, respectively. We also calculated the area under the CBF curve to fully represent the extent of hyperemia during CSD. The area increased by 30 +/- 8 (p<0.05), 72 +/- 31 (p<0.05) and 88 +/- 20% (p<0.05) of the control with 10(-6), 10(-5) and 10(-4) mol/l glyb, respectively. However, charybdotoxin (CTX), a Kca2+ antagonist showed no effect. The effect of glyb was inhibited by pretreatment with 5 mg/kg indomethacin. We conclude that activation of K(ATP), perhaps associated with neurons, plays an inhibitory role in the CSD-associated hyperemia via an indomethacin-sensitive mechanism.

Animals↗

Effect of mating system, flushing procedure, progesterone dose and donor ewe age on the yield and quality of embryos within a MOET program in sheep.

Multiple ovulation and embryo transfer (MOET) has the potential to increase the rates of genetic improvement in sheep. However, better realization of this potential requires a higher yield of transferable embryos. Thus we investigated some factors that may contribute to high embryo yield and quality under field conditions, as part of an ongoing MOET program. Comparison of the effects of 2 breeding systems (natural service plus laparoscopic intrauterine AI vs natural service only) on embryo yield and quality indicated that while AI did not affect embryo recovery, it significantly (P < 0.05) improved fertilization rate and embryo quality, and increased (P < 0.05) embryo survival rate after transfer to recipients. Two flushing procedures (the original semi-laparoscopic and a modified version) were compared for effects on embryo recovery. The modifications made to the original collection method increased (P < 0.001) embryo recovery from 69.0 +/- 2.4 to 83.2 +/- 0.6%. The effects of the progestagen priming dosage during superovulatory treatment and ewe age on MOET outcome were also investigated. Donor ewes primed with 30-mg progestagen sponges came into estrus 1.9 h earlier (P < 0.05) than those primed with 45-mg sponges, but there was no difference in ovulation rate or embryo recovery, or in embryo survival after transfer between the 2 regimens. However, Chi-square analysis indicated a significant benefit in favor of the higher progesterone dose on both fertilization (P < 0.01) and embryo quality (P < 0.001). Age of donor ewe did not significantly affect the timing of estrus, fertilization rate or embryo survival after transfer. While adult ewes had higher (P < 0.05) ovulation rates and embryo yields, shearling ewes produced a much higher proportion of Grade 1 embryos (P < 0.05).

Aging↗

Impaired microvascular response to cholinergic stimuli in primary Sjögren's syndrome.

OBJECTIVE: Signs of a parasympathetic dysfunction have been revealed in primary Sjögren's syndrome (SS). Its role in the pathogenesis and the clinical picture of the disease is not clear. To investigate the responsiveness of SS patients to a cholinergic agonist, a model was used involving examination of the cutaneous microcirculation. The microvascular response to the administration of carbachol was measured, a muscarinic cholinergic agonist. METHODS: Twenty two SS patients and 12 controls were examined. Carbachol and 0.9% saline solution were administered intracutaneously into the forearm skin at two distinct places. Skin blood flow (SBF) in the injected areas was measured continuously before and for 10 minutes after the injections by means of a laser Doppler perfusion monitor. The increase in SBF in response to carbachol (dSBF), reflecting vasodilatation, was calculated by a formula including the baseline and the maximum SBF values after the injections of carbachol and saline solution. RESULTS: The vasodilatation was significantly lower in SS patients than in the controls (mean dSBF: 2.1 (range: 1.0-4.5) versus 3.3 (range: 1.7-7.6), p=0.02). With non-responder patients defined as those in whom a smaller response was observed than in any of the controls, 11 of the 22 SS patients proved to be non-responders to carbachol. Comparisons of demographic, clinical and laboratory characteristics and HLA class II genotypes between responder and non-responder SS patients did not show any significant differences. CONCLUSIONS: A diminished or absent response to carbachol indicates a cholinergic dysfunction in SS patients. A disturbance in the neurotransmission at a receptorial or postreceptorial level is hypothesised. Unresponsiveness to cholinergic stimuli may contribute to exocrine insufficiency.

Adult↗

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↗