Combination of paracetamol or ketamine with meperidine enhances antinociception.

OBJECTIVES: Dealing with pain is one of the most important issues of medicine. All of the studies aim to find a drug or combination of drugs in order to have more effective analgesia and less side effects. In this study, we aimed to investigate the antinociceptive effects of combination of paracetamol or ketamine with meperidine. METHODS: In this study, we evaluated the systemic antinociceptive effects of meperidine, paracetamol, and ketamine one by one with their combinations. We used 50 mice (weighing 25-30 g), which were divided into 5 groups with each group consisting of 10 mice. Meperidine was applied to animals with increasing doses and their tail flick latencies (TFL) were noted at 20, 40, 60, 90, 120, 180, and 240 min. The same protocol was repeated after the combination of meperidine with paracetamol or ketamine. RESULTS: There was no analgesic effect on low doses of ketamine and paracetamol at TFL measurements. But the combination of low doses of these drugs with meperidine significantly increased TFL (p < 0.05). CONCLUSION: It was observed that meperidine + ketamine and meperidine + paracetamol combinations have potent analgesic effect.

The effects of L type calcium channels on the electroencephalogram recordings in WAG/RIJ rat model of absence epilepsy.

BACKGROUND: Epilepsy is one of the most important central nervous system disorder and 1% of the total world population suffers from this disorder which require a chronic drug treatment. Most of the researchers suggested that excessive calcium entry into neurons is the main triggering event in the initiation of epileptic discharges but the role of L type calcium channels has not been clarified in absence epilepsy. AIM: In this study, it is aimed to investigate the antiepileptic effects of nifedipine, an L type calcium channel blocker and BAY K8644, an L type calcium channel opener in a genetic model of absence epilepsy in WAG/Rij rats. MATERIALS AND METHODS: Thirty two WAG/Rij rats were allocated into four groups; sham (only saline injected), only nifedipine (an L type calcium channel blocker) injected group (40 µg/2 µl; 60 µg/2 µl; 80 µg/2 µl), only BAY K8644 (1,4 Dihydro-2,6-dimethyl-5-nitro-4-trifluoromethyl- phenyl-3-pyridine carboxylic acid methyl ester) (L-type Ca2+-channel activator) injected group (40 µg/2 µl; 60 µg/2 µl; 80 µg/2 µl) and combination of their most effective doses BAY K8644 (60 µg/2 µl) after nifedipine (60 µg/2 µl) injected group. All agents were given by intracerebroventricular injection. The beta, alpha, theta and delta wave ratios of electroencephalogram recordings and the frequency and duration of SWDs (spike and wave discharges) were analyzed and compared between four groups. RESULTS: Nifedipine increased the number and duration of spike wave discharges whereas BAY K8644 decreased both of them. When BAY K8644 was given after nifedipine, there was no significant difference with control group. CONCLUSIONS: L type calcium channels play an activator role on spike wave discharges and have positive effects on the duration and frequency.

The effect of sorafenib in postoperative adhesion formation in a rat uterine horn model.

OBJECTIVE: Postoperative adhesions are a serious problem. In this study, we aimed to observe the effects of sorafenib in postoperative adhesions and, to examine the effects of sorafenib on tissue levels of vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF). MATERIAL AND METHODS: Twenty female Wistar albino rats were randomized into two equal groups; sorafenib group (sorafenib treated) and control group; then all rats underwent laparotomy. Adhesions were developed by scalping on the anti-mesenteric surfaces of the right uterine horns. After 14 days, adhesions were investigated by using macroscopic, histopathological and immunohistochemical (for VEGF and PDGF) methods. RESULTS: The sorafenib group had lower scores of total adhesions [1 (0-2.5) vs 1.5 (1-4); p: 0.037], staining of VEGF [1 (0-1) vs 1 (1-3); p: 0.029] and PDGF [1 (0-2) vs 2 (1-3); p: 0.006], and vascular proliferation [1 (0-2) vs 2 (1-3); p: 0.038] than the control group. CONCLUSION: The findings of the present study show that sorafenib, a tyrosine kinase inhibitor, significantly reduced postoperative adhesion formation. This effect may be explained by inhibition of VEGF, PDGF, and thus vascular proliferation.

Determination of cerebellar volume in children and adolescents with magnetic resonance images.

Recent studies show that the cerebellum contributes to higher cognitive functions as well as its role on motor system. It is thought that higher cognitive functions continue to develop during childhood and adolescence; therefore, cerebellum develops significantly during these periods. For that reason, this study was carried out in order to determine cerebellar volumes of 90 healthy individuals (40 males, 50 females) aged between 6 and 17 years according to their gender. The individuals were divided into three age groups of 6-9, 10- -13, and 14-17 years, and their cerebellar volumes were found by means of stereological methods using their magnetic resonance images. The cerebellar volumes found were compared among the groups without discriminating genders, among groups according to gender, and again according to gender within each age group. The general average cerebellar volume of the age group 10-13 years was significantly higher than the other two age groups(p 〈 0.05). When the groups were compared according to gender, there was no important difference between the groups in women (p 〉 0.05); as for men, cerebellar volume only in the age group 10-13 years was significantly higher than that in age group 6-9 (p 〈 0.05). When cerebellar volume for ages 6-17 years was compared according to gender (without dividing into age group) there was no significant difference between men and women (p 〉 0.05). It was seen that the cerebellum develops from childhood to adolescence, and reaches peak levels between the ages 10-13 years for both genders.

Effects of methylene blue, pentoxyphylline and enoxaparin on postoperative adhesion formation and markers of angiogenesis in a rat uterine horn model.

OBJECTIVE: Postoperative adhesions still remain as a common and serious problem leading to morbidity, mortality and economic loss. Adhesions are the major cause of postoperative intestinal obstruction, infertility, and chronic pelvic pain. In this study, we aimed to compare adhesion prevention effects of pentoxyphylline, enoxaparin and methylene blue and to investigate the effects of these agents on angiogenesis, which is suggested as an important step in wound healing, in rat a uterine horn model. MATERIAL AND METHODS: Forty female Wistar albino rats were randomized into four subgroups and underwent laparotomy. Adhesions developed following cauterization at the anti-mesenteric surfaces of both uterine horns. After 14 days, adhesions were investigated by using macroscopic, histopathological and immunohistochemical [vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), transforming growth factor (TGF-beta), platelet-derived growth factor (PDGF)] methods. RESULTS: We found that enoxaparin significantly reduced adhesion formation. Pentoxyphylline had no significant effect on adhesion formation, whereas methylene blue had a significant decreasing effect on histopathologically determined adhesion markers and it may affect angiogenesis through PDGF. CONCLUSION: Among three agents, which were intraperitoneally given by a single dose manner in order to prevent postoperative adhesions, methylene blue and enoxaparin exhibited a positive effect, while no such effect was shown with pentoxyphylline.

Reduced uterine perfusion pressure model is not successful to mimic severe preeclampsia.

The aim of the study was to investigate maternal (hemoglobin, hematocrit, and biochemical parameters of blood and urine) and fetal parameters (number and weight of alive fetus) of preeclampsia in a rat model. Placental oxidative stress markers (protein carbonyl, malondialdehyde) and placental antioxidant values (CuZn-superoxide dismutase, glutathione peroxidase) were also measured. Preeclampsia was induced experimentally in timed-pregnant Sprague-Dawley rats by using the reduced uterine perfusion pressure (RUPP) model. Placental oxidative stress that plays a key role in the pathophysiology of placenta-related disorders, most notably preeclampsia (PE) and intrauterine growth restriction (IUGR) were demonstrated by using RUPP model. On day 14 of gestation, silver clips were placed around the aorta below the renal arteries and on the left and right uterine arcade at the ovarian artery. In the RUPP model animals (n = 15), when compared with the normotensive controls (n = 15), arterial pressure on day 19 of gestation was significantly higher in the RUPP rats (151.7 ± 17.6 mmHg) than normal pregnant rats (113.9 ± 11.4 mmHg). The RUPP rats showed a significant increase in protein excretion when compared with the normal pregnant rats (0.3 ± 0.04 vs 0.47 ± 0.07 g/dL) (p < 0.05). Associated with the hypertension in RUPP rats, placental levels of malondialdehyde (2.4 ± 0.2 vs. 1.6 ± 0.2 umol/gm tissue) and protein carbonyl (1.4 ± 0.3 vs. 0.9 ± 0.3 nmol/mg protein) were increased, while superoxid dismutase (0.03 vs 0.42 U/mg protein) and glutathione peroxidase (1.04 ± 0.31 vs 0.76 ± 0.22 U/g protein) were decreased. Pup number (6.6 ± 3.1 vs. 9.93 ± 2.0) and litter weight (17.4 ± 7.7 vs. 22.9 ± 6.7 g) were lower in the preeclamptic group. None of the complete blood counts and biochemical values other than sodium and chlorine were significantly different in preeclamptic group. Our findings suggest that the RUPP model cannot mimic severe preeclampsia; however, further studies using different settings may be helpful to obtain a preeclampsia model that is capable of successfully producing severe preeclampsia findings.

Correlation between birth weight, leptin, zinc and copper levels in maternal and cord blood.

Leptin and zinc are involved in the regulation of appetite. Copper is a trace element regulating the functions of several cuproenzymes that are essential for life. To evaluate the relationship between zinc and copper status and the leptin system in humans, we examined whether leptin concentrations in the mother and the newborn correlate with the weight of mother, placenta and newborn. A total of 88 pregnant women at 38-42 weeks' gestation were studied. All infants were categorized as small for gestational age (SGA) (n = 16), average for gestational age (AGA) (n = 59) or large for gestational age (LGA) (n = 13). Leptin, zinc, and copper levels were measured in maternal and cord serum at birth. Maternal BMI and placental weight of the LGA groups were significantly higher than those of the SGA and AGA groups. Cord and maternal leptin levels of the SGA groups were significantly lower than those of the AGA and LGA groups. Maternal serum leptin levels were positively correlated with BMI and maternal zinc levels in all groups. Cord serum leptin levels of all groups were positively correlated with birth weight and placental weight. Birth weight was negatively correlated with maternal and cord copper level of all groups. Umbilical leptin concentrations of SGA newborns correlated with leptin concentrations of their mothers. In all pregnancies, birth weight increases in association with increase in cord leptin level. Our results suggest that maternal zinc but not copper level has an effect on maternal serum leptin levels. The increase in copper level in both maternal and cord blood may contribute to restriction in fetal growth.

Correlation between birth weight, leptin, zinc and copper levels in maternal and cord blood

Leptin and zinc are involved in the regulation of appetite. Copper is a trace elementregulating the functions of several cuproenzymes that are essential for life. Toevaluate the relationship between zinc and copper status and the leptin system inhumans, we examined whether leptin concentrations in the mother and the newborncorrelate with the weight of mother, placenta and newborn. A total of 88 pregnantwomen at 38-42 weeks’ gestation were studied. All infants were categorized as smallfor gestational age (SGA) (n=16), average for gestational age (AGA) (n=59) or largefor gestational age (LGA) (n=13). Leptin, zinc, and copper levels were measured inmaternal and cord serum at birth. Maternal BMI and placental weight of the LGAgroups were significantly higher than those of the SGA and AGA groups. Cord andmaternal leptin levels of the SGA groups were significantly lower than those of theAGA and LGA groups. Maternal serum leptin levels were positively correlated withBMI and maternal zinc levels in all groups. Cord serum leptin levels of all groupswere positively correlated with birth weight and placental weight. Birth weight wasnegatively correlated with maternal and cord copper level of all groups. Umbilicalleptin concentrations of SGA newborns correlated with leptin concentrations of theirmothers. In all pregnancies, birth weight increases in association with increase in cordleptin level. Our results suggest that maternal zinc but not copper level has an effecton maternal serum leptin levels. The increase in copper level in both maternal andcord blood may contribute to restriction in fetal growth (AU)

No disponible

Correlation between birth weight, leptin, zinc andcopper levels in maternal and cord blood

Leptin and zinc are involved in the regulation of appetite. Copper is a trace elementregulating the functions of several cuproenzymes that are essential for life. Toevaluate the relationship between zinc and copper status and the leptin system inhumans, we examined whether leptin concentrations in the mother and the newborncorrelate with the weight of mother, placenta and newborn. A total of 88 pregnantwomen at 38-42 weeks’ gestation were studied. All infants were categorized as smallfor gestational age (SGA) (n=16), average for gestational age (AGA) (n=59) or largefor gestational age (LGA) (n=13). Leptin, zinc, and copper levels were measured inmaternal and cord serum at birth. Maternal BMI and placental weight of the LGAgroups were significantly higher than those of the SGA and AGA groups. Cord andmaternal leptin levels of the SGA groups were significantly lower than those of theAGA and LGA groups. Maternal serum leptin levels were positively correlated withBMI and maternal zinc levels in all groups. Cord serum leptin levels of all groupswere positively correlated with birth weight and placental weight. Birth weight wasnegatively correlated with maternal and cord copper level of all groups. Umbilicalleptin concentrations of SGA newborns correlated with leptin concentrations of theirmothers. In all pregnancies, birth weight increases in association with increase in cordleptin level. Our results suggest that maternal zinc but not copper level has an effecton maternal serum leptin levels. The increase in copper level in both maternal andcord blood may contribute to restriction in fetal growth (AU)

No disponible

Cervical spinal cord stimulation increases cerebral cortical blood flow in an experimental cerebral vasospasm model.

BACKGROUND: Cerebral microcirculatory changes during cerebral vasospasm after aneurysmal subarachnoid haemorrhage (SAH) are still controversial and uncertain. The aim of our study is to demonstrate that spinal cord stimulation (SCS) augments cerebral cortical microcirculatory blood flow in an experimental cerebral vasospasm model by using Laser Doppler Flowmetry (LDF). METHOD: The experiments were carried out on 24 New Zealand rabbits. Three experimental groups were designed. In group 1, Cerebral cortical blood flow (CCoBF) was evaluated by LDF in 8 rabbits. In group 2, Intracisternal saline injection and cervical epidural electrode placement without SCS were performed in 8 animals before LDF. In group 3, LDF was performed before and after SCS on the 4th day of SAH in 8 rabbits. CCoBF parameters obtained from LDF data were compared. FINDINGS: The occurrence of vasospasm after SAH was demonstrated with significant changes in LDF values. In all SAH animals, SCS resulted in significant increase (approximately 30%) in CCoBF. This increase was observed to continue even after the cessation of the stimulation. CONCLUSIONS: These results indicate that SCS improves cortical ischemia due to vasospasm after induced SAH. The cervical SCS may constitute a new therapeutic modality in treating disturbed CCoBF due to vasospasm.