Hyperemesis gravidarum affects maternal sanity, thyroid hormones and fetal health: a prospective case control study.

PURPOSE: Hyperemesis gravidarum (HG) is a condition of severe nausea or vomiting accompanied by various complications during pregnancy. In the present study, we aimed to demonstrate the effects of HG on mother and fetus health. METHODS: Control and case group were arranged from 50 healthy pregnant women and 50 pregnant women with HG. Information about the participant women was gathered with data collection form and Beck's Depression Inventory (BDI) and State Anxiety Inventory (SAI) were administered to the women. Following an abortion or delivery, the data about birth complications and neonatal health were collected. All laboratory results (blood count, thyroid hormones, electrolyte values and biochemical parameters) were gathered from the laboratory information system used in the hospital. RESULTS: It was found that in the case group, mean postpartum weight, serum hemoglobin, hematocrit and thyroid stimulant hormone levels were lower than control group (p < 0.01). Conversely, case group women have higher T3 and T4 levels than control group (p < 0.01). There was no significant difference between the two groups in terms of intrauterine growth retardation, low birth weight and abortion but it was observed that women with HG had often delivered prematurely. The mean scores of BDI and SAI in the case group were higher than those of control group. CONCLUSION: These results suggested that HG may have adverse effects on both mother and baby's health. Pregnant women with HG should be provided with training and consultancy services and be closely monitored in terms of anemia and thyroid hormones.

The effects of two different exercise programmes on adipose tissue hormones in sedentary middle-aged women.

Adipokines play an important role in obesity and related inflammatory disorders. We aimed to determine the effects of exercise training on serum adipokines. Forty sedentary women were randomly assigned to two groups as aerobic (AE) and core exercise (CE). The exercise programmes were performed 4 days a week for 16 weeks. Blood samples were taken before and after the 8 and 16 weeks training period. Percent changes of each parameter were calculated. Sixteen weeks of exercise caused significant decrease in body weight and fat mass (p < 0.001), significant increase in adiponectin (16.1% in AE, 15.8% in CE group, p < 0.05) and resistin levels (21.1% in AE and 26.6% in CE group, p < 0.05) but had no effect on leptin and ghrelin levels. Eight weeks of exercise had no effect on adipokines except leptin. These data suggest that both exercise programmes have improving effects on body composition, adiponectin and resistin levels.

Blocking of L-type calcium channels protects hippocampal and nigral neurons against iron neurotoxicity. The role of L-type calcium channels in iron-induced neurotoxicity.

Iron plays an important role in maintaining normal brain function. However, iron overload and enhanced hydroxyl radical formation have been implicated as the causative factors of some neurodegenerative disorders such as Parkinson's and Alzheimer's diseases. Calcium is also required for diverse physiological process including secretion of neurotransmitters, synaptic plasticity, gene expression and axonal growth. Iron and calcium are essential for neuronal function but, when present in excessive level, they induce neuronal damage and may even cause neuronal death. Some reports suggest that voltage gated calcium channels (VGCCs) are an alternate route for iron entry into neuronal cell lines under conditions of iron overload. The aim of the present study was to investigate the effects of L-type VGCCs on iron-induced neurotoxicity. Iron neurotoxicity was generated by intracerebroventricular FeCl3 injection. Nicardipine treatment (10 mg/kg/d) was applied to block L-type VGCCs for 10 d. Rats were perfused intracardially under deep urethane anaesthesia after treatment period. Removed brains were processed using the standard histological techniques. The numbers of neurons in hippocampus and substantia nigra of all rats were estimated by stereological techniques. Results of present study show that nicardipine decreased hippocampal and nigral neuron loss from 43.9% to 18.4% and 41.0% to 12.1%, respectively. Outcomes of the present study propose that blocking of L-type VGCCs may reduce the neurotoxic effects of iron by inhibiting the cellular influx of excessive calcium and/or iron ions.

Alpha-tocopherol decreases iron-induced hippocampal and nigral neuron loss.

There are many studies about iron-induced neuronal hyperactivity and oxidative stress. Some reports also showed that iron levels rise in the brain in some neurodegenerative diseases such as Parkinson's (PD) and Alzheimer's disease (AD). It has been suggested that excessive iron level increases oxidative stress and causes neuronal death. Tocopherols act as a free radical scavenger when phenoxylic head group encounters a free radical. We have aimed to identify the effect of alpha-tocopherol (Vitamin E) on iron-induced neurotoxicity. For this reason, rats were divided into three groups as control, iron, and iron + alpha-tocopherol groups. Iron chloride (200 mM in 2.5 microl volume) was injected into brain ventricle of iron and iron + alpha-tocopherol group rats. Same volume of saline (2.5 microl) was given to the rats belonging to control group. Rats of iron + alpha-tocopherol group received intraperitoneally (i.p.) alpha-tocopherol (100 mg/kg/day) for 10 days. After 10 days, rats were perfused intracardially under deep urethane anesthesia. Removed brains were processed using standard histological techniques. The numbers of neurons in hippocampus and substantia nigra of all rats were estimated by stereological techniques. Results of present study show that alpha-tocopherol decreased hippocampal and nigral neuron loss from 51.7 to 12.1% and 41.6 to 17.8%, respectively. Findings of the present study suggest that alpha-tocopherol may have neuroprotective effects against iron-induced hippocampal and nigral neurotoxicity and it may have a therapeutic significance for neurodegenerative diseases involved iron.

The antinociceptive effects of intravenous dexmedetomidine in colorectal distension-induced visceral pain in rats: the role of opioid receptors.

BACKGROUND: In comparison with cutaneous pain, the role of alpha(2)-adrenoceptor (alpha(2)-AR) agonists in visceral pain has not been extensively examined. We aimed to characterize the antinociceptive effect of IV dexmedetomidine on visceral pain in rats and to determine whether antinociception thus produced is mediated by opioid receptors. METHODS: Male Sprague Dawley rats (250-300 g) were instrumented with a venous catheter for drug administration and with enameled nichrome electrodes for electromyography of the external oblique muscles. Colorectal distension (CRD) was used as the noxious visceral stimulus, and the visceromotor response to CRD was quantified electromyographically before and 5, 15, 30, 60, 90, and 120 min after dexmedetomidine or clonidine administration. Antagonists were administered 10 min before dexmedetomidine. After confirmation of normal distribution of data, one-way analysis of variance with the Tukey-Kramer post hoc test was used for multiple comparison. RESULTS: IV administration of dexmedetomidine (2.5-20 microg/kg) and clonidine (10-80 microg/kg) produced a dose-dependent reduction in visceromotor response with 50% effective dose values of 10.5 and 37.6 microg/kg, respectively. Administration of the nonspecific alpha(2)-AR antagonist yohimbine (1 mg/kg), but not the peripherally restricted alpha(2)-AR antagonist MK-467 (1 mg/kg), abolished the antinociceptive effect of dexmedetomidine (10 microg/kg). In addition, inhibition of opioid receptors by naloxone (1 mg/kg) attenuated the antinociceptive effect of dexmedetomidine. CONCLUSION: Our data indicate that IV dexmedetomidine exerts pronounced antinociception against CRD-induced visceral pain and suggest that the antinociceptive effect of dexmedotimidine is mediated in part by opioid receptors, but peripheral alpha(2)-ARs are not involved.

Inhibition of neuronal nitric oxide synthase prevents iron-induced cerebellar Purkinje cell loss in the rat.

Iron plays an important role in maintaining normal brain function. However, in many neurodegenerative diseases abnormal iron accumulation in specific brain regions has been consistently reported. In this study, we investigated the neurotoxic effect of the intracerebroventricularly injected iron on the cerebellar Purkinje cells in the rat and the role of nitric oxide (NO) in this process. The role of NO in rats administered iron (FeCl36H2O) was examined with the use of a donor of NO, L-arginine (L-Arg) and a central selective inhibitor of NO synthase, 7-nitroindazole (7-NI). For this reason, rats were divided into 5 groups: control, iron-injected, iron plus L-Arg, iron plus 7-NI, and iron plus L-Arg plus 7-NI. Means (value +/- standard deviation) of the total numbers of Purkinje cells in the cerebellum were estimated as 337 +/- 23, 209 +/- 16, 167 +/- 19, 305 +/- 26, and 265 +/- 14 thousands in the control, iron, iron plus L-Arg, iron plus 7-NI, and iron plus L-Arg plus 7-NI groups, respectively. Iron treatment alone and the combination of iron and L-Arg caused a significant reduction in the total number of cerebellar Purkinje cells. Therefore, L-Arg increased the Purkinje cell loss induced by treatment with iron. These data show that inhibition of the neuronal NOS by 7-NI can prevent some of the deleterious effects of iron on cerebellar Purkinje cells. Presence of L-arginine decreased the neuroprotective effect of 7-NI.

Neuroprotective effect of aminoguanidine on iron-induced neurotoxicity.

Iron is a commonly used metal to induce neuronal hyperactivity and oxidative stress. Iron levels rise in the brain in some neurodegenerative disorders such as Parkinson's and Alzheimer's diseases. A body of evidence indicates a link between neuronal death and nitric oxide. The present study was performed to investigate whether nitric oxide produced by inducible nitric oxide synthase is involved in iron-induced neuron death. For this purpose rats were divided into four groups: control, iron, aminoguanidine and iron+aminoguanidine. Animals in iron and iron+aminoguanidine groups received intracerebroventricular FeCl3 injection (200 mM, 2.5 microl). Rats belonging to control and aminoguanidine groups received the same amount of saline into the cerebral ventricles. All animals were kept alive for 10 days following the operation and animals in aminoguanidine and iron+aminoguanidine groups received intraperitoneal aminoguanidine injections once a day (100mg/kg day) during this period. After 10 days, rats were perfused intracardially under deep urethane anesthesia. Removed brains were processed using the standard histological techniques. The total numbers of neurons in hippocampus of all rats were estimated with the unbiased stereological techniques. It was found that aminoguanidine decreased mean neuron loss from 43.4% to 20.3%. Results of the present study suggest that aminoguanidine may attenuate the neurotoxic effects of iron by inhibiting inducible nitric oxide synthase.

Role of nitric oxide synthesis inhibitors in iron-induced nigral neurotoxicity: a mechanistic exploration.

ABSTRACT In the central nervous system, nitric oxide (NO) has been suggested to be a cell-to-cell signaling molecule that regulates guanylyl cyclase, aconitase, and iron regulatory protein. NO is also one of the substances that is involved in neuronal death. On the other hand, iron overload and enhanced hydroxyl radical formation have been implicated as the causative factors of some neurodegenerative disorders. The present study was performed to clarify whether nitric oxide is involved in iron-induced neuron death. Neurotoxicity was produced by microinjection of iron chloride (200 mM, 2.5 muL) into the left cerebral ventricle. After the intracerebroventricular (ICV) injection, all animals were kept alive for 10 days. During this period, animals in the iron + L-NAME (N-nitro-L-arginine methyl ester) and iron + aminoguanidine groups received intraperitoneal (IP) L-NAME (30 mg/kg) and aminoguanidine (100 mg/kg) injections once a day, respectively. Rats belonging to the control group also received intraperitoneally the same amount of saline. After 10 days, the rats were perfused intracardially under deep urethane anesthesia. Removed brains were processed using the standard histological techniques. The total numbers of neurons in substantia nigra of all rats were estimated with stereological techniques. It was found that L-NAME significantly decreased nigral cell loss from 43.2% to 14.0%, while aminoguanidine did not affect cell loss. Results of the present study suggest that NOS inhibition by L-NAME seems to have neuroprotective effects on iron-induced nigral neurotoxicity.

Nitric oxide synthesis inhibition attenuates iron-induced neurotoxicity: a stereological study.

Iron overload and enhanced hydroxyl radical formation have been implicated as the causative factors of some neurodegenerative disorders. Therefore, iron is commonly used as a metal to induce neuronal hyperactivity and oxidative stress. A body of evidence indicates a relationship between iron-induced neuronal death and nitric oxide (NO). Data are, however, controversial because it is not clear whether NO has neuroprotective or neurotoxic effects on neurotoxicity. To determine the contribution of NO to iron-induced hippocampal cell loss, l-arginine, the NO synthesis precursor, and a nonselective nitric oxide synthase inhibitor N(G)-nitro-l-arginine methyl ester (l-NAME) were used. Animals were divided into four groups as follows: control, iron, iron+l-NAME and iron+l-arginine. Neurotoxicity was produced by microinjection of iron chloride (200 mM, 2.5 microl) into the left cerebral ventricle in iron-treated groups while control group rats received same amount of saline. After the intracerebroventricular injection, all animals were kept alive for 10 days. During this period, animals in iron+l-NAME and iron+l-arginine groups received intraperitoneal (i.p.) l-NAME (30 mg/kg) and l-arginine (1000 mg/kg) injections once a day, respectively. Rats belonging to control group also received the same amount of saline intraperitoneally. After 10 days, rats were perfused intracardially under deep urethane anesthesia. Removed brains were processed using the standard histological techniques. The total numbers of neurons in hippocampus of all rats were estimated with stereological techniques. It was found that l-NAME decreased iron-induced cell loss from 44.7 to 13.7%, while l-arginine increased cell loss from 44.7 to 57.5%. Results of the present study suggest that inhibition of NO synthesis may attenuate the neurotoxic effects of iron.

Neuroprotection by 7-nitroindazole against iron-induced hippocampal neurotoxicity.

(1) Iron plays an important role in maintaining normal brain function. In some neurodegenerative disorders including Parkinson's and Alzheimer's disease, iron levels rise in the brain. It is known that higher iron levels induce neuronal hyperactivity and oxidative stress. A body of evidence indicates a relationship between neuronal death and nitric oxide (NO). The aim of present study was to evaluate the effects of NO produced by neuronal nitric oxide synthase (nNOS) on iron-induced neuronal death. (2) Animals were classified into four groups: control, iron, iron+7-nitroindazole, and iron+vehicle. Rats in iron, iron+7-nitroindazole, and iron+vehicle groups received intracerebroventricular (i.c.v.) FeCl3 injection (200 mM, in 2.5 microl). Rats belonging to control groups received the same amount of saline into the cerebral ventricles. All animals were kept alive for 10 days following the operation. Animals in iron+7-nitroindazole group received intraperitoneal 7-nitroindazole (30 mg/kg/day) injections once a day during this period, while the rats belonging to vehicle group received daily intraperitoneal injection of peanut oil. After 10 days, rats were perfused intracardially under deep urethane anesthesia. Removed brains were processed using the standard histological techniques. (3) The total number of neurons in hippocampus of all rats was estimated with the unbiased stereological techniques. Results of present study show that 7-nitroindazole decreased mean neuron loss from 43% to 11%. Treatment of peanut oil alone did not affect iron-induced hippocampal cell loss with respect to iron group values. (4) Findings of our study suggest that 7-nitroindazole may have neuroprotective effects against iron-induced hippocampal neurotoxicity by inhibiting nNOS.

Anticonvulsive effects of quinine on penicillin-induced epileptiform activity: an in vivo study.

Epilepsy is an important problem in neurological disorders. The common features of all types of epilepsy are the synchronized and uncontrolled discharges of nerve cell assemblies. Recent studies claimed that gap junctions have a critical role in epileptic neuronal events. The aim of present study is to investigate the effects of connexin36 (Cx36) channel blocker quinine on penicillin-induced experimental epilepsy. For this purpose, 4 months old male Wistar rats were used in the present study. Permanent screw electrodes allowing EEG monitoring from conscious animals and permanent cannula providing the administration of the substances to the brain ventricle were placed into the cranium of rats under general anesthesia. At the end of the postoperative recovery period, epileptiform activity was generated by injecting 300 IU crystallized penicillin through the ventricular cannula. When the epileptiform activity, monitored from a digital recording system, reached maximal frequency and amplitude, quinine (200, 400 or 1000 nmol) was administered similar to penicillin. Effects of quinine on epileptiform activity were assessed by both electrophysiological and behavioral analysis. Quinine suppressed epileptiform activity by decreasing the amplitude and frequency of epileptiform spikes and by attenuating the epileptiform behavior. The outcomes of this study suggest that the blockade of Cx36 channels may contribute to the amelioration of epileptic activity.

Anticonvulsive effects of carbenoxolone on penicillin-induced epileptiform activity: an in vivo study.

Epilepsy is an important problem in neurological disorders. Recent studies claimed that gap junctions have a critical role in epileptic neuronal events. The aim of present study is to investigate the effects of gap junction blocker carbenoxolone on penicillin-induced experimental epilepsy. For this purpose, 4-month-old male Wistar rats were used in the present study. Permanent screw electrodes allowing EEG monitoring from conscious animals and permanent cannula providing the administration of the substances to the brain ventricle were placed into the cranium of rats under general anesthesia. At the end of the postoperative recovery period, epileptiform activity was generated by injecting 300 IU crystallized penicillin through the ventricular cannula. Epileptiform activity monitored from a digital recording system, when it reached its maximum intensity, carbenoxolone (100, 200, 500 nmol) was applied in the same way with penicillin. Effects of carbenoxolone on epileptiform activity were assessed by both electrophysiological and behavioral analysis. Carbenoxolone suppressed epileptiform activity by decreasing the amplitude and frequency of epileptiform spikes and by attenuating the epileptiform behavior. The results of this study suggest that the blockade of electrical synapses may contribute to the prevention and amelioration of epileptic activity.

The effects of octanol on penicillin induced epileptiform activity in rats: an in vivo study.

The common features of all types of epilepsy are the synchronized and uncontrolled discharges of nerve cell assemblies. The reason for the pathologically synchronized discharges of the neuron is not exactly known yet. Recent reports claim that gap junctions have a critical role in neuronal synchronization. The present study was planned to investigate the effects of octanol, a gap junction blocker, on penicillin-induced experimental epilepsy. Permanent screw electrodes allowing EEG monitoring from conscious animals and permanent cannula providing the administration of the substances to the brain ventricle were placed into the cranium of rats under general anesthesia. After the postoperative recovery period, epileptiform activity was generated by injecting 300 IU crystallized penicillin through the ventricular cannula. When epileptiform activity, monitored from a digital recording system, reached at its maximum intensity, octanol was applied in the same way as penicillin administered. Application of octanol caused an inhibition in the epileptiform activity. Vehicle solution alone did not affect the epileptiform activity. Results of this study suggest that the blockade of electrical synapses may contribute to the prevention and amelioration of epileptic activity. Production of gap junction blockers selective for connexin types is needed. Further studies on the differential roles of gap junctions on certain epileptiform activities are required.

Anticonvulsive effects of nimodipine on penicillin-induced epileptiform activity.

The common features of all types of epilepsy are synchronized and uncontrolled discharges of nerve cell assemblies. It is believed that calcium ions play an important role in the generation of epileptic activity. Excessive calcium influx into neurons is the first step toward a seizure. The aim of the present study is to investigate whether the calcium channel blocker nimodipine has anticonvulsive effects. The left cerebral cortex was exposed by craniotomy in anaesthetized rats. An epileptic focus was produced by injection of penicillin G potassium (500 units) into the somatomotor cortex. After the epileptiform activity reached maximum frequency and amplitude; nimodipine was injected into the same area. Application of nimodipine caused an inhibition in the electrocorticograms (ECoG). Solvent alone did not affect the epileptiform activity. The results of this study indicate that nimodipine may have anticonvulsant effects.

A calcium channel blocker flunarizine attenuates the neurotoxic effects of iron.

Iron is a metal highly concentrated in liver and brain tissue, and known to induce neuronal hyperactivity and oxidative stress. It has been established that iron levels rise in the brain in some neurodegenerative diseases such as Parkinson's and Alzheimer's diseases (AD). A body of evidence indicates a link between neuronal death and intracellular excessive calcium accumulation. The aim of the present study was to investigate the effects of a calcium antagonist, flunarizine, on neurotoxicity induced by intracerebroventricular (i.c.v.) iron injection. For this reason rats were divided into three groups as control, iron and iron+flunarizine groups. Animals in iron and iron+flunarizine groups received i.c.v. FeCl(3) injection (200 mM, 2.5 microl), while control rats received the same amount of saline into the cerebral ventricles. Rats in iron+flunarizine group also received i.c.v. flunarizine (1 microM, 2 microl) following FeCl(3) injection. All animals were kept alive for ten days following the operation and animals in iron+flunarizine group received intraperitoneal (i.p.) flunarizine injections once a day (10 mg/kg/day) during this period. After ten days, rats were sacrificed. The total numbers of neurons in hippocampus of all rats were estimated with the latest, unbiased stereological techniques. Findings of the present study suggest that flunarizine may attenuate the neurotoxic effects of iron injection by inhibiting the cellular influx of excessive calcium ions.