Investigation of the protective effects of piceatannol on experimental subarachnoid hemorrhage in rats.

BACKGROUND: Subarachnoid hemorrhage (SAH) is one of the most prevalent brain injuries in humans which has poor prognosis and high mortality rates. Due to several medical or surgical treatment methods, a gold standard method doesn't exist for SAH treatment. Piceatannol (PCN), a natural analog of resveratrol, was reported to reduce inflammation and apoptosis promising a wide range of therapeutic alternatives. In this study, we aimed to investigate the effects of PCN in an experimental SAH model. The alleviating effects of PCN in the hippocampus in an experimental SAH model were investigated for the first time. METHODS AND RESULTS: In this study, 27 Wistar Albino male rats (200-300 g; 7-8 week) were used. Animals were divided into three groups; SHAM, SAH, and SAH + PCN. SAH model was created with 120 µl of autologous arterial tail blood to prechiasmatic cisterna. 30 mg/kg PCN was administered intraperitoneally at 1st h after SAH. Neurological evaluation was performed with Garcia's score. RT-PCR was performed for gene expression levels in the hippocampus. Pyknosis, edema, and apoptosis were evaluated by H&E and TUNEL staining. Our results indicated that PCN administration reduced apoptosis (P < 0.01), cellular edema, and pyknosis (P < 0.05) in the hippocampus after SAH. Moreover, PCN treatment significantly decreased the expression levels of TNF-α (P < 0.01), IL-6 (P < 0.05), NF-κB (P < 0.05), and Bax (P < 0.05) in the hippocampus. CONCLUSIONS: Our results demonstrated that PCN might be a potential therapeutic adjuvant agent for the treatment of early brain injury (EBI) following SAH. Further studies are required to clarify the underlying mechanisms and treatment options of SAH.

The role of AQP3 and AQP4 channels in cisplatin-induced cardiovascular edema and the protective effect of melatonin.

BACKGROUND: The present study evaluates the development of edema, the change in the AQP3, AQP4, p53 and Bax gene expressions, and the protective effects of melatonin in rat hearts administered with cisplatin. METHODS AND RESULTS: A total of 28 Wistar albino rats were divided into four groups. The vehicle was administered intraperitoneally (i.p.) to the rats in the control group. The melatonin group (Mel) received melatonin at a dose of 10 mg/kg for 13 days. The cisplatin group (Cis) received cisplatin on days 1, 5, 9 and 13 at a dose of 4 mg/kg. The rats in the cisplatin + melatonin (Cis+Mel) group underwent the procedures both in the Mel and Cis groups. Blood and left ventricular samples were taken and analyzed on day 14 of the study. AQP3, p53 and Bax gene expressions were found to be significantly increased following cisplatin administration compared to the control, while melatonin administration significantly decreased the expression of these genes (p < 0.05). Melatonin administration also significantly decreased the level of AQP4 gene expression compared to the cis. On histological examination, congestion, hemorrhage, extracellular and intracellular edema, and degenerative changes were significantly more common in the Cis than in the control. Melatonin administration significantly decreased intracellular edema (p = 0.010) and degenerative changes (p = 0.010), and the improvement in extracellular edema was close to statistical significance (p = 0.051) in melatonin. CONCLUSIONS: These results indicate that melatonin had an ameliorative effect on myocardial edema and AQP channels, and that it may be used as a protective molecule against myocardial edema secondary to cisplatin administration.

Melatonin ameliorates sodium valproate-induced hepatotoxicity in rats.

Valproic acid (VPA) is a anticonvulsant and mood-stabilizing agent used to treat epilepsy in patients of all ages. However, it can cause hepatotoxicity with increased oxidative stress. Melatonin (MEL) is known as antioxidant and antiinflammatory agent. Therefore, the present study designed to investigate the probable protective role of melatonin against VPA-induced liver toxicity. For that purpose, 28 Wistar rats were randomly selected and divided into four groups, namely the Group C (vehicle), VPA (500 mg/kg/day VPA), MEL + VPA (10 mg/kg/day melatonin + 500 mg/kg/day VPA) and MEL (10 mg/kg/day melatonin). The agents were given by oral gavage for 14 days. Blood and liver tissue samples from all the rats were harvested on the 15th day of experiment. Biochemical analyses were conducted on the blood samples. The levels of malondialdehyde (MDA), superoxide dismutase (SOD), alpha glutathione S-transferases (α-GST), nuclear factor-κB (NF-κB), myeloperoxidase (MPO) and changes in gene expression were examined in the liver tissues. Also, liver histopathological analyses were conducted. VPA administration significantly increased the levels of α-GST, MDA, NF-κB and of IL-1ß, TNF-α gene expression in the liver compared to Group C. Moreover, vacuolization, hydropic degeneration, inflammatory cell infiltration, and sinusoidal congestion were commonly detected in the VPA-treated group along with the highest apoptotic index (TUNEL staining) values. Melatonin administration was revealed to exhibit powerful protective properties at cellular, inflammatory and oxidative level activities against VPA-induced liver toxicity. Therefore, melatonin administration may be used as an adjuvant therapy against to VPA-induced liver toxicity.

Adalimumab mitigates ovarian ischemia-reperfusion injury in rats by regulating oxidative stress, apoptosis and resolution of inflammation.

AIM: Ovarian torsion is a rare but an important reason of acute lower abdominal pain in women and associated with serious morbidity and mortality, if not treated promptly. The aim of this study was to evaluate the effects of an antitumor necrosis factor-α antibody on ovarian torsion in a rat model of ischemia-reperfusion (I/R) injury. METHODS: Forty female Wistar Albino rats were used in the present study. The rats were randomly divided into four groups: group I (sham), group II (I/R), group III (I/R + isotonic saline) and group IV (I/R + adalimumab). The I/R model was induced by torsion of both ovaries. Immunohistochemical staining for interleukin-1ß (IL-1ß), nuclear factor-κB (NF-κB), and inducible nitric oxide synthase was performed. Tissue and serum oxidative stress markers in conjunction with apoptotic index (AI) with the terminal deoxynucleotidyl transferase dUTP nick end labeling method were also calculated. RESULTS: Tissue total oxidant status, oxidative stress index and nitric oxide values were significantly decreased, and tissue total antioxidant status was found to be increased in group IV. Inflammation, vascular congestion and hemorrhagia were significantly lower in adalimumab-treated group. Serum oxidative stress markers and tissue malondialdehyde levels did not differ in study groups. The AI was significantly increased in groups 2 and 3. Adalimumab treatment significantly decreased the AI. CONCLUSION: Adalimumab therapy in rats attenuated I/R induced ovarian injury, possibly suppressing inflammation, inhibiting oxidative stress, and altering apoptotic pathways.

Hyperbaric oxygen treatment ameliorates gentamicin-induced nephrotoxicity and expression of kidney injury molecule 1 in the rat model.

In recent years hyperbaric oxygen (HBO2) therapy has been considered as an effective method for the treatment of gentamicin (GM)-induced renal toxicity. However, the findings related to the use of HBO2 for GM toxicity are limited and contradictory. The aim of this study is to investigate the protective role of HBO2 on GM-induced nephrotoxicity. For this purpose, Wistar albino rats (n=28) were randomly divided into four equal groups: C, HBO2, GM and GM+HBO2. GM (100 mg/kg, ip) and HBO2 were applied over seven days. On the eighth day blood and kidney tissue samples were harvested. The albumin, creatinine, and urea levels were determined from serum samples. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activities, malondialdehyde (MDA), total antioxidant status (TAS) and total oxidant status (TOS) values were analyzed spectrophotometrically. The relative expression level of TNF-α, IL-1ß and Kim-1 gene were determined by qRT-PCR assays; histopathologic investigation was completed in kidney tissue samples. Serum urea, albumin and creatinine levels significantly increased in the GM group compared to the GM+HBO2 group. For antioxidant parameters the GM+HBO2 group was not statistically different from the C group but was significantly different compared with the GM group. TNF-α, IL-1ß and Kim-1 gene expression levels in the GM group were statistically increased compared to the GM+HBO2 group (p=0.015, p=0.024, p=0.004) respectively. Severe tubular necrosis, epithelial desquamation and mild peritubular hemorrhage were observed in the GM-administrated group, while HBO2 exposure ameliorated these alterations. In conclusion, HBO2 exposure may be defined as a potential method for the prevention of GM-induced renal toxicity.

Comparison of the effects of various airway devices on hemodynamic response and QTc interval in rabbits under general anesthesia.

UNLABELLED: In this study, we aimed to compare the effects of various airway devices on QTc interval in rabbits under general anesthesia. The subjects were randomly separated into four groups: Group ETT, Group LMA, Group PLA, Group V-gel. Baseline values and hearth rate, mean arterial pressure and ECG was obtained at the 1st, 5th and 30th minutes after administration of anesthesia and placement of airway device and, QTc interval was evaluated. Difference was observed between ET group and V-gel group in the 5th minute mean arterial pressure values (p < 0.05). It was observed that QTc intervals at the 1st and 5th minute in the ET group significantly increased when compared with the other groups (p < 0.05). Again, it was observed that QTc interval of ET group at the 15th and 30th minute was longer when compared with PLA and V-gel groups (p < 0.05). It was also observed that QTc interval of LMA Group at the 5th minute after intubation significantly increased when compared with V-gel group (p < 0.05). It was observed that HR values of ETT group at the 1st, 5th and 15th minutes after intubation increased with regards to PLA and V-gel groups (p < 0.05). It was determined that the 30th minute hearth rate of ETT group was higher when compared to V-gel group (p < 0.05). CONCLUSION: In our study we observed that V-gel Rabbit affected both hemodynamic response and QT interval less than other airway devices.

Melatonin regulates oxidative stress and apoptosis in fetal hearts of pinealectomised RUPP rats.

OBJECTIVE: This study aimed to investigate the effects of melatonin on cardiac oxidative stress and apoptosis in the fetal heart in RUPP rats. METHODS: The fetal heart samples were obtained from melatonin administrated RUPP rats. RESULTS: Our results indicate that preeclampsia exacerbated by melatonin deficiency triggers hypoxic conditions, both mis/un-folded protein response, oxidative stress-induced DNA damage and apoptosis. Melatonin treatment provided significant therapeutic effects on fetal hearts via regulating all these stress response at cellular and molecular levels. CONCLUSION: Melatonin may be considered as a potential molecule for development of preventive strategies to reduce the PE induced risk of cardiovascular diseases in offspring.

The correlation between the plasma nitric oxide levels and QT/QTc interval in conscious rabbits.

The current study was undertaken to investigate the effects of NOx (plasma concentrations of nitrate plus nitrite which are plasma nitric oxide (NO) metabolites) over QT interval and to determine the level of correlation between them in conscious rabbits. For this purpose, twenty-one New Zealand rabbits (5-7 months old) were used and randomly assigned into the following three groups: control (CG; n = 7, 1 ml isotonic NaCl solution per animal/day), L-arginine (ARG-G; n = 7, L-arginine solution 200 mg/kg/day) and L-NAME (NAME-G; n = 7, L-NAME solution 100 mg/kg/day). Injections were performed intraperitoneally at 9:00 a.m. for 9 days. Blood samples were collected 2 h after the injections on day 1, 5 and 9 and the concentration of plasma NOx was determined using a colorimetric method. ECG was also recorded 2 h after the injection on 1st, 5th and 9th days. The heart rate, QT intervals, corrected QT intervals (QTc) and QT dispersion (QTd), QTc dispersion (QTcd) values were calculated from the ECG recordings. Statistically significant differences were observed between HR, QT and QTc values in all groups for all days (p < 0.001). QTd and QTcd values were found statistically significant different in NAME-G compared to CG and ARG-G (p < 0.001). It was also determined that there was a statistically significant correlation between the NOx and HR and QT and QTc in all days. It is concluded from this study that NO is an important molecule for the electrical activation of heart and has effects on the duration of QT/QTc interval, which should be taken into consideration by the physicians. In addition, application of the L-arginine should be further studied.

Melatonin attenuates caspase-dependent apoptosis in the thoracic aorta by regulating element balance and oxidative stress in pinealectomised rats.

The aim of this study was to explain the possible mechanisms by which melatonin deficiency results in cardiovascular injury and to investigate the effects of melatonin administration on important signalling pathways and element equilibrium in the thoracic aorta (TA). For this purpose, we analysed the cellular and molecular effects of melatonin deficiency or administration on oxidative stress, DNA damage, molecular chaperone response, and apoptosis induction in TA tissues of pinealectomised rats using ELISA, RAPD, qRT-PCR, and Western blot assays. The results showed that melatonin deficiency led to an imbalance in essential element levels, unfolded or misfolded proteins, increased lipid peroxidation, and selectively induced caspase-dependent apoptosis in TA tissues without significantly affecting the Bcl-2/BAX ratio (2.28 in pinealectomised rats, 2.73 in pinealectomised rats treated with melatonin). In pinealectomised rats, the genomic template stability (80.22%) was disrupted by the significantly increased oxidative stress, and heat shock protein 70 (20.96-fold), TNF-α (1.73-fold), caspase-8 (2.03-fold), and caspase-3 (2.87-fold) were markedly overexpressed compared with the sham group. Melatonin treatment was protective against apoptosis and inhibited oxidative damage. In addition, melatonin increased the survivin level and improved the regulation of element equilibrium in TA tissues. The results of the study indicate that melatonin deficiency induces TNF-α-related extrinsic apoptosis signals and that the administration of pharmacological doses of melatonin attenuates cardiovascular toxicity by regulating the increase in the rate of apoptosis caused by melatonin deficiency in TA tissue of Sprague-Dawley rats.

The Role of Melatonin in Oxidative Stress, DNA Damage, Apoptosis and Angiogenesis in Fetal Eye under Preeclampsia and Melatonin Deficiency Stress.

Aim: The aim of this study was to investigate the possible mechanisms of ocular damage induced by pinealectomy (PNX) and preeclampsia (PE), and to determine the cellular and molecular effects of melatonin treatment on oxidative stress, DNA damage, molecular chaperone responses, induction of apoptosis and angiogenesis in the fetal eye of both PNX and PNX+PE animals. Material and Methods: We analysed therapeutic potential of melatonin on fetal eye damage in PNX and PNX+PE animals using Malondialdehyde (MDA), Random Amplified Polymorphic DNA (RAPD), qRT-PCR and Western blot assays. Results: Our study presents three preliminary findings: (a) in fetal eye tissues, PNX and PNX+PE significantly induce oxidative damage to both DNA and protein contents, leading to a dramatic increase in caspase-dependent apoptotic signalling in both mitochondrial and death receptor pathways; (b) the same conditions trigger hypoxia biomarkers in addition to significant overexpression of HIF1-α, HIF1-ß, MMP9 and VEGF genes in the fetal eye; (c) finally, melatonin regulates not only the expression of genes encoding antioxidant enzymes and increase in DNA damage as well as lipid peroxidation but also limits programmed cell death processes in the fetal eye of PNX and PNX+PE animals . Furthermore, melatonin can relatively modulate genes in the HIF1 family, TNF-α and VEGF, thus acting as a direct anti-angiogenic molecule. In conclusion, both PNX and PNX+PE induce ocular damage at both cellular and molecular levels in fetal eye tissue of rats. Conclusion: Our results clearly indicate the potential of melatonin as a preventative therapeutic intervention for fetal ocular damage triggered by both PNX and PNX+PE.

Does the lower nitric oxide level cause cardiovascular changes in major depressed women?

In the recent years, studies have revealed higher incidence of cardiovascular diseases in patients with major depression (MD). A role of plasma nitric oxide (NO) levels in these diseases has been suggested. Hence, aim of the current study was to determine plasma NO, QT, corrected QT (QTc) and systolic and diastolic blood pressures (SBP-DBP) in healthy women (HW) and in women with MD and to interrelate these values with plasma NO levels. Thirty MD women (average 32 years old) and 28 HW (average 28-years old) were included in this study. Nitric oxide values were determined from plasma by spectrophotometric method. Blood pressure was measured in the left arm using an auscultation method. QT and QTc values were obtained from electrocardiographic records. For the calculation of QTc values Bazett's formula was applied. MD group had significantly lower plasma NO levels compared to HW (12.7 +/- 1.4 vs. 21.82 +/- 3.5 microM, respectively, p < 0.05). Mean SBP and DBP were higher in MD group (120/72 vs. 109/65 mmHg; p < or = 0.001). In MD patients, QT and QTc intervals were significantly longer compared to the HW (p < 0.01 and p < 0.001, respectively). There was a significant negative correlation between plasma NO levels and SBP in MD group (r = -0.50; p < 0.01). There was no relationship between plasma NO levels and QT or QTc intervals. In conclusion, lower plasma NO levels, longer QT and QTc intervals and higher SBP and DBP values in MD patients suggest (1) that cardiovascular disease risk is higher in these patients and (2) this needs a special attention by the clinicians.

Effects of xylazine, medetomidine, detomidine, and diazepam on sedation, heart and respiratory rates, and cloacal temperature in rock partridges (Alectoris graeca).

In this study, heart and respiratory rates, cloacal temperature, and quality of sedation were evaluated before (0 min) and after (10, 20, and 30 min) i.m. administration of xylazine (10 mg/kg; n = 7), medetomidine (75 li; n = 6), detcmidine (0.3 mg/kg; n = 6), or diazepam (6 mg/kg; n = 7) in rock partridges (Alectoris graeca). All partridges recovered from sedation without any disturbance. Xylazine and diazepam administration did not induce significant changes in heart rate, which did decrease significantly after medetomidine and detomidine administration (P < 0.001). Mean respiratory rate was decreased dramatically at 20 and 30 min after xylazine (P < 0.001) and medetomidine (P < 0.005) administration, and at all stages of sedation after detomidine injection (P < 0.001), whereas there was not any significant change after diazepam injection. In all groups, cloacal temperature measured at 10, 20, and 30 min tended to decrease compared with baseline values. Sedative effects of the drugs started within 2.1+/-0.2 min for detomidine, 2.6 +/- 0.4 min for diazepam, 3.1 -+/-.4 min for xylazine, and 4.8+/-0.8 min for medetomidine application. There was an extreme variability in time to recovery for each drug: 205 +/-22.2 min for xylazine, 95 -12.2 min for medetomidine, 260+/-17.6 min for detomidine, and 149 + 8.3 min for diazepam. In conclusion, xylazine, medetomidine, detomidine, and diazepam produced sedation, which could permit some clinical procedures such as handling and radiographic examination of partridges to occur. Of the four drugs, xylazine produced stronger and more efficient sedation compared to the others, which could permit only minor procedures to be performed. However, depending on the drug used, monitoring of heart and respiratory rates and cloacal temperature might be required.

Major Ozonated Autohemotherapy Preconditioning Ameliorates Kidney Ischemia-Reperfusion Injury.

Medical ozone has therapeutic properties as an antimicrobial, anti-inflammatory, modulator of antioxidant defense system. Major ozonated autohemotherapy (MOA) is a new therapeutic approach that is widely used in the treatment of many diseases. The objective of the present study was to determine whether preischemic application of MOA would attenuate renal ischemia-reperfusion injury (IRI) in rabbits. Twenty-four male New Zealand white rabbits were divided into four groups, each including six animals: (1) Sham-operated group, (2) Ozone group (the MOA group without IRI), (3) IR group (60 min ischemia followed by 24 h reperfusion), and (4) IR + MOA group (MOA group). The effects of MOA were examined by use of hematologic and biochemical parameters consisting of neutrophil to lymphocyte ratio (NLR), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), ischemia-modified albumin (IMA), total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI). In addition, the histopathological changes including the tubular brush border loss (TBBL), tubular cast (TC), tubular necrosis (TN), intertubular hemorrhage and congestion (IHC), dilatation of bowman space (DBS), and interstitial inflammatory cells infiltration (IECI) were evaluated. In the IR group, compared to the Sham group, biochemical parameters indicating oxidative stress, NLR, IL-6, TNF-α, IMA, TOS, and OSI have increased. MOA reduced inflammation and oxidative stress parameters. Although TAS values have decreased in the IR group and increased in the MOA-pretreated group, no significant changes in TAS values were detected between the IR and MOA groups. The total score was obtained by summing all the scores from morphological kidney damage markers. The total score has increased with IR damage when compared with the Sham group (13.83 ± 4.30 vs 1.51 ± 1.71; p = 0.002). But, the total score has decreased significantly after application of MOA (5.01 ± 1.49; p = 0.002; compared with the IR group). MOA preconditioning is effective in reducing tissue damage induced in kidney ischemia-reperfusion injury. The protective effect of MOA is mediated via reducing inflammatory response and regulating of reactive oxygen species (ROS). Renal histology also showed convincing evidence regarding MOA's protective nature against kidney injury induced renal ischemia-reperfusion. Consequently, MOA might be helpful in protecting the kidneys from IR-induced damage in humans, probably through the anti-inflammatory effect and reducing the total oxidant status.

Evidence of three maternal lineages in Near Eastern sheep supporting multiple domestication events.

The variability of mtDNA was analysed in local sheep breeds reared throughout Turkey, for which a fragment of the D-loop region and the complete cytochrome b were sequenced. Phylogenetic analyses performed independently for the D-loop and the Cyt b gene revealed three clearly separated clusters indicating three major maternal lineages, two of which had been previously described as types B and A. The new type, C, was present in all the breeds analysed and showed considerable mtDNA variability. Divergence time was obtained on the basis of Cyt b gene and was estimated to be around 160,000-170,000 years ago for lineages B and A, whereas the divergence of lineage C proved to have occurred earlier (between 450,000 and 750,000 years ago). These times greatly predate domestication and suggest that the origin of modern sheep breeds was more complex than previously thought and that at least three independent sheep domestication events occurred. Our results, together with archaeological information and the current wild sheep populations in the Near East region support the high importance of this area in the sheep domestication process. Finally, the evidence of a third maternal lineage has important implications regarding the history of modern sheep.

The investigation of airway management capacity of v-gel and cobra-PLA in anaesthetised rabbits.

PURPOSE: To evaluate the applicability and airway management capacity of v-gel® and Cobra PLA in rabbit anaesthesia during assisted (AV) or controlled ventilation (CV). METHODS: This study was carried out in 44 adult New Zealand white rabbit. Baseline arterial pH, PaCO2 and PaO2 values were recorded. Anaesthesia was induced with 5 mg/kg xylasine and 35 mg/kg ketamine HCI combination. AV rabbits were assigned as; control (CG-AV; n=5), LMA (LMA-AV; n=5), cobra PLA (PLA-AV; n=5) and v-gel (v-gelAV; n=5). Rabbits have CV were also assigned as; ET (ET-CV; n=6), LMA (LMA-CV; n=6), cobraPLA (PLA-CV; n=6) and v-gel (v-gelCV; n=6). All measurements were repeated 1st, 5th, 15th and 30th mins during anaesthesia. RESULTS: The less insertion time, number of attempt and complications are recorded in v-gel applied rabbits compared to other apparatus. For arterial pH values significant differences are recorded in especially at 15th and 30th min between groups of CV (p<0.005 or p<0.001). All groups had similar results with each other during anaesthesia for PaCO2 except for LMA-CV group. CONCLUSION: The v-gel may be used as airway device in rabbit anaesthesia undergoing AV or CV and also can be a suitable alternative to endotracheal tubes and laryngeal mask airway.

Blood gas analyzer utility in evaluating oxygen kinetics of the aqueous humor.

PURPOSE: To measure the partial pressure of oxygen (PO2) and carbon dioxide (PCO2) and the pH of aqueous humor (AH) and arterial blood samples from rabbits using a blood gas analyzer. METHODS: Twenty New Zealand rabbits were anesthetized intramuscularly with ketamine and xylazine and were then allowed to breathe room air. Using a gas blood analyzer, arterial blood and AH samples were analyzed for PO2, PCO2, and pH. RESULTS: The mean arterial blood pressure was 87.14 ± 15.0 mmHg. The mean blood and AH PO2 were 95.18 ± 11.76 mmHg and 88.83 ± 9.92 mmHg, the mean blood and AH PCO2 were 25.86 ± 5.46 mmHg and 29.50 ± 5.36 mmHg, and the mean blood and AH pH were 7.38 ± 0.06 and 7.33 ± 0.09, respectively. CONCLUSIONS: The blood gas analyzer was easily employed to evaluate the aqueous humor in rabbits. When comparing the results of studies evaluating aqueous PO2, care should be taken to determine the methods used in these studies.

Tylosin does not affect GnRH-induced LH secretion in rams.

The aim of this study was to investigate the effect of a therapeutic dose of Tylosin (Tylan 50) on gonadotropin releasing hormone (GnRH)-induced luteinizing hormone (LH) secretion in sheep. A total of 10 mature rams were divided into two groups by balancing body weights (bw) and body condition scores. Five of the rams received 10mg/kg Tylosin intramuscularly (i.m., Tylosin group), while the other five were given placebo (Control group), for 5 days. On Day 5, all the rams were injected intravenously (i.v.) with the GnRH agonist Ovarelin at 0.1 microg/kg bw. Blood samples were collected at -30, 0, 30, 60, 90, 120, 150, 180, 210, 240, and 270 min for measuring LH levels in the plasma. Three days after the cessation of Tylosin application (Day 8) the injection of GnRH was repeated at the same dose. Although LH secretion appeared to be lower on Day 8 compared to Day 5, there were no significant differences between the groups for the mean LH concentrations, total LH secretion, peak LH concentrations, timing of LH peak, duration of LH secretion, and LH secretions on Days 5 and 8. These results indicate the absence of a negative effect of a therapeutic dose of Tylosin on GnRH-induced LH secretion in rams.

Electrocardiography of rock partridges (Alectoris graeca) and chukar partridges (Alectoris chukar).

Standard limb, six lead (I, II, III, aVR, aVL, and aVF) electrocardiograms (ECGs) were recorded in 10 awake mature rock partridges (Alectoris graeca) and 10 chukar partridges (Alectoris chukar). Durations and amplitudes of P and T waves and QRS complexes, durations of P-Q and Q-T intervals, and mean heart rates were calculated from the lead II ECGs. All observable P and T waves were negative in aVR and aVL, whereas they were positive in all remaining leads. The most frequent forms of QRS complex were r-s (r-S) and q-r (q-R). A Q wave was observed in all aVR and aVL leads in both species. Chukar partridges had significantly higher amplitudes of P and T waves and QRS complexes than rock partridges. Mean heart rates were 310+/-15 beats/min and 317+/-19 beats/min for chukar partridges and rock partridges, respectively. Mean electrical axes, calculated from leads II and III, were -99+/-6.3 degrees and -95+/-1.7 degrees for chukar partridges and rock partridges, respectively. Clear ECGs were easily obtainable without anesthesia or sedation.

Comparison of effects of sugammadex and neostigmine on QTc prolongation in rabbits under general anesthesia.

PURPOSE: To compare the effects of sugammadex and neostigmine, used to antagonize the effects of rocuronium, on the QTc interval. METHODS: This study used 10 adult New Zealand white rabbits of 2.5-3.5 kg randomly divided into two groups: sugammadex group (Group S, n:5) and neostigmine group (Group N, n:5). For general anesthesia administering 2 mg/kg iv propofol and 1 mcg/kg iv fentanyl, 0.6 mg/kg iv rocuronium was given. Later to provide reliable airway for all experimental animals V-Gel Rabbit was inserted. The rabbits were manually ventilated by the same anesthetist. After the V-Gel Rabbit was inserted at 2, 5, 10, 20, 25, 27, 30 and 40 minutes measurements were repeated and recorded. At 25 minutes after induction Group N rabbits were given 0.05 mg/kg iv neostigmine + 0.01 mg/kg iv atropine. Group S were administered 2 mg/kg iv sugammadex. RESULTS: Comparing the QTc interval in the rabbits in Group S and Group N, in the 25th, 27th and 30th minute after muscle relaxant antagonist was administered the QTc interval in the neostigmine group rabbits was significantly increased (p<0.05). CONCLUSION: While sugammadex, administered to antagonize the effect of rocuronium, did not significantly affect the QTc interval, neostigmine+atropine proloned the QTc interval.