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Adult Male Sprague (adult + male_sprague)
Selected AbstractsThe combined neuroprotective effects of lidocaine and dexmedetomidine after transient forebrain ischemia in ratsACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 9 2009T. GOYAGI Background: We investigated whether coadministration of lidocaine and dexmedetomidine would reduce brain injury following transient forebrain ischemia in rats to a greater extent than either drug alone. Methods: Adult male Sprague,Dawleyrats were anesthetized with halothane to maintain normocapnia and normoxia. Rats received subcutaneous injection of saline 1 ml/kg, lidocaine 10 mg/kg, dexmedetomidine 3 ,g/kg, or lidocaine 10 mg/kg plus dexmedetomidine 3 ,g/kg. Thirty minutes after the drug injection, forebrain ischemia was induced by hemorrhagic hypotension and occlusion of the bilateral carotid arteries, and was confirmed by isoelectric EEG. At the end of 10-min ischemia, rats were reperfused. The same dose of drugs was administered 3, 24, and 48 h after ischemia. Neurological examination was done at 1, 2, and 7 days after ischemia. Seven days after ischemia, the brain was stained with hematoxylin and eosin. We counted ischemic cells in the CA1 hippocampal region, striatum, and cerebral cortex. We also measured extracellular glutamate and norepinephrine concentration in hippocampal CA1 in the four groups. Results: As compared with saline-treated rats, rats receiving dexmedetomidine plus lidocaine showed less than neurological deficit scores at 2 and 7 days after ischemia, and had less ischemic cells in the CA1 region. However, administration of dexmedetomidine plus lidocaine did not alter the area under the glutamate concentration curve and norepinephrine concentration during ischemia in the CA1 region, compared with saline-treated rats. Conclusions: Our results suggest coadministration of lidocaine and dexmedetomidine improves the neurological outcome without alteration of glutamate and norepinephrine concentrations during forebrain ischemia in rats. [source] Protective effects of baicalin on ligature-induced periodontitis in ratsJOURNAL OF PERIODONTAL RESEARCH, Issue 1 2008X. Cai Background and Objective:, Baicalin is a flavonoid compound purified from the medicinal plant, Scutellaria baicalensis Georgi, and has been reported to possess anti-inflammatory and antioxidant activities. The purpose of this study was to test the ability of baicalin to influence the progression of experimental periodontitis in rats, as well as the expression of cyclooxygenase-2 and inducible nitric oxide synthase. Material and Methods:, Adult male Sprague,Dawley rats were subjected to placement of a nylon thread around the bilateral lower first molars and killed after 7 d. Baicalin (50, 100 or 200 mg/kg) was supplied to the animals by oral gavage, starting 1 d before the induction of periodontitis. The ligature group consisted of rats subjected to periodontitis and receiving vehicle (0.5% carboxymethylcellulose) alone. The alveolar bone loss and the area fraction occupied by collagen fibers were assessed. The expression of cyclooxygenase-2 and inducible nitric oxide synthase protein in the gingiva were detected by immunohistochemistry and western blotting. Results:, Baicalin-treated groups presented with lower alveolar bone loss than that of the ligature group, reaching statistical significance at the dose of 200 mg/kg (p = 0.009). The area fraction of collagen fibers was significantly higher in the baicalin (200 mg/kg)-treated group than in the ligature group (p = 0.047). Baicalin treatment significantly down-regulated the protein expression for cyclooxygenase-2 (p = 0.000) and inducible nitric oxide synthase (p = 0.003), compared with the ligature group. Conclusion:, Baicalin protects against tissue damage in ligature-induced periodontitis in rats, which might be mediated, in part, by its inhibitory effect on the expression of cyclooxygenase-2 and inducible nitric oxide synthase. These activities could support the continued investigation of baicalin as a potential therapeutic agent in periodontal disease. [source] NF-,B involvement in the induction of high affinity CAT-2 in lipopolysaccharide-stimulated rat lungsACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2004C.-J. Huang Background:, Endotoxemia stimulates nitric oxide (NO) biosynthesis through induction of inducible NO synthase (iNOS). Cellular uptake of l -arginine, the sole substrate for iNOS, is an important mechanism regulating NO biosynthesis by iNOS. The isozymes of type-2 cationic amino acid transporters, including CAT-2, CAT-2A, and CAT-2B, constitute the most important pathways responsible for trans -membrane l -arginine transportation. Therefore, regulation of CAT-2 isozymes expression may constitute one of the downstream regulatory pathways that control iNOS activity. We investigated the time course of enzyme induction and the role of nuclear factor-,B (NF-,B) in CAT-2 isozymes expression in lipopolysaccharide-(LPS) treated rat lungs. Methods:, Adult male Sprague,Dawley rats were randomly given intravenous injections of normal saline (N/S), LPS, LPS plus NF-,B inhibitor pre-treatment (PDTC, dexamethasone, or salicylate), or an NF-,B inhibitor alone. The rats were sacrificed at different times after injection and enzyme expression and lung injury were examined. Pulmonary and systemic NO production were also measured. Results:, LPS co-induced iNOS, CAT-2, and CAT-2B but not CAT-2A expression in the lungs. Furthermore, NF-,B actively participated in LPS-induction of iNOS, CAT-2, and CAT-2B. LPS induced pulmonary and systemic NO overproduction and resulted in lung injuries. Attenuation of LPS-induced iNOS, CAT-2, and CAT-2B induction significantly inhibited NO biosynthesis and lessened lung injury. Conclusion:, NF-,B actively participates in the induction of CAT-2 and CAT-2B in intact animals. Our data further support the idea that CAT-2 and CAT-2B are crucial in regulating iNOS activity. [source] Cannabinoid modulation of limbic forebrain noradrenergic circuitryEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 2 2010Ana F. Carvalho Abstract Both the endocannabinoid and noradrenergic systems have been implicated in neuropsychiatric disorders. Importantly, low levels of norepinephrine are seen in patients with depression, and antagonism of the cannabinoid receptor type 1 (CB1R) is able to induce depressive symptoms in rodents and humans. Whether the interaction between the two systems is important for the regulation of these behaviors is not known. In the present study, adult male Sprague,Dawley rats were acutely or chronically administered the CB1R synthetic agonist WIN 55,212-2, and ,2A and ,1 adrenergic receptors (AR) were quantified by Western blot. These AR have been shown to be altered in a number of psychiatric disorders and following antidepressant treatment. CB1R agonist treatment induced a differential decrease in ,2A- and ,1-ARs in the nucleus accumbens (Acb). Moreover, to assess long-lasting changes induced by CB1R activation, some of the chronically treated rats were killed 7 days following the last injection. This revealed a persistent effect on ,2A-AR levels. Furthermore, the localization of CB1R with respect to noradrenergic profiles was assessed in the Acb and in the nucleus of the solitary tract (NTS). Our results show a significant topographic distribution of CB1R and dopamine beta hydroxylase immunoreactivities (ir) in the Acb, with higher co-localization observed in the NTS. In the Acb, CB1R-ir was found in terminals forming either symmetric or asymmetric synapses. These results suggest that cannabinoids may modulate noradrenergic signaling in the Acb, directly by acting on noradrenergic neurons in the NTS or indirectly by modulating inhibitory and excitatory input in the Acb. [source] Effect of systemic parathyroid hormone (1,34) and a , -tricalcium phosphate biomaterial on local bone formation in a critical-size rat calvarial defect modelJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 5 2010Jonathan I. Yun Yun JI, Wikesjö UME, Borke JL, Bisch FC, Lewis JE, Herold RW, Swiec GD, Wood JC, McPherson III JC. Effect of systemic parathyroid hormone (1,34) and a ,-tricalcium phosphate biomaterial on local bone formation in a critical-size rat calvarial defect model. J Clin Periodontol 2010; 37: 419,426 doi: 10.1111/j.1600-051X.2010.01547.x Abstract Objective: The objective of this study was to evaluate local bone formation following systemic administration of parathyroid hormone (1,34) (PTH), a surgically implanted synthetic , -tricalcium phosphate (, -TCP) bone biomaterial serving as a matrix to support new bone formation. Materials and Methods: Critical-size, 8 mm, calvarial through-and-through osteotomy defects were surgically created in 100 adult male Sprague,Dawley rats. The animals were randomized into five groups of 20 animals each to receive one of the following treatments: PTH (15 ,g PTH/kg/day; subcutaneously), PTH/, -TCP, , -TCP, or particulate human demineralized freeze-dried bone (DFDB), and sham-surgery controls. Ten animals/group were euthanized at 4 and 8 weeks post-surgery for radiographic and histometric analysis. Results: The histometric analysis showed that systemic PTH significantly enhanced local bone formation, bone fill averaging (±SE) 32.2±4.0% compared with PTH/, -TCP (15.7±2.4%), , -TCP (12.5±2.3%), DFDB (14.5±2.3%), and sham-surgery control (10.0±1.5%) at 4 weeks (p<0.014). Systemic PTH showed significantly enhanced bone formation (41.5±4.0%) compared with PTH/, -TCP (22.4±3.0%), , -TCP (21.3±4.4%), and with the sham-surgery control (23.8±4.2%) at 8 weeks (p<0.025). The DFDB group showed significantly increased bone formation from 4 (14.5±2.3%) to 8 weeks (32.0±3.2%) (p<0.006). The PTH/, -TCP and , -TCP groups both showed limited biomaterials resorption. The radiographic analysis was not diagnostic to distinguish local bone formation from the radiopaque , -TCP biomaterial. Conclusions: Systemic administration of PTH significantly stimulates local bone formation. Bone formation was significantly limited by the , -TCP biomaterial. [source] Effects of Ethanol on Extracellular Levels of Adenosine in the Basal Forebrain: An In Vivo Microdialysis Study in Freely Behaving RatsALCOHOLISM, Issue 5 2010Rishi Sharma Background:, Adenosine is implicated to play a pivotal role in mediating many neuronal responses to ethanol. While in vitro studies performed in cell culture have demonstrated that acute ethanol exposure increases extracellular adenosine levels, this effect has not been demonstrated, in vivo, in the brain. We performed an in vivo microdialysis study to examine the effects of local ethanol perfusion on extracellular levels of adenosine in the basal forebrain (BF). Methods:, Under sterile conditions and using a standard surgical protocol, adult male Sprague,Dawley rats were implanted with unilateral microdialysis guide cannula targeted toward the BF. Following postoperative recovery, the microdialysis probe was inserted. After allowing at least 12 to 16 hours for probe insertion recovery, the experiment was begun. Artificial cerebrospinal fluid (aCSF) was perfused (0.7 ,l/min) for 80 minutes, and 4 × 20-minute pre-ethanol baseline samples were collected. Subsequently, 30, 100, and 300 mM doses of ethanol were perfused. Each ethanol dose was perfused for 80 minutes, and 4 × 20-minute samples were collected. Finally, aCSF was perfused, and 4 × 20 postethanol samples were collected. Adenosine in the microdialysate was separated and measured with HPLC coupled with an UV detector. On completion, the animals were euthanized, brain removed and processed for histology. Results:, Local ethanol perfusion in the BF produced a significant increase in extracellular adenosine with the highest dose of 300 mM ethanol producing a 4-fold increase. Cresyl violet (Nissl) staining did not indicate any toxic damage in the area surrounding the probe tip. Choline acetyltransferase immunohistochemistry revealed that all microdialysis probe sites were localized in the BF. Conclusion:, Our study is the first to demonstrate that ethanol acts directly in the brain to increase extracellular adenosine. [source] Pretreatment with melatonin exerts anti-inflammatory effects against ischemia/reperfusion injury in a rat middle cerebral artery occlusion stroke modelJOURNAL OF PINEAL RESEARCH, Issue 2 2004Zhong Pei Abstract:, Inflammatory response following cerebral ischemia/reperfusion plays a key pathogenic role in ischemic cerebral damage. Nitric oxide (NO), cyclooxygenase-2 (COX-2) and myeloperoxidase (MPO) are important inflammatory mediators. Neuronal NO synthase (nNOS) is a major initial source of excessive NO during ischemia/reperfusion. Induction of COX-2 and infiltration of polymorphonuclear cells expressing MPO are critical factors in delayed inflammatory damage. Previously, we demonstrated that administration of melatonin before ischemia significantly reduced the infarct volume in a rat middle cerebral artery occlusion (MCAO) stroke model. In this study, we examined the effect of pretreatment with melatonin at 5 mg/kg on the immunoreactivity (ir) for nNOS, COX-2, MPO, and glial fibrillary acidic protein (GFAP) at 24, 48, and 72 hr after right-sided endovascular MCAO for 1 hr in adult male Sprague,Dawley rats. Melatonin did not affect the hemodynamic parameters. When compared with rats with sham MCAO, ischemia/reperfusion led to an ipsilateral increase in cells with positive ir for nNOS (similar at all times) and in ir-GFAP (similar at all times). Ischemia/reperfusion led to appearance of cells with positive ir for COX-2 (greatest at 24 hr with a tendency to increase again at 72 hr) or MPO (greatest at 24 hr). A single dose of melatonin significantly lessened the ipsilateral increase in cells with positive ir for nNOS, COX-2 or MPO, but did not influence the ipsilateral change in ir-GFAP. Our results suggest that melatonin treatment mediates neuroprotection against ischemia/reperfusion injury partly via inhibition of the consequential inflammatory response. [source] Bone healing with electric current: a histological assessmentORTHODONTICS & CRANIOFACIAL RESEARCH, Issue 3 2000Hui-Ling Chen Skeletal relapse is a major concern after correction of retrognathism with surgical mandibular advancement. It was hypothesized that the stimulation from a direct electric current can accelerate the osseous repair through the enhancement of the maturation of fibrocartilage. Furthermore, this stimulation may enhance the mechanical properties of the facial osteotomy site and reduce the skeletal relapse. The purpose of the present study was to examine the osteotomy site histologically and determine the effect of post-surgical electrical stimulation on the healing of a facial osteotomy site in a rat model. Three groups of adult male Sprague,Dawley rats, 15 in each group (direct electric current, electric sham, and control), were used to generate data. Electrodes were placed in both the direct electric current and the electric sham groups. A 20-,A direct current was delivered to the osteotomy site only in the direct electric current group. Histological slides of the osteotomy site for each animal were prepared and interpreted to characterize the healing process of the osteotomy site for each animal. The results showed no statistically significant difference among the three groups of animals (p>0.005). An examination with histology earlier in the healing process and the utilization of an experimental animal with a larger jaw are suggested for any further investigation that involves electrical stimulation and osseous healing in a facial osteotomy site. [source] | |||||||||||||