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Vivo Rat Model (vivo + rat_model)
Selected AbstractsAge-Related Increase in Atrial Fibrillation Induced by Transvenous Catheter-Based Atrial Burst Pacing: An In Vivo Rat Model of Inducible Atrial FibrillationJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 1 2010DONGZHU XU M.D. AF Rat Model Induced by Transvenous Catheter Pacing.,Introduction: Large animal models of atrial fibrillation (AF) are well established, but limited experimental reports exist on small animal models. We sought to develop an in vivo rat model of AF using a transvenous catheter and to evaluate the model's underlying characteristics. Methods and Results: Echocardiogram, surface electrocardiogram (ECG), and atrial effective refractory period (AERP) were recorded at baseline in young (3 months) and middle-aged (9 months) Wistar rats. AF inducibility and duration were measured through transvenous electrode catheter in young (n = 11) and middle-aged rats (n = 11) and middle-aged rats treated with either pilsicainide (1 mg/kg iv, n = 7) or amiodarone (10 mg/kg iv, n = 9). Degrees of interstitial fibrosis and cellular hypertrophy in the atria were assessed histologically. The P-wave duration and AERP were significantly longer and echocardiographic left atrial dimension significantly larger in middle-aged versus young rats. AF was inducible in >90% of all procedures in both untreated rat groups, whereas AF inducibility was reduced by the antiarrhythmic drugs. The AF duration was significantly longer in middle-aged than in young rats and was significantly shortened by treatment with either pilsicainide or amiodarone. Histologic analysis revealed significant increases in atrial interstitial fibrosis and cellular diameter in middle-aged versus young rats. Conclusions: Transvenous catheter-based AF is significantly longer in middle-aged than in young rats and is markedly reduced by treatment with antiarrhythmic drugs. This rat model of AF is simple, reproducible, and reliable for examining pharmacologic effects on AF and studying the process of atrial remodeling.(J Cardiovasc Electrophysiol, Vol. 21, pp. 88,93, January 2010) [source] Sex differences in long bone fatigue using a rat modelJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 10 2006Luisa D. Moreno Abstract Stress fractures can occur because of prolonged exercise and are associated with cyclic loading. Fatigue is the accumulated damage that results from cyclic loading and bone fatigue damage is of special concern for athletes and army recruits. Existing literature shows that the rates of stress fracture for female athletes and female army recruits are higher than their male counterparts. In this study, we used an ex vivo rat model to investigate the fatigue response of female and male bones. We determined the strain versus number of cycles to failure (S/N) for each sex and found that for a certain initial strain (5,000,7,000 µ,) female bones have shorter fatigue life. To further characterize the bone response to fatigue, we also determined the creep that occurred during the fatigue test. From the creep data, for a certain strain range, female bones accumulated greater residual strains and reached the critical strain at a faster rate. In summary, this study demonstrates that female rat bones have a lower resistance to fatigue in the absence of a physiological response such as muscle fatigue or osteogenic adaptation. From these results, we hypothesized that creep was the underlying mechanism that accounted for the fast deterioration of female bones during fatigue. © 2006 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 24:1926,1932, 2006 [source] A caspase inhibitor, IDN-6556, ameliorates early hepatic injury in an ex vivo rat model of warm and cold ischemia,LIVER TRANSPLANTATION, Issue 3 2007Niel C. Hoglen This study examined the efficacy of the caspase inhibitor, IDN-6556, in a rat model of liver ischemia-reperfusion injury. Livers from male Sprague-Dawley rats were reperfused for 120 minutes after 24 hours of 4°C cold storage in University of Wisconsin solution. Portal blood flow measurements estimated sinusoidal resistance, and bile production, alanine aminotransferase activities, and Suzuki scores were evaluated as parameters of hepatocyte/liver injury. Treated livers were exposed to 25 or 50 ,M of IDN-6556 in University of Wisconsin storage solution and/or the perfusate. All treatment regimens with IDN-6556 significantly improved portal blood flow measured at 120 minutes, and significant improvements were seen as early as 30 minutes when inhibitor was also present in the perfusate (P < 0.01). All treatment groups with IDN-6556 significantly increased bile production by 3-4-fold compared with controls (P < 0.01), and reductions in alanine aminotransferase activities were seen within 90 minutes of reperfusion (P < 0.05). These data were confirmed by improved Suzuki scores (less sinusoidal congestion, necrosis, and vacuolization) in all treated groups. Livers from the IDN-6556,treated groups had markedly reduced caspase activities and TUNEL (terminal deoxynucleotidyl transferase dUTP nick-end labeling)-positive cells, suggesting reductions in apoptosis. IDN-6556 present in cold storage media ameliorated liver injury due to cold ischemia and reperfusion injury and may be a rational therapeutic approach to reduce the risk of liver ischemia in the clinical setting. Liver Transpl 13: 361,366, 2007. © 2007 AASLD. [source] Ischemic preconditioning attenuates the oxidant-dependent mechanisms of reperfusion cell damage and death in rat liverLIVER TRANSPLANTATION, Issue 11 2002Barbara Cavalieri In an in vivo rat model of liver ischemia followed by reperfusion a consistent appearance of necrosis and activation of biochemical pathways of apoptosis was reproduced and monitored after 30 minutes reperfusion. Preconditioning by application of a short cycle of ischemia-reperfusion (10 minutes + 10 minutes) positively conditioned recovery of the organ at reperfusion, attenuating both necrotic and apoptotic events. Preconditioning at least halved cell oxidative damage occurring early at reperfusion, and as a major consequence, the increase of cytolysis and apoptosis occurring at reperfusion was about 50% less. The attenuation of both pathways of cell death by preconditioning appeared at least partly related to its modulate action on H2O2 and 4-hydroxy-2,3-trans-nonenal production. The overall data point to a marked diminished oxidant generation and oxidative reactions as one major possible mechanism through which ischemic preconditioning exerts protection against necrotic and apoptotic insult to the postischemic liver. [source] The phosphatidylinositol 3-kinase,Akt pathway protects cardiomyocytes from ischaemic and hypoxic apoptosis via mitochondrial functionCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2010Hua-Pei Song Summary 1.,After a severe burn, a marked decrease in myocardial blood flow results in ischaemic and hypoxic injury, which subsequently leads to apoptosis or necrosis. Phosphatidylinositol 3-kinase (PI3-K)/Akt is an important intracellular signal transduction molecule that regulates cell proliferation, differentiation, glucose metabolism and migration. However, the function and mechanisms of the PI3-K,Akt pathway in cardiomyocyte apoptosis after a burn remain unclear. 2.,In the present study, an in vivo rat model of burn injury and an in vitro hypoxic model using rat cardiomyocytes were established. In burned rats, the expression of PI3-K and phosphorylated (p-) Akt expression increased, as did myocardial apoptosis. Inhibition of the PI3-K,Akt pathway with 1.4 mg/kg LY294002 caused a significant increase in the myocardial apoptotic index compared with hypoxia alone in the in vivo model. 3.,Cardiomyocytes cultured under hypoxic conditions exhibited increased apoptosis, decreased cell viability, enhanced caspase 3 activity, a decreased mitochondrial membrane potential, increased cytoplasmic calcium transients and increased p53 and Bax mRNA expression. Pretreatment with 50 ,mol/L LY294002 significantly enhanced all these negative indicators compared with hypoxia alone. In contrast, pretreatment of cells with 200 ng/mL insulin-like growth factor-1, an activator of PI3-K,Akt, significantly ameliorated the effects of hypoxia, although control levels were not reached. 4.,These findings indicate that activation of the PI3-K,Akt pathway induced by ischaemia and hypoxia after a severe burn can protect cardiomyocytes from apoptosis. This anti-apoptotic effect is most likely mediated via the mitochondria and changes in p53 and Bax gene expression, intracellular [Ca2+] and caspase 3 activity. [source] | ||||||||||