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Статті в журналах з теми "Ex-vivo rat model"

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Автор: Grafiati

Опубліковано: 12 червня 2021

Оновлено: 1 лютого 2022

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1

Citak, N., S. Arni, J. Cehn, L. Ceulemans, I. Schmitt-Opitz, and I. Inci. "Subnormothermic Ex Vivo Lung Perfusion Improves Graft Preservation in Rat Ex Vivo Lung Perfusion Model." Journal of Heart and Lung Transplantation 39, no. 4 (April 2020): S354. http://dx.doi.org/10.1016/j.healun.2020.01.416.

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2

Kural, Mehmet H., Guohao Dai, Laura E. Niklason, and Liqiong Gui. "An Ex Vivo Vessel Injury Model to Study Remodeling." Cell Transplantation 27, no. 9 (August 10, 2018): 1375–89. http://dx.doi.org/10.1177/0963689718792201.

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Objective: Invasive coronary interventions can fail due to intimal hyperplasia and restenosis. Endothelial cell (EC) seeding to the vessel lumen, accelerating re-endothelialization, or local release of mTOR pathway inhibitors have helped reduce intimal hyperplasia after vessel injury. While animal models are powerful tools, they are complex and expensive, and not always reflective of human physiology. Therefore, we developed an in vitro 3D vascular model validating previous in vivo animal models and utilizing isolated human arteries to study vascular remodeling after injury. Approach: We utilized a bioreactor that enables the control of intramural pressure and shear stress in vessel conduits to investigate the vascular response in both rat and human arteries to intraluminal injury. Results: Culturing rat aorta segments in vitro, we show that vigorous removal of luminal ECs results in vessel injury, causing medial proliferation by Day-4 and neointima formation, with the observation of SCA1+ cells (stem cell antigen-1) in the intima by Day-7, in the absence of flow. Conversely, when endothelial-denuded rat aortae and human umbilical arteries were subjected to arterial shear stress, pre-seeding with human umbilical ECs decreased the number and proliferation of smooth muscle cell (SMC) significantly in the media of both rat and human vessels. Conclusion: Our bioreactor system provides a novel platform for correlating ex vivo findings with vascular outcomes in vivo. The present in vitro human arterial injury model can be helpful in the study of EC-SMC interactions and vascular remodeling, by allowing for the separation of mechanical, cellular, and soluble factors.

3

Ohsumi, Akihiro, Takashi Kanou, Aadil Ali, Zehong Guan, David M. Hwang, Thomas K. Waddell, Stephen Juvet, Mingyao Liu, Shaf Keshavjee, and Marcelo Cypel. "A method for translational rat ex vivo lung perfusion experimentation." American Journal of Physiology-Lung Cellular and Molecular Physiology 319, no. 1 (July 1, 2020): L61—L70. http://dx.doi.org/10.1152/ajplung.00256.2019.

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The application of ex vivo lung perfusion (EVLP) has significantly increased the successful clinical use of marginal donor lungs. While large animal EVLP models exist to test new strategies to improve organ repair, there is currently no rat EVLP model capable of maintaining long-term lung viability. Here, we describe a new rat EVLP model that addresses this need, while enabling the study of lung injury due to cold ischemic time (CIT). The technique involves perfusing and ventilating male Lewis rat donor lungs for 4 h before transplanting the left lung into a recipient rat and then evaluating lung function 2 h after reperfusion. To test injury within this model, lungs were divided into groups and exposed to different CITs (i.e., 20 min, 6 h, 12 h, 18 h and 24 h). Experiments involving the 24-h-CIT group were prematurely terminated due to the development of severe edema. For the other groups, no differences in the ratio of arterial oxygen partial pressure to fractional inspired oxygen ([Formula: see text]/[Formula: see text]) were observed during EVLP; however, lung compliance decreased over time in the 18-h group ( P = 0.012) and the [Formula: see text]/[Formula: see text] of the blood from the left pulmonary vein 2 h after transplantation was lower compared with 20-min-CIT group ( P = 0.0062). This new model maintained stable lung function during 4-h EVLP and after transplantation when exposed to up to 12 h of CIT.

4

Abubakar, Adamu Abdul, Sahar Mohammed Ibrahim, Ahmed Khalaf Ali, Kareem Obayes Handool, Mohammad Shuaib Khan, Mohamed Noordin Mustapha, Tengku Azmi Ibrahim, Ubedullah Kaka, and Loqman Mohamad Yusof. "Postnatal ex vivo rat model for longitudinal bone growth investigations." Animal Models and Experimental Medicine 2, no. 1 (February 20, 2019): 34–43. http://dx.doi.org/10.1002/ame2.12051.

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5

Hoff, Catherine M. "Ex vivo and in vivo gene transfer to the peritoneal membrane in a rat model." Nephrology Dialysis Transplantation 16, no. 3 (March 1, 2001): 666–68. http://dx.doi.org/10.1093/ndt/16.3.666.

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6

Sierakowiak, Adam, Anna Mattsson, Marta Gómez-Galán, Teresa Feminía, Lisette Graae, Sahar Nikkhou Aski, Peter Damberg, Mia Lindskog, Stefan Brené, and Elin Åberg. "Hippocampal Morphology in a Rat Model of Depression: The Effects of Physical Activity." Open Neuroimaging Journal 9, no. 1 (January 30, 2015): 1–6. http://dx.doi.org/10.2174/1874440001509010001.

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Accumulating in vivo and ex vivo evidences show that humans suffering from depression have decreased hippocampal volume and altered spine density. Moreover, physical activity has an antidepressant effect in humans and in animal models, but to what extent physical activity can affect hippocampal volume and spine numbers in a model for depression is not known. In this study we analyzed whether physical activity affects hippocampal volume and spine density by analyzing a rodent genetic model of depression, Flinders Sensitive Line Rats (FSL), with Magnetic Resonance Imaging (MRI) and ex vivo Golgi staining. We found that physical activity in the form of voluntary wheel running during 5 weeks increased hippocampal volume. Moreover, runners also had larger numbers of thin spines in the dentate gyrus. Our findings support that voluntary wheel running, which is antidepressive in FSL rats, is associated with increased hippocampal volume and spine numbers.

7

Bouckaert, Charlotte, Emma Christiaen, Jeroen Verhoeven, Benedicte Descamps, Valerie De Meulenaere, Paul Boon, Evelien Carrette, Kristl Vonck, Christian Vanhove, and Robrecht Raedt. "Comparison of In Vivo and Ex Vivo Magnetic Resonance Imaging in a Rat Model for Glioblastoma-Associated Epilepsy." Diagnostics 11, no. 8 (July 21, 2021): 1311. http://dx.doi.org/10.3390/diagnostics11081311.

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Magnetic resonance imaging (MRI) is frequently used for preclinical treatment monitoring in glioblastoma (GB). Discriminating between tumors and tumor-associated changes is challenging on in vivo MRI. In this study, we compared in vivo MRI scans with ex vivo MRI and histology to estimate more precisely the abnormal mass on in vivo MRI. Epileptic seizures are a common symptom in GB. Therefore, we used a recently developed GB-associated epilepsy model from our group with the aim of further characterizing the model and making it useful for dedicated epilepsy research. Ten days after GB inoculation in rat entorhinal cortices, in vivo MRI (T2w and mean diffusivity (MD)), ex vivo MRI (T2w) and histology were performed, and tumor volumes were determined on the different modalities. The estimated abnormal mass on ex vivo T2w images was significantly smaller compared to in vivo T2w images, but was more comparable to histological tumor volumes, and might be used to estimate end-stage tumor volumes. In vivo MD images displayed tumors as an outer rim of hyperintense signal with a core of hypointense signal, probably reflecting peritumoral edema and tumor mass, respectively, and might be used in the future to distinguish the tumor mass from peritumoral edema—associated with reactive astrocytes and activated microglia, as indicated by an increased expression of immunohistochemical markers—in preclinical models. In conclusion, this study shows that combining imaging techniques using different structural scales can improve our understanding of the pathophysiology in GB.

8

Ma, Zhe, Sheng-jun Wang, Chuan-fu Li, Xiang-xing Ma, and Tao Gu. "Increased metabolite concentration in migraine rat model by proton MR spectroscopy in vivo and ex vivo." Neurological Sciences 29, no. 5 (October 2008): 337–42. http://dx.doi.org/10.1007/s10072-008-0991-5.

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9

Savolainen-Peltonen, H., L. Petrov, and P. Hayry. "RAT AORTIC ALLOGRAFT EXPLANT ASSAY AS AN EX VIVO MODEL OF ALLOGRAFT ARTERIOSCLEROSIS." Transplantation 78 (July 2004): 623. http://dx.doi.org/10.1097/00007890-200407271-01678.

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10

Liu, Mingyao, Lorraine Tremblay, Stephen D. Cassivi, Xiao-Hui Bai, Eric Mourgeon, Andrew F. Pierre, Arthur S. Slutsky, Martin Post, and Shaf Keshavjee. "Alterations of nitric oxide synthase expression and activity during rat lung transplantation." American Journal of Physiology-Lung Cellular and Molecular Physiology 278, no. 5 (May 1, 2000): L1071—L1081. http://dx.doi.org/10.1152/ajplung.2000.278.5.l1071.

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Decreased nitric oxide (NO) production has been reported during lung transplantation in patients. To study the effects of ischemia and reperfusion on endogenous NO synthase (NOS) expression, both an ex vivo and an in vivo lung injury model for transplantation were used. Donor rat lungs were flushed with cold low-potassium dextran solution and subjected to either cold (4°C for 12 h) or warm (21°C for 4 h) ischemic preservation followed by reperfusion with an ex vivo model. A significant increase in inducible NOS and a decrease in endothelial NOS mRNA was found after reperfusion. These results were confirmed in a rat single-lung transplant model after warm preservation. Interestingly, protein contents of both inducible NOS and endothelial NOS increased in the transplanted lung after 2 h of reperfusion. However, the total activity of NOS in the transplanted lungs remained at very low levels. We conclude that ischemic lung preservation and reperfusion result in altered NOS gene and protein expression with inhibited NOS activity, which may contribute to the injury of lung transplants.

11

Stadler, Michaela, Vincent Nuyens, and Jean G. Boogaerts. "Intralipid minimizes hepatocytes injury after anoxia-reoxygenation in an ex vivo rat liver model." Nutrition 23, no. 1 (January 2007): 53–61. http://dx.doi.org/10.1016/j.nut.2006.08.014.

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12

PAPEGAY, Berengere, Michaela STADLER, Vincent Nuyens, Isabelle SALMON, Veronique KRUYS, and Jean G. BOOGAERTS. "Alanine minimises hepatocyte injury after ischemia-reperfusion in an ex vivo rat liver model." BIOCELL 38, no. 1 (2014): 25–32. http://dx.doi.org/10.32604/biocell.2014.38.025.

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13

Ganugula, Raghu, Meenakshi Arora, and Majeti N. V. Ravi Kumar. "Ex Vivo Rat Eye Model for Investigating Transport of Next Generation Precision-Polyester Nanosystems." ACS Applied Materials & Interfaces 9, no. 31 (July 26, 2017): 25668–71. http://dx.doi.org/10.1021/acsami.7b07896.

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14

Boyle, Erin C., Heike Dombrowsky, Jürgen Sarau, Janin Braun, Martin Aepfelbacher, Ingmar Lautenschläger, and Guntram A. Grassl. "Ex vivo perfusion of the isolated rat small intestine as a novel model ofSalmonellaenteritis." American Journal of Physiology-Gastrointestinal and Liver Physiology 310, no. 2 (January 15, 2016): G55—G63. http://dx.doi.org/10.1152/ajpgi.00444.2014.

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Using an ex vivo perfused rat small intestinal model, we examined pathological changes to the tissue, inflammation induction, as well as dynamic changes to smooth muscle activity, metabolic competence, and luminal fluid accumulation during short-term infection with the enteropathogenic bacteria Salmonella enterica serovar Typhimurium and Yersinia enterocolitica. Although few effects were seen upon Yersinia infection, this system accurately modeled key aspects associated with Salmonella enteritis. Our results confirmed the importance of the Salmonella Pathogenicity Island 1 (SPI1)-encoded type 3 secretion system (T3SS) in pathology, tissue invasion, inflammation induction, and fluid secretion. Novel physiological consequences of Salmonella infection of the small intestine were also identified, namely, SPI-1-dependent vasoconstriction and SPI-1-independent reduction in the digestive and absorptive functions of the epithelium. Importantly, this is the first small animal model that allows for the study of Salmonella-induced fluid secretion. Another major advantage of this model is that one can specifically determine the contribution of resident cell populations. Accordingly, we can conclude that recruited cell populations were not involved in the pathological damage, inflammation induction, fluid accumulation, nutrient absorption deficiency, and vasoconstriction observed. Although fluid loss induced by Salmonella infection is hypothesized to be due to damage caused by recruited neutrophils, our data suggest that bacterial invasion and inflammation induction in resident cell populations are sufficient for fluid loss into the lumen. In summary, this model is a novel and useful tool that allows for detailed examination of the early physiopathological effects of Salmonella infection on the small intestine.

15

Eriksson, Johanna, Helena Thörn, Erik Sjögren, Lisa Holmstén, Katarina Rubin, and Hans Lennernäs. "Pulmonary Dissolution of Poorly Soluble Compounds Studied in an ex Vivo Rat Lung Model." Molecular Pharmaceutics 16, no. 7 (May 28, 2019): 3053–64. http://dx.doi.org/10.1021/acs.molpharmaceut.9b00289.

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16

Shoji, T., M. Omasa, T. Nakamura, T. Yoshimura, H. Yoshida, K. Ikeyama, T. Fukuse, and H. Wada. "Mild Hypothermia Ameliorates Lung Ischemia Reperfusion Injury in an ex vivo Rat Lung Model." European Surgical Research 37, no. 6 (2005): 348–53. http://dx.doi.org/10.1159/000090335.

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17

Ohsumi, A., T. Kanou, T. K. Waddell, M. Liu, S. Keshavjee, and M. Cypel. "The Establishment of an Ex Vivo Lung Perfusion in a Rat Lung Transplantation Model." Journal of Heart and Lung Transplantation 35, no. 4 (April 2016): S179—S180. http://dx.doi.org/10.1016/j.healun.2016.01.498.

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18

Montero-Bullon, Javier-Fernando, Susana S. Aveiro, Tânia Melo, Tânia Martins-Marques, Diana Lopes, Bruna Neves, Henrique Girão, M. Rosário M Domingues, and Pedro Domingues. "Cardiac phospholipidome is altered during ischemia and reperfusion in an ex vivo rat model." Biochemistry and Biophysics Reports 27 (September 2021): 101037. http://dx.doi.org/10.1016/j.bbrep.2021.101037.

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19

Roffia, Valentina, Antonella De Palma, Caterina Lonati, Dario Silvestre, Rossana Rossi, Marco Mantero, Stefano Gatti, et al. "Proteome Investigation of Rat Lungs subjected to Ex Vivo Perfusion (EVLP)." Molecules 23, no. 12 (November 22, 2018): 3061. http://dx.doi.org/10.3390/molecules23123061.

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Ex vivo lung perfusion (EVLP) is an emerging procedure that allows organ preservation, assessment and reconditioning, increasing the number of marginal donor lungs for transplantation. However, physiological and airflow measurements are unable to unveil the molecular mechanisms responsible of EVLP beneficial effects on lung graft and monitor the proper course of the treatment. Thus, it is urgent to find specific biomarkers that possess these requirements but also accurate and reliable techniques that identify them. The purpose of this study is to give an overview on the potentiality of shotgun proteomic platforms in characterizing the status and the evolution of metabolic pathways during EVLP in order to find new potential EVLP-related biomarkers. A nanoLC-MS/MS system was applied to the proteome analysis of lung tissues from an optimized rat model in three experimental groups: native, pre- and post-EVLP. Technical and biological repeatability were evaluated and, together with clustering analysis, underlined the good quality of data produced. In-house software and bioinformatics tools allowed the label-free extraction of differentially expressed proteins among the three examined conditions and the network visualization of the pathways mainly involved. These promising findings encourage further proteomic investigations of the molecular mechanisms behind EVLP procedure.

20

Prantil, Rachelle L., Ron J. Jankowski, Yasuhiro Kaiho, William C. de Groat, Michael B. Chancellor, Naoki Yoshimura, and David A. Vorp. "Ex vivo biomechanical properties of the female urethra in a rat model of birth trauma." American Journal of Physiology-Renal Physiology 292, no. 4 (April 2007): F1229—F1237. http://dx.doi.org/10.1152/ajprenal.00292.2006.

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Stress urinary incontinence (SUI) is the involuntary release of urine during sudden increases in abdominal pressures. SUI is common in women after vaginal delivery or pelvic trauma and may alter the biomechanical properties of the urethra. Thus we hypothesize that injury due to vaginal distension (VD) decreases urethral basal tone and passive stiffness. This study aimed to assess the biomechanical properties of the urethra after VD in the baseline state, where basal muscle tone and extracellular matrix (ECM) are present, and in the passive state, where inactive muscle and ECM are present. Female rat urethras were isolated in a rat model of acute SUI induced by simulated birth trauma. Our established ex vivo system was utilized, wherein we applied intraluminal static pressures ranging from 0 to 20 mmHg. Outer diameter was measured via a laser micrometer. Measurements were recorded via computer. Urethral thickness was assessed histologically. Stress-strain responses of the urethra were altered by VD. Quantification of biomechanical parameters indicated that VD decreased baseline stiffness. The passive peak incremental elastic modulus of the distal segment in VD urethras was less than for controls (1.84 ± 0.67 vs. 1.19 ± 0.70 × 106 dyne/cm2, respectively; P = 0.016). An increase was noted in passive low-pressure compliance values in proximal VD urethras compared with controls (9.44 ± 2.43 vs. 4.62 ± 0.60 mmHg−1, respectively; P = 0.04). Biomechanical analyses suggest that VD alters urethral basal tone, proximal urethral compliance, and distal stiffness. Lack of basal smooth muscle tone, in combination with these changes in the proximal and distal urethra, may contribute to SUI induced by VD.

21

Ishikawa, Makoto, Takeshi Yoshitomi, Douglas F. Covey, Charles F. Zorumski, and Yukitoshi Izumi. "TSPO activation modulates the effects of high pressure in a rat ex vivo glaucoma model." Neuropharmacology 111 (December 2016): 142–59. http://dx.doi.org/10.1016/j.neuropharm.2016.09.001.

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22

Scott, A. "High strain mechanical loading rapidly induces tendon apoptosis: an ex vivo rat tibialis anterior model." British Journal of Sports Medicine 39, no. 5 (May 1, 2005): e25-e25. http://dx.doi.org/10.1136/bjsm.2004.015164.

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23

Omasa, Mitsugu, Tatsuo Fukuse, Shinya Toyokuni, Yoichi Mizutani, Hiroshi Yoshida, Kazuyuki Ikeyama, Seiki Hasegawa, and Hiromi Wada. "Glycine ameliorates lung reperfusion injury after cold preservation in an ex vivo rat lung model." Transplantation 75, no. 5 (March 2003): 591–98. http://dx.doi.org/10.1097/01.tp.0000053200.98125.14.

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24

Peng, Chung-Kan, Kun-Lun Huang, Chou-Chin Lan, Yu-Juei Hsu, Geng-Chin Wu, Chia-Hui Peng, Chin-Pyng Wu, and Khee-Siang Chan. "Experimental chronic kidney disease attenuates ischemia-reperfusion injury in an ex vivo rat lung model." PLOS ONE 12, no. 3 (March 14, 2017): e0171736. http://dx.doi.org/10.1371/journal.pone.0171736.

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25

Amersi, Farin F., Sally K. Nelson, Douglas G. Farmer, Hirohisa Kato, Judy Melinek, Joseph Zaky, Jerzy W. Kupiec-Weglinski, Lawrence D. Horwitz, Ronald W. Busuttil, and Marcus A. Horwitz. "BUCILLAMINE, A DIFFUSIBLE ANTIOXIDANT, PREVENTS ISCHEMIA/REPERFUSION INJURY IN AN EX-VIVO RAT LIVER MODEL." Transplantation 69, Supplement (April 2000): S198—S199. http://dx.doi.org/10.1097/00007890-200004271-00328.

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26

Haam, Seokjin, Kentaro Noda, Brian J. Philips, Takashi Harano, Pablo G. Sanchez, and Norihisa Shigemura. "Cyclosporin A Administration During Ex Vivo Lung Perfusion Preserves Lung Grafts in Rat Transplant Model." Transplantation 104, no. 9 (March 20, 2020): e252-e259. http://dx.doi.org/10.1097/tp.0000000000003237.

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27

Becerra, D. C., H. Linge, S. C. Jeffs, S. Roberts, J. O, and H. Ott. "Normothermic Liquid Ventilation Attenuates Inflammation from Ischemia-Reperfusion Injury in an Ex Vivo Rat Model." Journal of Heart and Lung Transplantation 40, no. 4 (April 2021): S344. http://dx.doi.org/10.1016/j.healun.2021.01.971.

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28

Ehrsam, J. P., S. Arni, J. Chen, H. Rodriguez Cetina Biefer, I. Opitz, and I. Inci. "Nicotinamide Adenine Dinucleotide (NAD+) Improves Lung Function in Rat Lung Ex-Vivo Lung Perfusion Model." Journal of Heart and Lung Transplantation 40, no. 4 (April 2021): S347. http://dx.doi.org/10.1016/j.healun.2021.01.978.

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29

Grupcheva, Christina N., Wilda T. Laux Fenton, Colin R. Green, and Charles NJ McGhee. "In vivo and ex vivo in situ confocal analysis of a rat model demonstrating transient ‘epithelialization of the endothelium’." Clinical & Experimental Ophthalmology 30, no. 3 (May 24, 2002): 191–95. http://dx.doi.org/10.1046/j.1442-9071.2002.00524.x.

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30

Su, Haili, Yongfeng Du, Yunqiu Qian, Yujin Zong, Jun Li, Ran Zhuang, Jianguo He, Zhangrui Wei, Jun Zhang, and Xiaodong Zhou. "Targeted Ultrasound Contrast Imaging of Matrix Metalloproteinase-2 in Ischemia–Reperfusion Rat Model: Ex Vivo and In Vivo Studies." Molecular Imaging and Biology 13, no. 2 (June 11, 2010): 293–302. http://dx.doi.org/10.1007/s11307-010-0350-9.

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31

Castillo, Felipe, Daniel R. González, and Rodrigo Moore-Carrasco. "Effects of Phaseolus vulgaris Extract on Lipolytic Activity and Differentiation of 3T3-L1 Preadipocytes into Mature Adipocytes: A Strategy to Prevent Obesity." Journal of Nutrition and Metabolism 2019 (April 28, 2019): 1–8. http://dx.doi.org/10.1155/2019/5093654.

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Background. Overweight and obesity are defined as abnormal or excessive fat accumulation that may be harmful for health. A global trend in this area is the search for natural compounds that have a proven beneficial effect and no clinical complications. Phaseolus vulgaris (bean) is a vegetable highly consumed worldwide. One of its effects, the most reported, is weight reduction in overweight individuals. Objective. The objective of this study was to investigate the antiobesity activity of this legume in mature 3T3-L1 adipocytes and in rat white adipose tissue in an ex vivo model. Design. Mature adipocytes 3T3-L1 and rat adipose tissue were treated with bean extracts. We quantified lipolysis in mature 3T3-L1 adipocytes and in rat white adipose tissue in an ex vivo model. Results. In an ex vivo assay with adipose tissue, methanolic and aqueous green bean extracts increased glycerol release to the medium compared to control (p<0.05 and p<0.001 respectively). Treatment of 3T3-L1 adipocytes with green bean extracts (800 and 1000 µg/mL) increased glycerol release significantly (p<0.0001). Extracts at concentrations between 500 and 1000 µg/mL reduced intracellular triglyceride accumulation by 34.4% and 47.1% compared to control (p<0.0001). Discussion. Our results propose that bioactive compounds of green beans exert a direct mechanism on adipocytes through lipolysis. Conclusion. We have identified a novel capacity of bean extracts related to lipolytic activity both in vitro and ex vivo, resulting in a powerful lipolytic effect. Moreover, we also found that bean extracts has an antiadipogenic effect during the differentiation of 3T3-L1 preadipocytes. These results suggest that bean is a good candidate for the development of functional ingredients that can help reduce the high rates of death from cardiovascular diseases associated with obesity.

32

Klotman, P. E., S. R. Smith, B. D. Volpp, T. M. Coffman, and W. E. Yarger. "Thromboxane synthetase inhibition improves function of hydronephrotic rat kidneys." American Journal of Physiology-Renal Physiology 250, no. 2 (February 1, 1986): F282—F287. http://dx.doi.org/10.1152/ajprenal.1986.250.2.f282.

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Twenty-four hours of complete unilateral ureteral obstruction (UUO) produces intense renal vasconstriction in the rat even after release of obstruction. In the ex vivo perfused hydronephrotic rabbit kidney, bradykinin stimulates increased production of the vasoconstrictor autocoid thromboxane. In the present study, we measured basal and bradykinin-stimulated thromboxane and prostaglandin E2 production by UUO and contralateral rat kidneys perfused ex vivo. Furthermore, we evaluated thromboxane synthetase inhibition by imidazole and by two of its substituted derivatives, UK 37248 and UK 38485, in vitro. We compared these in vitro findings with in vivo measurements of renal hemodynamics and excretory function before and after the intrarenal artery administration of thromboxane synthetase inhibitors. Both basal and bradykinin-stimulated thromboxane and prostaglandin E2 production were significantly increased in hydronephrotic kidneys. Imidazole and its substituted congeners were effective inhibitors of bradykinin-stimulated thromboxane B2 production in vitro. However, the substituted imidazoles were more potent, more efficacious, and more selective for thromboxane synthetase inhibition than the parent compound. In vivo, administration of imidazole into the renal artery of the UUO kidney improved function slightly, whereas administration of UK 37248 or UK 38485 doubled renal blood flow and excretory function but did not restore them to normal. We conclude that the hydronephrotic rat kidney produces increased amounts of the vasoconstrictor eicosanoid thromboxane and that thromboxane is an important mediator of vasoconstriction in this model of disease.

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Yoshihara, Hikari A. I., Jessica A. M. Bastiaansen, Corinne Berthonneche, Arnaud Comment, and Juerg Schwitter. "An intact small animal model of myocardial ischemia-reperfusion: Characterization of metabolic changes by hyperpolarized 13C MR spectroscopy." American Journal of Physiology-Heart and Circulatory Physiology 309, no. 12 (December 15, 2015): H2058—H2066. http://dx.doi.org/10.1152/ajpheart.00376.2015.

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Hyperpolarized carbon-13 magnetic resonance spectroscopy (13C MRS) enables the sensitive and noninvasive assessment of the metabolic changes occurring during myocardial ischemia-reperfusion. Ischemia-reperfusion models using hyperpolarized 13C MRS are established in heart preparations ex vivo and in large animals in vivo, but an in vivo model in small animals would be advantageous to allow the study of reperfusion metabolism with neuroendocrine and inflammatory responses intact with the option to perform a greater number of experiments. A novel intact rat model of ischemia-reperfusion is presented that incorporates hyperpolarized 13C MRS to characterize reperfusion metabolism. Typically, in an in vivo model, a tissue input function (TIF) is required to account for apparent changes in the metabolism of injected hyperpolarized [1-13C]pyruvate resulting from changes in perfusion. Whereas the measurement of a TIF by metabolic imaging is particularly challenging in small animals, the ratios of downstream metabolites can be used as an alternative. The ratio of [13C]bicarbonate:[1-13C]lactate (RatioBic/Lac) measured within 1–2 min after coronary release decreased vs. baseline in ischemic rats ( n = 10, 15-min occlusion, controls: n = 10; P = 0.017 for interaction, 2-way ANOVA). The decrease in oxidative pyruvate metabolism [RatioBic/Lac(Ischemia)/RatioBic/Lac(Baseline)] modestly correlated with area at risk ( r = 0.66; P = 0.002). Hyperpolarized 13C MRS was also used to examine alanine production during ischemia, which is observed in ex vivo models, but no significant change was noted; metrics incorporating [1-13C]alanine did not substantially improve the discrimination of ischemic-reperfused myocardium from nonischemic myocardium. This intact rat model, which mimics the human situation of reperfused myocardial infarction, could be highly valuable for the testing of new drugs to treat reperfusion injury, thereby facilitating translational research.

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Posma, Rene A., Leonie H. Venema, Tobias M. Huijink, Andrie C. Westerkamp, A. Mireille A. Wessels, Nynke J. De Vries, Frank Doesburg, et al. "Increasing metformin concentrations and its excretion in both rat and porcine ex vivo normothermic kidney perfusion model." BMJ Open Diabetes Research & Care 8, no. 1 (August 2020): e000816. http://dx.doi.org/10.1136/bmjdrc-2019-000816.

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IntroductionMetformin can accumulate and cause lactic acidosis in patients with renal insufficiency. Metformin is known to inhibit mitochondria, while renal secretion of the drug by proximal tubules indirectly requires energy. We investigated whether addition of metformin before or during ex vivo isolated normothermic machine perfusion (NMP) of porcine and rat kidneys affects its elimination.Research design and methodsFirst, Lewis rats were pretreated with metformin or saline the day before nephrectomy. Subsequently, NMP of the kidney was performed for 90 min. Metformin was added to the perfusion fluid in one of three different concentrations (none, 30 mg/L or 300 mg/L). Second, metformin was added in increasing doses to the perfusion fluid during 4 hours of NMP of porcine kidneys. Metformin concentration was determined in the perfusion fluid and urine by liquid chromatography-tandem mass spectrometry.ResultsMetformin clearance was approximately 4–5 times higher than creatinine clearance in both models, underscoring secretion of the drug. Metformin clearance at the end of NMP in rat kidneys perfused with 30 mg/L was lower than in metformin pretreated rats without the addition of metformin during perfusion (both p≤0.05), but kidneys perfused with 300 mg/L trended toward lower metformin clearance (p=0.06). Creatinine clearance was not different between treatment groups. During NMP of porcine kidneys, metformin clearance peaked at 90 min of NMP (18.2±13.7 mL/min/100 g). Thereafter, metformin clearance declined, while creatinine clearance remained stable. This observation can be explained by saturation of metformin transporters with a Michaelis-Menten constant (95% CI) of 23.0 (10.0 to 52.3) mg/L.ConclusionsMetformin was secreted during NMP of both rat and porcine kidneys. Excretion of metformin decreased under increasing concentrations of metformin, which might be explained by saturation of metformin transporters rather than a self-inhibitory effect. It remains unknown whether a self-inhibitory effect contributes to metformin accumulation in humans with longer exposure times.

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Bladt, S., and H. Wagner. "Inhibition of MAO by Fractions and Constituents of Hypericum Extract." Journal of Geriatric Psychiatry and Neurology 7, no. 1 (January 1994): 57–59. http://dx.doi.org/10.1177/089198879400700115.

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The inhibition of monoamine oxidase (MAO) by six fractions from hypericum extract and three characteristic constituents (as pure substances) were analyzed in vitro and ex vivo to study the antidepressive mechanism of action. Rat brain homogenates were used as the in vitro model, while the ex vivo analysis was performed after intraperitoneal application of the test substances to albino rats. Massive inhibition of MAO-A could be shown with the total extract and all fractions only at the concentration of 10-3 mol/L. At 10-4 mol/L, one fraction rich in flavonoides showed an inhibition of 39%, and all other fractions demonstrated less than 25% inhibition. Using pure hypericin as well as in all ex vivo experiments, no relevant inhibiting effects could be shown. From the results it can be concluded that the clinically proven antidepressive effect of hypericum extract cannot be explained in terms of MAO inhibition.

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Bladt, S., and H. Wagner. "Inhibition of MAO by Fractions and Constituents of Hypericum Extract." Journal of Geriatric Psychiatry and Neurology 7, no. 1_suppl (January 1994): 57–59. http://dx.doi.org/10.1177/089198879400701s15.

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The inhibition of monoamine oxidase (MAO) by six fractions from hypericum extract and three characteristic constituents (as pure substances) were analyzed in vitro and ex vivo to study the antidepressive mechanism of action. Rat brain homogenates were used as the in vitro model, while the ex vivo analysis was performed after intraperitoneal application of the test substances to albino rats. Massive inhibition of MAO-A could be shown with the total extract and all fractions only at the concentration of 10-3 mol/L. At 10-4 mol/L, one fraction rich in flavonoides showed an inhibition of 39%, and all other fractions demonstrated less than 25% inhibition. Using pure hypericin as well as in ex vivo experiments, no relevant inhibiting effects could be shown. From the results it can be concluded that the clinically proven antidepressive effect of hypericum extract cannot be explained in terms of MAO inhibition.

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Zhou, Yan, Xinqiao Zhou, Wenjuan Zhou, Qingfeng Pang, and Zhiping Wang. "The protective effect of dexmedetomidine in a rat ex vivo lung model of ischemia-reperfusion injury." Acta Cirurgica Brasileira 33, no. 1 (January 2018): 1–13. http://dx.doi.org/10.1590/s0102-865020180010000001.

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Puppi, Juliana, Michel Modo, Anil Dhawan, Sharon C. Lehec, Ragai R. Mitry, and Robin D. Hughes. "Ex Vivo Magnetic Resonance Imaging of Transplanted Hepatocytes in a Rat Model of Acute Liver Failure." Cell Transplantation 23, no. 3 (April 2014): 329–43. http://dx.doi.org/10.3727/096368913x663596.

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39

Bujak-Giżycka, Beata, Józef Madej, Maciej Suski, Katarzyna Kuś, Stefan Zorad, Rafał Olszanecki, and Ryszard Korbut. "Metabolism of angiotensin-(1-12) in adipose tissue – ex vivo study in rat model of hypertension." Pharmacological Reports 65 (May 2013): 33. http://dx.doi.org/10.1016/s1734-1140(13)71306-9.

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40

Burki, Sarah, Kentaro Noda, Brian J. Philips, Murugesan Velayutham, Sruti Shiva, Pablo G. Sanchez, Ajay Kumar, and Jonathan D'Cunha. "Impact of triptolide during ex vivo lung perfusion on grafts after transplantation in a rat model." Journal of Thoracic and Cardiovascular Surgery 161, no. 1 (January 2021): e65-e74. http://dx.doi.org/10.1016/j.jtcvs.2019.12.104.

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Armstrong, D., M. Farrell, G. M. Murphy, and R. H. Dowling. "The Differing Gastrotoxicity of Various Bile Acids; Studies with an ex vivo Rat Gastric Chamber Model." Clinical Science 73, s17 (December 1, 1987): 45P. http://dx.doi.org/10.1042/cs073045p.

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Biesalski, H. K., L. Engel, E. Stofft, and A. Zschäbitz. "An ex vivo model of the rat trachea to study the effect of inhalable toxic compounds." Research in Experimental Medicine 196, no. 4 (1996): 195. http://dx.doi.org/10.1007/s004330050027.

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Biesalski, H. K., L. Engel, E. Stofft, and A. Zschäbitz. "An ex vivo model of the rat trachea to study the effect of inhalable toxic compounds." Research in Experimental Medicine 196, no. 1 (December 1996): 195–210. http://dx.doi.org/10.1007/bf02576842.

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Ohsumi, A., K. Marseu, P. Slinger, K. McRae, T. Waddell, M. Liu, S. Keshavjee, and M. Cypel. "Protective Effect of Anesthetic Preconditioning During Ex Vivo Lung Perfusion in a Rat Lung Transplantation Model." Journal of Heart and Lung Transplantation 36, no. 4 (April 2017): S375—S376. http://dx.doi.org/10.1016/j.healun.2017.01.1068.

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Knecht, Camila, Cecilia L. Balaban, Joaquín V. Rodríguez, Eduardo A. Ceccarelli, Edgardo E. Guibert, and Germán L. Rosano. "Proteome variation of the rat liver after static cold storage assayed in an ex vivo model." Cryobiology 85 (December 2018): 47–55. http://dx.doi.org/10.1016/j.cryobiol.2018.10.003.

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Fukuse, Tatsuo, Johannes M. Albes, Yutaka Takahashi, Harald Brandes, Bernard Hausen, and Hans-Joachim Schäfers. "Influence of Red Blood Cells on Lung Function in an ex Vivo Rat Heart-Lung Model." Journal of Surgical Research 59, no. 3 (September 1995): 399–404. http://dx.doi.org/10.1006/jsre.1995.1182.

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Dutta, Mousumi, and Goutam Paul. "BISPHENOL A DOSE- AND TIME-DEPENDENTLY INDUCES OXIDATIVE STRESS IN RAT LIVER MITOCHONDRIA EX VIVO." Asian Journal of Pharmaceutical and Clinical Research 11, no. 9 (September 7, 2018): 98. http://dx.doi.org/10.22159/ajpcr.2018.v11i9.26750.

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Objective: The probable toxic effects of bisphenol A (BPA) on different physiological functions have been reported in animal models. The role of BPA in mitochondrial oxidative stress has not been reported till date. The present study is aimed to elucidate dose- and time-dependent oxidative stress generation by BPA, respectively, in rat liver mitochondria in ex vivo model. Methods: The incubation mixture of BPA-treated groups containing mitochondria, 50 mM potassium phosphate buffer (pH 7.4), and different concentrations of BPA (20–160 μM/ml) (dissolved in 12% DMSO) in a final volume of 1.0 ml was incubated at 37°C in incubator for different time durations (30 min–2 h). Whereas, the incubation mixture of control group contained DMSO (12%), mitochondria and 50 mM potassium phosphatebuffer (pH 7.4).’ will be replaced by ‘Whereas, the incubation mixture of control group contained the same constituents except BPA. Result: We have observed significant decrease in mitochondrial intactness incubated with BPA in dose- and time-dependent manner under bright field and confocal microscopic study compared to control. Further, we have observed a decrease in mitochondrial reduced glutathione (GSH) content and increase in lipid peroxidation and protein carbonylation levels in dose- and time-dependent manner in BPA-exposed mitochondria. We have found a significant increase in the activity of Mn-superoxide dismutase and decrease in the activities of GSH peroxidase, GSH reductase, pyruvate dehydrogenase, and other three enzymes of Kreb’s cycle dose and time dependently in BPA-exposed mitochondria. The results indicate that exposure to BPA leads to decrease in intactness of mitochondria and increase in oxidative stress in mitochondria isolated from rat liver in a dose- and time-dependent manner. Conclusion: It can be concluded that the incubation of mitochondria isolated from rat liver with BPA, caused oxidative stress-mediated damages in mitochondria in both dose- and time-dependent manners.

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Martin, Dan, and Mircea Radu Gorgan. "Step training in a rat model for complex aneurysmal vascular microsurgery." Romanian Neurosurgery 29, no. 4 (December 1, 2015): 493–502. http://dx.doi.org/10.1515/romneu-2015-0066.

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Abstract Introduction: Microsurgery training is a key step for the young neurosurgeons. Both in vascular and peripheral nerve pathology, microsurgical techniques are useful tools for the proper treatment. Many training models have been described, including ex vivo (chicken wings) and in vivo (rat, rabbit) ones. Complex microsurgery training include termino-terminal vessel anastomosis and nerve repair. The aim of this study was to describe a reproducible complex microsurgery training model in rats. Materials and methods: The experimental animals were Brown Norway male rats between 10-16 weeks (average 13) and weighing between 250-400g (average 320g). We performed n=10 rat hind limb replantations. The surgical steps and preoperative management are carefully described. We evaluated the vascular patency by clinical assessment-color, temperature, capillary refill. The rats were daily inspected for any signs of infections. The nerve regeneration was assessed by foot print method. Results: There were no case of vascular compromise or autophagia. All rats had long term survival (>90 days). The nerve regeneration was clinically completed at 6 months postoperative. The mean operative time was 183 minutes, and ischemia time was 25 minutes.

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Panda, Siva Prasad, Asit Kumar Sarangi, and Uttam Prasad Panigrahy. "ISOLATION OF CUCURBITACIN-B FROM CUCUMIS CALLOSUS AND ITS HYPOGLYCEMIC EFFECT IN ISOLATED RAT ENTEROCYTES." International Journal of Pharmacy and Pharmaceutical Sciences 10, no. 5 (May 1, 2018): 123. http://dx.doi.org/10.22159/ijpps.2018v10i5.25788.

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Objective: The pericarp of fruits of Cucumis callous (Rottl.) Cogn. (Cucurbitaceae) is traditionally used for curing diabetes, epilepsy, and diarrhea. It has an active compound include Cucurbitacin-B (CuB), which acts as a potent inducer of CYP450 of rat enterocytes. This study was conducted with the aim of elaborating and reconciling our previous finding on the glucose-lowering effect of Cucumis callosus (Rottl.) Cogn. fruits.Methods: In vivo hypoglycemic potential for methanolic pericarp extracts from C callosus (MPCC, 350 mg/kg b.w. p. o), methanolic seed extract of C callosus (MSCC, 250 mg/kg b.w. p. o) and CuB (80 µg/kg b.w. p. o) were studied in streptozotocin (STZ, 55 mg/kg b.w. i. p) induced diabetic rats. Metformin (25 mg/kg b.w. p. o) served as reference drug. Ex vivo model of intestinal tissue preparation of Swiss albino rats named Single Pass Intestinal Perfusion (SPIP) technique was performed for ex vivo hypoglycemic study. The glucose levels in the serosal fluid were determined by commercially available glucose oxidase kit and compared with the standard drug metformin (0.1 mg/kg).Results: In vivo results showed that administration of MPCC (350 mg/kg b.w. p. o) and Cucurbitacin-B (80 µg/kg b.w. p. o) produced the hypoglycemic effect. The MPCC (1.4 mg/kg) and CuB (0.4 µg/kg) produced hypoglycemic effect in ex vivo technique. These effects are due to induction of 0.53 mµmoles of CYP450 proteins with maximum absorption at 454 mµ in rat enterocytes.Conclusion: The present investigation gave evidence that bitter pericarp of C callosus fruit has a hypoglycemic effect due to the presence of Cucurbitacin B as phytoconstituent but seeds did not have such effects.

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Patel, Mihir K., Kiranj K. Chaudagar, and Anita A. Mehta. "ROLE OF NITRIC OXIDE (NO) IN CAPSAICIN MEDIATED ANTI-PLATELET ACTIVITY IN IN VITRO, IN VIVO, EX-VIVO MODEL OF PLATELET AGGREGATION ASSAY AND ARTERIAL THROMBOSIS IN RAT: POTENTIAL THERAPEUTIC TARGET?" International Journal of Pharmacy and Pharmaceutical Sciences 10, no. 4 (April 1, 2018): 44. http://dx.doi.org/10.22159/ijpps.2018v10i4.22474.

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Objective: Although recent advances in the treatment of congestive heart disease, mortality among patients’ remains a questionable remark. Therefore, we evaluated the role of capsaicin on in vitro and ex vivo platelet aggregation induced by Adenosine Di-Phosphate (ADP) as well as in in vivo thrombosis models and role of NO, KATP was also identified in the capsaicin-induced anti-platelet animal model as well as in vivo model of arterial thrombosis.Methods: According to body weight wistar rats were divided into five groups. Group I and Group II was treated with saline and capsaicin (3 mg/kg, i. v), while animals from Group III were treated with N(ω)-nitro-L-arginine methyl ester (L-NAME) (30 mg/kg, i. v) 30 min before administration of capsaicin (3 mg/kg, i. v). Group IV animals were treated with glibenclamide (10 mg/kg,i. v) 30 min before administration of capsaicin (3 mg/kg, i. v). Group V was considered as a positive control and administered clopidogrel (30 mg/kg, p. o). Animals were subjected for in vitro, ex-vivo platelet aggregation assay. ADP (30µM) was utilized as an aggregating agent in these experiments. After these assays; animals of each group were subjected for subaqueous tail bleeding time in a rat model and FeCl3-induced arterial thrombosis model in rats.Results: In ADP-induced in vitro platelet aggregation, a significant reduction in % platelet aggregation was observed at 50µM (64.35±4.641) and 100µM (52.72±4.192) concentration of capsaicin as compared to vehicle control (85.82±3.716). Capsaicin (3 mg/kg, i. v) also showed a significant reduction (49.53±4.075) in ex-vivo ADP-induced platelet aggregation as compared to vehicle control (89.38±2.057). In FeCl3 induced arterial thrombosis model, Capsaicin (3 mg/kg, i. v) exhibited an increase in time to occlusion in this rodent model and presence of the L-NAME and glibenclamide had inhibited the activity of capsaicin.Conclusion: In our study, capsaicin (50 µM, 100µM) exhibited potent anti-platelet activity in ADP-induced platelet aggregation, similarly capsaicin exhibited significant anti-platelet action in the ex-vivo study. Moreover, the presence of L-NAME and glibenclamide inhibited the anti-thrombotic and anti-platelet action of capsaicin. Therefore, it was concluded that NO and KATP may be involved in the anti-thrombotic action of capsaicin.