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In treatment of hypovolemia it is important to reestablish normal tissue hemodynamics after fluid resuscitation. Vascular endothelial growth factor (VEGF) and VEGF receptors (VEGFR) have been identified as important in many physiological and pathological processes. In this study, we aimed to investigate the histo-physiological effects of VEGF, VEGFR-1 (flt-1) and VEGFR-2 (KDR/flk-1) in resuscitation with different plasma substitutes on lung tissues after acute hemorrhage in rats. Male Sprague-Dawley rats (n=25) were used in this study. The left femoral vein and artery were cannulated for the administration of volume expanders and for direct measurement of mean arterial blood pressure (MAP) (Power-Lab) and heart rate (HR). Fifteen rats were bled (5 ml/10 min) and infused (5 ml/5 min) with one of three randomly selected fluids: (a) dextran-70 (Macrodex); (b) gelatin (Gelofusine); or (c) physiological saline (PS, 0.9% isotonic saline) solutions. Five rats were bled and none were infused (hypovolemia group) and five rats were untreated as the control group. At the end of the experiment, rats were sacrificed and lung tissues were removed for routine processing and paraffin wax embedding. Sections of tissue were stained with hematoxylin and eosin (H&E) and selected blocks were then prepared for indirect immunohistochemical labeling for anti-VEGF, anti-VEGFR-1 and anti-VEGFR-2 primary antibodies. It was observed that both MAP and HR decreased parallel to blood withdrawn in this time interval. The MAP and HR were restored in the following periods. In the control rats, positive immunoreactivity of VEGF and its receptors (VEGFR-1 and VEGFR-2) were detected in respiratory epithelial cells, respiratory and vascular smooth muscle cells, alveolar cells and endothelial cells. While strong immunoreactivities of VEGF and VEGFR-1 were observed in the hypovolemia group, only moderate immunoreactivity of VEGFR-2 was seen in this group. Moderately strong immunolabeling of VEGF and VEGFR-1 were observed in the dextran-70, gelatin and PS resuscitated groups, whereas only weak immunolabeling of VEGFR-2 was observed in these groups. In summary, the vascular protecting effects of these factors were observed with fluid resuscitation, contributing to the pathophysiological changes seen in hypovolemia. 相似文献
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Gastric outlet obstruction is commonly caused by gastric ulcers, pyloric stenosis, foreign bodies, and compression of the duodenum by pancreatic cancer and other intra-abdominal masses. There is no report on Riedel's lobe of the liver as a cause of this condition. This is the first report to describe Riedel's lobe of the liver as a cause of gastric outlet obstruction. An 81-year-old woman who complained of severe nausea and abdominal discomfort was admitted to our clinic. The physical examination revealed a mass in the right upper quadrant of the abdomen. An exploratory laparotomy showed an approximately 10x6-cm tongue-like mass arising from the left lobe of the liver, extending to the umbilicus and compressing the prepyloric area of the stomach. The nature and location of the mass were compatible with Riedel's lobe. A cholecystectomy was performed and the compressing mass was fixed to the abdominal wall with a simple suture. The patient did well postoperatively and was discharged from the hospital. We also reviewed the English-language literature to provide an update on this subject. 相似文献
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Muhammed Yildirim Mustafa Kaplan Alpaslan Tanoglu Zafer Kucukodaci Yesim Onal Tastan 《Scandinavian journal of gastroenterology》2020,55(2):236-241
AbstractBackground: To investigate the protective efficacy of pentoxifylline through biochemical parameters and histopathological scores in a caerulein- and alcohol-induced experimental model of chronic pancreatitis in rats.Methods: A model of chronic pancreatitis with caerulein and alcohol was created in female rats of the genus Sprague Dawley. Pentoxifylline was administered in doses of 25?mg/kg (low dose) and 50?mg/kg (high dose) as a protective agent. Each group contained 8 animals. The groups were: group 1 (control group); caerulein?+?alcohol, group 2 (low-dose pentoxifylline group); caerulein?+?alcohol?+?pentoxifylline 25?mg/kg, group 3 (high-dose pentoxifylline group); caerulein?+?alcohol?+?pentoxifylline 50?mg/kg, group 4 (placebo); caerulein?+?alcohol?+?saline, group 5 (sham group); only saline injection.Rats were sacrificed 12?h after the last injection, and TNF-α, TGF-β, MDA, and GPx concentrations were measured in blood samples. The histopathologic examination was conducted by a pathologist who was unaware of the groups.Results: The biochemical results of the treatment groups (group 2 and group 3) were statistically significantly lower compared with the control group (group 1) (p?<?.05). The difference between the low-dose treatment group (group 2) and high-dose treatment group (group 3) was significant in terms of biochemical parameters (p?<?.05). The difference between group 2 and the control group was not significant in terms of histopathologic scores (p?>?.05), whereas the difference between the group 3 and the control group was statistically significant (p?<?.05).Conclusions: As a result, pentoxifylline, which has anti-inflammatory and antioxidant properties, was shown to have protective efficacy in an experimentally generated model of chronic pancreatitis. 相似文献
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Bahceci F Sari R Sarikaya M Atik E Karincaoglu Y Sevinc A 《Journal of the National Medical Association》2004,96(6):844-846
Autosomal dominant polycystic kidney disease is a multisystem disorder characterized by multiple, bilateral renal cysts and is also associated with cysts in other organs, such as the liver, pancreas, and arachnoid membranes. Dermatomyositis is a disease which mainly involves the skin and muscles, although occasionally other organs are affected. In this report, a 56-year-old male patient with a four-year history of autosomal dominant polycystic kidney disease was presented. Renal failure was exacerbated by a coexisting dermato-polymyositis. Prednisone treatment with hemodialysis improved the situation. This is the first report renal failure in a patient with autosomal dominant polycystic kidney disease and dermato-polymyositis. 相似文献
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