Presence of ascites in bullfrog breeders reared and kept on a frog farm / Presença de ascite em reprodutores de rã-touro criados e mantidos em ranário

Ascites is a pathology characterized by the extravasation of fluid from blood vessels and its accumulation in the abdominal cavity, caused by several associated factors. In this paper, we report the occurrence of this syndrome in breeding male and female Bullfrogs fed a commercial fish feed with 40% crude protein. Liver malformation was already observed due to lack of protein deposition in adult animals from the same spawning. The culture of ascitic fluid showed absence of bacterial growth. Kidney histopathology showed, in both sexes, a large number of tubular structures with strongly eosinophilic hyaline material suggesting colloid growth in both the cortical region and spinal cord. The analysis also revealed granulomas in various stages of development, many showing central necrotic material. The kidneys, glomerular, were mostly hypoplastic, with enlarged Bowman space, and many were hyalinized or hemorrhagic; the parenchyma showed dystrophic calcification, and many tubules containing fibrinoid material. The liver displayed a large amount of melanomacrophages in the parenchyma and foci of mono-lymphocytic hepatitis and marked cytoplasmic rarefaction, as well as several hepatocytes with pyknotic nuclei and necrotic cells and dissociation of the hepatic trabeculae. Ascites may be caused by the lesions observed in these organs.(AU)

A ascite é uma condição patológica que se caracteriza pelo extravasamento do líquido dos vasos sanguíneos e por seu acúmulo na cavidade abdominal provocado por uma somatória de fatores. É considerada uma síndrome de caráter multifatorial e, uma vez desencadeado o processo ascítico, esse se torna, na maioria dos casos, irreversível. O objetivo deste trabalho foi relatar a ocorrência dessa síndrome em machos e fêmeas reprodutores de rã-touro (Lithobates catesbeianus), alimentados com ração comercial para peixes, com 40% de proteína bruta, durante três anos e já sendo observada má formação de fígado, por falta de deposição proteica, em animais adultos da mesma desova. A cultura do líquido ascítico demonstrou ausência de crescimento bacteriano. Na histopatologia, observou-se, para ambos os sexos, nos rins, grande número de estruturas tubulares com material fortemente eosinofílico e hialino, sugerindo coloide, tanto na região cortical como na medular. Visualizaram-se também granulomas em vários estágios de desenvolvimento, muitos apresentando material necrótico central. Ainda se pôde observar que os aparelhos renais, os glomérulos, em sua maioria, estavam hipoplásicos e com aumento do espaço de Bowman, e muitos hialinizados ou hemorrágicos; além de calcificação distrófica no parênquima e nos dos túbulos, havia material fibrinoide no seu interior. No fígado, pôde-se ver grande quantidade de melanomacrófagos no parênquima e focos de hepatite monolinfocitária e acentuada rarefação citoplasmática, assim como vários hepatócitos com núcleo em picnose e células em necrose e dissociação das trabéculas hepáticas. A causa da ascite pode ser devido às lesões observadas nesses órgãos.(AU)

Presence of ascites in bullfrog breeders reared and kept on a frog farm / Presença de ascite em reprodutores de rã-touro criados e mantidos em ranário

Ascites is a pathology characterized by the extravasation of fluid from blood vessels and its accumulation in the abdominal cavity, caused by several associated factors. In this paper, we report the occurrence of this syndrome in breeding male and female Bullfrogs fed a commercial fish feed with 40% crude protein. Liver malformation was already observed due to lack of protein deposition in adult animals from the same spawning. The culture of ascitic fluid showed absence of bacterial growth. Kidney histopathology showed, in both sexes, a large number of tubular structures with strongly eosinophilic hyaline material suggesting colloid growth in both the cortical region and spinal cord. The analysis also revealed granulomas in various stages of development, many showing central necrotic material. The kidneys, glomerular, were mostly hypoplastic, with enlarged Bowman space, and many were hyalinized or hemorrhagic; the parenchyma showed dystrophic calcification, and many tubules containing fibrinoid material. The liver displayed a large amount of melanomacrophages in the parenchyma and foci of mono-lymphocytic hepatitis and marked cytoplasmic rarefaction, as well as several hepatocytes with pyknotic nuclei and necrotic cells and dissociation of the hepatic trabeculae. Ascites may be caused by the lesions observed in these organs.(AU)

A ascite é uma condição patológica que se caracteriza pelo extravasamento do líquido dos vasos sanguíneos e por seu acúmulo na cavidade abdominal provocado por uma somatória de fatores. É considerada uma síndrome de caráter multifatorial e, uma vez desencadeado o processo ascítico, esse se torna, na maioria dos casos, irreversível. O objetivo deste trabalho foi relatar a ocorrência dessa síndrome em machos e fêmeas reprodutores de rã-touro (Lithobates catesbeianus), alimentados com ração comercial para peixes, com 40% de proteína bruta, durante três anos e já sendo observada má formação de fígado, por falta de deposição proteica, em animais adultos da mesma desova. A cultura do líquido ascítico demonstrou ausência de crescimento bacteriano. Na histopatologia, observou-se, para ambos os sexos, nos rins, grande número de estruturas tubulares com material fortemente eosinofílico e hialino, sugerindo coloide, tanto na região cortical como na medular. Visualizaram-se também granulomas em vários estágios de desenvolvimento, muitos apresentando material necrótico central. Ainda se pôde observar que os aparelhos renais, os glomérulos, em sua maioria, estavam hipoplásicos e com aumento do espaço de Bowman, e muitos hialinizados ou hemorrágicos; além de calcificação distrófica no parênquima e nos dos túbulos, havia material fibrinoide no seu interior. No fígado, pôde-se ver grande quantidade de melanomacrófagos no parênquima e focos de hepatite monolinfocitária e acentuada rarefação citoplasmática, assim como vários hepatócitos com núcleo em picnose e células em necrose e dissociação das trabéculas hepáticas. A causa da ascite pode ser devido às lesões observadas nesses órgãos.(AU)

Endocrine effects of tobacco smoke exposure during lactation in weaned and adult male offspring.

Children from pregnant smokers show more susceptibility to develop obesity in adult life. Previously, we failed to demonstrate a program for obesity in rat offspring only when the mothers were exposed to tobacco smoke during lactation. Here, we studied the short- and long-term effects of smoke exposure (SE) to both dams and their pups during lactation on endocrine and metabolic parameters. For this, we designed an experimental model where nursing rats and their pups were divided into two groups: SE group, exposed to smoke in a cigarette smoking machine (four times/day, from the third to the 21st day of lactation), and group, exposed to filtered air. Pups were killed at 21 and 180 days. At weaning, SE pups showed lower body weight (7%), length (5%), retroperitoneal fat mass (59%), visceral adipocyte area (60%), and higher subcutaneous adipocyte area (95%) with hypoinsulinemia (-29%), hyperthyroxinemia (59%), hypercorticosteronemia (60%), and higher adrenal catecholamine content (+58%). In adulthood, SE offspring showed higher food intake (+10%), body total fat mass (+50%), visceral fat mass (retroperitoneal: 55%; mesenteric: 67%; and epididymal: 55%), and lower subcutaneous adipocyte area (24%) with higher serum glucose (11%), leptin (85%), adiponectin (1.4-fold increase), total triiodothyronine (71%), free thyroxine (57%), TSH (36%), triglycerides (65%), VLDL cholesterol (+66%), and HDL cholesterol (91%) levels and lower corticosteronemia (41%) and adrenal catecholamine content (57%). Our present findings suggest that tobacco SE to both dams and their pups during lactation causes malnutrition in early life that programs for obesity and hormonal and metabolic disturbances in adulthood, only if the pups are submitted to the same smoke environment as the mother.

Protective effects of human amniotic fluid stem cells in a model of aorta allograft vasculopathy in rats.

BACKGROUND: Chronic allograft vasculopathy (CAV) is an important cause of graft loss. Considering the immune inflammatory events involved in the development of CAV, therapeutic approaches to target this process are of relevance. Human amniotic fluid-derived stem cells (hAFSCs), a class of fetal, pluripotent stem cells with intermediate characteristics between embryonic and adult stem cells, display immunomodulatory properties. hAFSCs express mesenchymal and embryonic markers, show high proliferation rates; however, they do not induce tumor formation, and their use does not raise ethical issues. Thus, we sought to investigate the effect of hAFSC on CAV in a model of aorta transplantation. METHODS: Orthotopic aorta transplantation was performed using Fisher (F344) rats as donors and Lewis rats as recipients. Rats were divided into three groups: syngeneic (SYNG), untreated F344 receiving aorta from F344 (n = 8); allogeneic (ALLO), Lewis rats receiving allogeneic aorta from F344 (n = 8); and ALLO + hAFSC, ALLO rats treated with hAFSC (10(6) cells; n = 8). Histological analysis and immunohistochemistry were performed 30 days posttransplantation. RESULTS: The ALLO group developed a robust aortic neointimal formation (208.7 ± 25.4 µm) accompanied by a significant high number of ED1+ (4845 ± 841 cells/mm2) and CD43+ cells (4064 ± 563 cells/mm2), and enhanced expression of α-smooth muscle actin in the neointima (25 ± 6%). Treatment with hAFSC diminished neointimal thickness (180.7 ± 23.7 µm) and induced a significant decrease of ED1+ (1100 ± 276 cells/mm2), CD43+ cells (1080 ± 309 cells/µm2), and α-smooth muscle actin expression 8 ± 3% in the neointima. CONCLUSIONS: These preliminary results showed that hAFSC suppressed inflammation and myofibroblast migration to the intima, which may contribute to ameliorate vascular changes in CAV.

Developmental plasticity in adrenal function and leptin production primed by nicotine exposure during lactation: gender differences in rats.

Neonate male rats whose mothers were nicotine-treated during lactation have higher adiposity, hyperleptinemia, and adrenal dysfunction. At adulthood, they still present higher adiposity and hyperleptinemia, but there was no report about their adrenal function. Also, there was no report of this developmental plasticity on females. Here, we evaluated the adrenal function and leptin content in adipocytes and muscle of male and female adult offspring whose mothers were nicotine-treated during lactation. On the 2nd postnatal day (PN2), dams were subcutaneously implanted with osmotic minipumps releasing nicotine (NIC-6 mg/kg/day) or saline for 14 days (12 litters/group and 2 rats/litter). Male and female offspring were killed on PN180. Significant data were p<0.05. Male NIC offspring presented higher adrenal catecholamine content (+ 89%) and TH expression (+ 38%), lower "in vitro" catecholamine release (- 19%), and higher adrenergic ß3 receptor (ADRB3, + 59%) content in visceral adipose tissue (VAT). Serum corticosterone was higher (+ 77%) in male NIC group, coherent with the increase of both CRH and ACTH immunostaining in hypothalamus and pituitary, respectively. Leptin content was higher in VAT (+ 23%), which may justify the observed hyperleptinemia. Female NIC offspring presented lower ADRB3 content in VAT (- 39%) and lower leptin content in subcutaneous adipose tissue (SAT) (- 46%), but higher leptin content in soleus muscle (+ 22%), although leptinemia was normal. We evidenced a sex dimorphism in the model of maternal nicotine exposure during lactation. The adrenal function in adult offspring was primed only in male offspring while the female offspring displayed relevant alterations in leptin content on muscle and adipocytes.

Effects of tobacco smoke exposure during lactation on nutritional and hormonal profiles in mothers and offspring.

Exposure to tobacco smoke is related to changes in energy balance regulation and several endocrine dysfunctions. Previously, we showed that maternal nicotine (the main addictive compound of tobacco) exposure exclusively during lactation affects biochemical profiles in mothers, milk, and pups. As the possible consequences for mothers and offspring of maternal smoking during lactation are still unknown, we evaluated the effects of tobacco smoke exposure on nutritional, biochemical, and hormonal parameters in dams and pups at weaning. After 72 h from birth, lactating rats were divided into two groups: smoke-exposed (S) in a cigarette-smoking machine, 4 × 1 h per day throughout the lactation period without pups; control (C), rats were treated the same as the experimental group but exposed to filtered air. Dams and pups were killed at weaning (21 days of lactation). Body weight and food intake were evaluated. Milk, blood, visceral fat, adrenal, and carcass were collected. S dams showed hyperprolactinemia (+50%), hypoinsulinemia (-40%), hypoleptinemia (-46%), as well as lower triglycerides (-53%) and very low-density lipoprotein cholesterol (-50%). Milk of S dams had higher lactose (+52%) and triglycerides (+78%). S pups presented higher body protein (+17%), lower total (-24%) and subcutaneous fat contents (-25%), hypoglycemia (-11%), hyperinsulinemia (+28%), hypocorticosteronemia (-40%), lower adrenal catecholamine content (-40%), hypertriglyceridemia (+34%), higher high-density lipoprotein cholesterol (+16%), and lower low-density lipoprotein cholesterol (-45%). In conclusion, tobacco smoke exposure leads to changes in nutritional, biochemical, and hormonal parameters in dams and, passively through the milk, may promote several important metabolic disorders in the progeny.

Spontaneous rupture of giant hepatic hemangioma: a rare source of hemoperitoneum. Case report.

BACKGROUND: Hemoperitoneum due to spontaneous rupture of a hepatic hemangioma is a rare and serious clinical event with a high mortality rate. CASE REPORT: 25-year-old woman under hormonal treatment for pregnancy with abdominal pain with distension followed by vomits, palpable epigastric mass and paleness of the skin and mucosas. Computed tomography of the abdomen without oral and venous contrast showed a heterogeneous and capsulated tumor of the liver. Exploratory laparotomy was carried out that revealed a large tumor occupying the gastro-hepatic site with partial rupture of the tumor's capsule with bleeding. Because of the close relationship between the tumor and the retro-hepatic inferior vena cava, the partial resection of the tumor was realized. The patient had a good post-operative evolution. The study of the tumor revealed hepatic hemangioma. CONCLUSION: Hepatic Hemangiomas may evolve to spontaneous rupture leading to hemorrhagic acute abdomen. Surgery is mandatory and the resection of the Hemangioma will depend on the clinical condition of the patient and on the relationship of the tumor with the vascular structures of the liver. Partial resection is a safe choice that saves lives in urgency situations, as the one described herein.

Effectiveness of thalidomide and tamoxifen in preventing neointimal hyperplasia in experimental vascular injury in rats.

INTRODUCTION: Chronic allograft vasculopathy is an important cause of graft loss. Considering the inflammatory response in the development of chronic vascular lesions, therapeutic approaches to target the inflammatory process may be useful. We sought to investigate the possible protective effects on balloon catheter-induced vascular injury of thalidomide and tamoxifen, 2 drugs with powerful anti-inflammatory, immunomodulatory, and antifibrotic effects, using an animal model that mimics the morphologic features of chronic allograft vasculopathy. METHODS: Male Wistar rats subjected to balloon catheter carotid injury (INJ) were treated with thalidomide (100 mg/kg), or tamoxifen (10 mg/kg), or vehicle. Contralateral right carotid arteries were used as uninjured controls. Morphometric and immunohistochemical analyses were performed at 14 days postinjury. RESULTS: Injured carotid arteries showed marked neointimal hyperplasia, which was significantly inhibited among animals treated with thalidomide or tamoxifen: neointimal/media ratios of 1.4 +/- 0.4 versus 0.2 +/- 0.1 versus 0.4 +/- 0.2, for INJ, INJ + Thalid, and INJ + Tamox; respectively (P < .001). The endothelial cell loss was significantly less pronounced among animals subjected to carotid balloon injury that were treated with thalidomide (24 +/- 14 vs 1 +/- 1 cells per section in INJ, respectively (P < .05). Therapy with either thalidomide or tamoxifen effectively maintained alpha-smooth muscle actin expression in the media, similar to uninjured arteries. In this setting, tamoxifen was additionally effective to prevent the migration of myofibroblasts in to the intima. CONCLUSION: Thalidomide and tamoxifen were effective to reduce neointimal hyperplasia secondary to vascular damage. The vasculoprotective effects of thalidomide were more pronounced to preserve endothelial cells, whereas tamoxifen inhibited smooth muscle cell migration and proliferation. A possible beneficial effect of combined therapy with thalidomide plus tamoxifen should be addressed in future studies.

Subcapsular hematoma of the liver due to intercostal anesthesic blockage after cholecystectomy: case report.

The subcapsular hematoma of the liver (SHL) are the results of injuries such as liver needle biopsy, liver trauma, pregnancy illnesses, parasitic diseases and others. The approach of these lesions depends on the various clinical presentations of subcapsular hematoma of the liver because it may be small with minimal clinical repercussion, managed only by ultrasound observation. In some situations the SHL may present large dimensions with hemodinamic instability. A case of subcapsular hematoma of the liver secondary to anesthetic intercostal blockade to control the postoperative pain after cholecystectomy is reported. A 34-year-old woman was submitted to intercostal anesthetic blockade after cholecystectomy for treatment of cholelithiasis. The blockade evolved with pain in right flank followed of mucocutaneous pallor and fall of the haematocrit and hemoglobin levels. At relaparotomy, subcapsular hematoma of the liver was proven and tamponed with compresses. The patient had good postoperative evolution being discharged from hospital, after removing the compresses. In conclusion, the intercostal anesthesic blockade, as any other medical procedure, is not exempt of complications. Therefore, it must be carried through in well selected cases; Anyway nowadays, there are efficient drugs for the control of postoperative pain.

Anti-inflammatory activities of Ph CL28A in rats in vivo.

The anti-inflammatory effects of Ph CL28A, a potentiator of prostacyclin output and inhibitor of leukotriene (LT) synthesis, were assessed in two models of acute inflammation. In paw oedema induced by carrageenan in rats, Ph CL28A (10-100 mg/kg), given i.p. at the same time as the carrageenan, inhibited oedema for up to 4 h. When indomethacin or Ph CL28A was given locally into the paw with carrageenan, indomethacin inhibited oedema formation but Ph CL28A potentiated the oedema for up to 4 h. As Ph CL28A does not inhibit cyclo-oxygenase, its anti-inflammatory effects in this model may reflect its ability to increase prostacyclin output. In pleurisy induced by carrageenan in rats, there were increases in leukocytes, LTB4, thromboxane B2 (TxB2) and 6-oxo-prostaglandin F1 alpha (6-oxo-PGF1 alpha) in the pleural fluid over 3 h. In this model, Ph CL28A (30 mg/kg) given i.p. decreased leukocyte numbers and LTB4 but did not affect TxB2 or 6-oxo-PGF1 alpha. Indomethacin decreased both prostanoids but did not affect leukocyte accumulation. The beneficial effects of Ph CL28A in two different models of acute inflammation suggests that it may have potential as an anti-inflammatory agent.