O propósito deste estudo foi comparar a biocompatibilidade do cimento Portland modificado (CPM) com agregado de trióxido mineral (MTA) no subcutâneo de um modelo murino. Foram usados 24 ratos Wistar macho. No tecido subcutâneo dorsal de cada animal se colocaram 3 tubos de silicone. Um contendo MTA, outro CPM e o último vazio. Os animais foram sacrificados em 3 grupos de 8 aos 7, 14 e 30 dias. As amostras se fixaram em formol e se coloriram com hematoxilina - eosina, Masson e Luna. No dia 7 os tubos vazios mostraram uma leve infiltração de células inflamatórias. No grupo CPM, se observou um infiltrado inflamatório com alguns eosinófilos e tecido conectivo imaturo. O grupo MTA mostrou um infiltrado similar sem eosinófilos e abundante necrose de tecido e numerosas células gigantes multinucleadas do tipo corpo estranho. Ao dia 14, o infiltrado crônico com eosinófilos persistiu em contato com CPM. No grupo MTA, a necrose e células multinucleadas afastadas ainda se podiam observar. Ao dia 30, os 3 grupos mostraram tecido fibroso maduro. Estes resultados mostram uma resposta diferente aos materiais avaliados no presente estudo. Apesar do que MTA e CPM causaram um infiltrado crônico, no grupo MTA predominou a necrose e as células gigantes, enquanto isso, no grupo CPM se observaram grandes quantidades de eosinófilos.

The purpose of this study was compare the biocompatibility of modified Portland cement (CPM) and mineral trioxide aggregate (MTA) in a subcutaneous rat model. Twenty-four male Wistar rats were used. Three silicon tubes were placed on the dorsal subcutaneous tissue of each animal: one tube contained MTA, one tube contained CPM and the other was an empty tube. The rats were sacrificed in 3 groups of 8 animals at 7, 14 and 30 postoperative days, respectively. Tissue samples were fixed in 10% buffered formalin, embedded in paraffin, and serial sections were cut and stained with hematoxylin and eosin, Masson Trichrome and Luna's stain. At day 7, the empty tubes displayed a mild inflammatory infiltrate. In the CPM group, an inflammatory infiltrate was observed with some eosinophils and immature connective tissue. The MTA group showed a similar infiltrate without eosinophils and presence of abundant necrotic tissue and numerous multinucleate foreign body giant cells. At day 14, the chronic infiltrate with eosinophils persisted when in contact with CPM. In the MTA group, necrosis and distant giant cells could still be seen. At day 30, all 3 groups showed mature fibrous collagenous tissue. These findings indicate a different response to the materials evaluated in this study. Although, MTA and CPM induced a chronic inflammatory infiltrate, necrosis and multinucleated foreign body giant cells predominated in the MTA group, while in the CPM group numerous eosinophils were seen at all the observational periods.

Objective The aim of the present study was to assess the morphology of early atherosclerotic lesions in coronary arteries from sudden infant death syndrome (SIDS) victims in order to recognize atherogenic mechanisms. Material and Methods We examined 52 victims of SIDS and 16 controls with known causes of infant death. The principal coronary arteries were serially cut and stained with hematoxilin-eosin, Azan, Alcian blue, acetic orcein, CD68, CD34 and α-SM actin, with subsequent histomorphometric analysis of the lesions. Results Preatherosclerotic lesions were found in 44.2% in SIDS group (23/52) and only in 6.3% in controls (1/16) (p=0.0062). Smooth muscle cells lost polarity, infiltrating the subedothelium, with rupture of the internal elastic membrane (IEM) in most cases. Angiogenesis was not observed. When muscular and elastic intimal thickening was present in the SIDS group, the results were as follows: neointimal thickness, 58.3±17.8 mm; affected perimeter of the EIM, 45.6%; area of neointimal proliferation, 0.03±0.01 mm²; and luminal area, 0.21±0.1 mm² with a luminal stenosis of 13.8±5%. Conclusions Preatherosclerotic lesions develop early in SIDS victims, and they are significantly more frequent than in controls. Smooth muscle cells are fundamental in its genesis.

Objetivo El presente estudio se llevó a cabo con el propósito de caracterizar morfológicamente lesiones ateroscleróticas precoces en arterias coronarias de víctimas del "síndrome de muerte súbita infantil" (SMSI) para conocer los mecanismos aterogénicos. Material y métodos Se efectuó el examen de 52 víctimas de SMSI y de 16 casos controles fallecidos de causas conocidas. Las principales arterias coronarias se cortaron serialmente y se tiñeron con hematoxilina-eosina, Azán, azul alciano, orceína acética, CD68, CD34 y α-SM-actina y se realizó histomorfometría de las lesiones. Resultados Se encontraron lesiones preateroscleróticas en el 44,2% del grupo SMSI (23/52) y en sólo el 6,3% del grupo control (1/16) (p = 0,0062). Las células musculares lisas perdieron la polaridad, infiltrándose en el subendotelio, en gran parte de los casos con rotura de la membrana elástica interna (MEI). No se observó neoangiogénesis. En el grupo SMSI con engrosamiento musculoelástico intimal, el espesor neointimal fue de 58,3 ± 17,8 mm, el perímetro de la MEI afectado fue del 45,6%, el área de proliferación neointimal fue de 0,03 ± 0,01 mm² y el área luminal fue de 0,21 ± 0,1 mm² con 13,8% ± 5% de estenosis luminal. Conclusiones Las lesiones preateroscleróticas se desarrollan temprano en víctimas del SMSI y son significativamente más frecuentes que en los controles. Las células musculares lisas tienen un papel fundamental en su génesis.

We have recently reported serious lesions in the carotid glomus and the autonomic ganglia of SHR rats, and suggested that this effect was due more to an increase in blood pressure than to aging. Subsequently we showed, also in SHR rats, that compared to atenolol, ramipril exerts a protective effect on these structures, well beyond the reduction in blood pressure. Since there are no studies describing the changes caused by AT1 blockade on glomus morphology in normotensive rats, we undertook the present study with the goal of assessing the effect of losartan on the glomus of male Wistar rats treated during 8 months. Fourteen rats aged 4 weeks were divided into two groups: control and losartan (10 mg/kg/day in drinking water). Systolic blood pressure (SBP) was recorded at initiation and monthly thereafter. At the age of 9 months, the rats were sacrificed and their carotid glomus extracted, stained with hematoxilin-eosin and Masson's trichromic and processed for histomorphometry with an image analyzer. In the control group, SBP was 115 ± 8.1 mm Hg, whereas in the losartan group it was 105 ± 8.3 mm Hg (p = 0.0375). As to histomorphometry, the treated group exhibited a larger glomus area compared to the control group (497.931± 48.783 versus 59.668 ± 6.196 µm²; p < 0.0001) and a wall/ lumen ratio in the glomus arterioles of 0.7 ± 0.1 versus 2.7± 0.6, respectively (p < 0.0001). The control group exhibited a decrease in the glomus area and an increase in wall/lumen ratio, suggesting that the atrophy observed with increasing age in the structures analyzed is related to arterial blood supply.

Recientemente comunicamos lesiones graves en el glomus carotídeo y los ganglios autonómicos de ratas SHR y sugerimos que este efecto se debía más al aumento de la presión arterial que al envejecimiento. Posteriormente demostramos, en SHR, que el ramipril, en comparación con el atenolol, ejerce un efecto protector sobre estas estructuras más allá de la reducción de la presión arterial. Teniendo en cuenta que no existen trabajos que describan los cambios que origina el bloqueo AT1 sobre la morfología del glomus en ratas normotensas, se realizó el presente estudio con el objetivo de evaluar el efecto del losartán sobre esta estructura de ratas Wistar macho tratadas durante 8 meses. Se emplearon 14 ratas de 4 semanas de edad, divididas en grupos control y losartán (10 mg/ kg/día en el agua de bebida). La presión sistólica (PAS) se registró al inicio y luego mensualmente. A la edad de 9 meses se sacrificaron las ratas y se extrajeron los glomus carotídeos, se tiñeron con hematoxilina-eosina y tricrómico de Masson y se procesaron para histomorfometría con un analizador de imágenes. El grupo control registró una PAS de 115 ± 8,1, mientras que en el grupo losartán fue de 105 ± 8,3 mm Hg (p = 0,0375). Histomorfométricamente, el grupo tratado mostró un área mayor del glomus con respecto al control (497.931 ± 48.783 versus 59.668 ± 6.196 µm²; p< 0,0001) y una relación pared/luz en las arteriolas glómicas de 0,7 ± 0,1 versus 2,7 ± 0,6, respectivamente (p < 0,0001). El grupo control mostró disminución del área glómica y un aumento de la relación pared/ luz, lo cual sugiere que la atrofia de las estructuras estudiadas a través del aumento de la edad se vincula con el aporte nutricio arterial.

Background Formation of reactive oxygen species during post ischemic reperfusion in experimental models induces "oxidative stress", which may exert deleterious effects on myocardium. Since during cardioplegic arrest patients undergo ischemia/ reperfusion, it has been proposed that oxidative stress might occur during cardiac surgery. However, this phenomenon has not been yet fully characterized. Study Aim To correlate glutathione release (the initial step of oxidative stress) with markers of progression of oxidant injury, such as peroxidation of membrane lipids and development of ultrastructural alterations. Methods and Results We systematically investigated changes in several markers of oxidative stress and tissue injury occurring during post ischemic reperfusion in 24 patients undergoing coronary artery bypass. Trans-cardiac blood sampling and tissue biopsies were taken at baseline and after reperfusion following an average 40.9±11.9 min cardioplegic arrest. Glutathione release was negligible at baseline (0.02±0.04 µmol/ L), but markedly increased 15 min after reperfusion (1.10±0.40 µmol/L; p< 0.05); concurrently, tissue concentration of the antioxidant ubiquinol decreased from 144.5±52.0 to 97.6±82.0 nmol/g (p< 0.05). Even though these changes document exposure of the heart to oxidants, this was not accompanied by biochemical alterations indicative of cell injury, since neither coronary sinus blood nor cardiac biopsies showed increased lipid peroxidation. Furthermore, electron microscopy showed no major ultrastructural alterations. Conclusions Although an excess of oxidant production occurs in patients undergoing cardiac surgery, in our settings, cardiac oxidative stress did not progress to membrane damage and irreversible injury.

Introducción En modelos experimentales, la formación de especies reactivas del oxígeno durante la reperfusión posisquémica induce "estrés oxidativo" que afecta al miocardio. Dado que los pacientes sometidos a cardioplejía sufren isquemia-reperfusión, se sugirió que en ellos habría estrés oxidativo. Sin embargo, este fenómeno aún no se ha caracterizado correctamente. Objetivo El propósito del presente trabajo fue correlacionar la liberación de glutatión (el paso inicial de estrés oxidativo) con marcadores de progresión del daño oxidativo, como peroxidación de lípidos de membrana y desarrollo de alteraciones ultraestructurales. Material y métodos En 24 pacientes sometidos a cirugía de puente aortocoronario se investigaron cambios en varios marcadores de estrés oxidativo y daño tisular durante la reperfusión posisquémica. Se obtuvieron muestras de sangre y biopsias cardíacas basales y luego de la reperfusión a 40,9 ± 11,9 minutos de la cardioplejía. La liberación de glutatión basal fue insignificante (0,02 ± 0,04 µmol/L), pero aumentó a los 15 minutos de la reperfusión (1,10 ± 0,40 µmol/L; p < 0,05); también disminuyeron los niveles tisulares de ubiquinol, de 144,5 ± 52 a 97,6± 82 nmol/g (p < 0,05). Aunque estos cambios documentan el estrés oxidativo cardíaco, no hubo alteraciones bioquímicas indicativas de daño celular, ya que no se produjo un incremento de marcadores de peroxidación lipídica, tanto en sangre del seno coronario como en las biopsias cardíacas. Tampoco se observaron alteraciones ultraestructurales importantes. Conclusiones A pesar de observarse estrés oxidativo en pacientes sometidos a cirugía cardíaca, en las condiciones descriptas, no induce lesiones progresivas de membranas ni daño celular irreversible.