A novel dissector device that separates anatomic structures during laparoscopic surgery.

OBJECTIVE: To describe a novel dissector device useful in laparoscopy, better definition of anatomic structures to have a better dissection, separation, and cleaning of the structures. METHOD: The endoscopic dissector DisePad was designed and developed at the experimental surgery department of Centro Médico Nacional 20 de Noviembre, and properly patented at Instituto Mexicano de la Propiedad Industrial (title 3512). RESULTS: The tip of the device is the most important component, by its direct contact with the different tissues, consists of a cotton-polyester black cloth impregnated with a special gel immersed into a hot saline solution. Once soaked the tip maintains the solution temperature on itself. CONCLUSIONS: This device has been used in 364 laparoscopic procedures demonstrating, its utility to visualize, separate and clean anatomical structures without thermal lesion, tear, hemorrhage or visceral perforation.

OBJETIVO: Describir un nuevo dispositivo disector en laparoscopia, con una mejor definición de las estructuras anatómicas para obtener una mejor disección,separación y limpieza de las estructuras. MÉTODO: El disector endoscópico DisePad fue diseñado y desarrollado en el servicio de cirugía experimental del Centro Médico Nacional 20 de Noviembre, y patentado ante el Instituto Mexicano de la Propiedad Industrial (registro n.º 3512). RESULTADOS: El componente más importante del disector es la punta que tiene contacto con los tejidos: es una tela de algodón-poliéster negra impregnada en un gel (patentado) que, al ser sumergido en un termo con solución salina caliente, permite retener la temperatura. CONCLUSIONES: Este dispositivo ha sido utilizado en 364 procedimientos quirúrgicos por vía laparoscópica y ha demostrado ser útil para visualizar, separar y limpiar estructuras anatómicas sin producir daño por lesión térmica, desgarre, hemorragia ni perforación visceral.

Piroxicam and meloxicam ameliorate hepatic oxidative stress and protein carbonylation in Kupffer and sinusoidal endothelial cells promoted by ischemia-reperfusion injury.

The present study was aimed to assess the effect of protein carbonylation (PC) in hepatic cells and effects of nonsteroidal anti-inflammatory drugs (NSAIDs) on indicators of tissue damage induced by liver ischemia-reperfusion injury (LIRI). Warm ischemia was performed by partial vascular occlusion during 90 min in Wistar rats. In serum, we determined the catalytic activity of Alanine Aminotransferase, Aspartate Aminotransferase, Lacticate Dehydrogenase, and Ornithine Carbamoyltransferase. In liver samples, we studied cellular alterations by means of histologic studies, lipid peroxidation, PC by immunohistochemistry, apoptosis and reactive oxygen species in bile by electron paramagnetic resonance. Based on PC data, sinusoidal endothelial cells (SEC) and Kupffer cells (KC) were the first to exhibit LIRI-associated oxidative damage and prior to parenchymal cells. Administration of piroxicam or meloxicam during the pre-ischemic period produced a highly significant decrease in all studied injury indicators. No significant differences were revealed between the protective action of the two drugs. The data shown here suggest the potential use of NSAIDs such as piroxicam or meloxicam in minimizing ischemic event-caused damage in liver. We also propose that PC may be employed as an adequate tool to assess tissue damage after oxidative stress.

Factors in the pathophysiology of the liver ischemia-reperfusion injury.

Hepatic ischemia-reperfusion injury is commonplace in liver surgery, particularly in hepatic transplantation, hepatic resection, and trauma. The signaling events contributing to local hepatocellular damage are diverse and complex and involve the interaction between hepatocytes, sinusoidal endothelial cells, Kupffer cells, as well as infiltrating neutrophils, macrophages, and platelets. Signaling mediators include cytokines, reactive oxygen and nitrogen species, calcium, complement, and several transcription factors. The purpose of this review article was to summarize the factors that contribute to the pathophysiology of hepatic ischemia-reperfusion injury.