Background: Pulmonary loborraphy can be performed using manual sutures and staples, although other methods such as tissue adhesives are also cited in the veterinary literature. However, despite the wide availability, no efficient suture material has yet been recognized that is completely safe in preventing any air leakage, a complication that is heavily investigated in medicine and not uncommon in veterinary medicine, despite the few studies and reports in dogs. Although the surgery is well tolerated in the canine species, failure in pulmonary aerostasis is still a reality, since all the methods described so far eventually lead to air leakage after the use of the partial lobectomy technique in the lungs. Within this context, the aim of this research was to compare the effectiveness of different hermetic sealing methods after partial lobectomy of the right caudal lung lobe (RCLL) in dogs. Using 30 cadaver models of canine lungs obtained immediately after death. The 30 cadavers models were divided in 6 groups: G1 - cobbler suture associated with simple continuous; G2 - overlapping continuous suture associated with simple continuous suture; G3 - Ford interlocking suture; G4 - Stapling device; G5 - Tissue glue (cyanoacrylate). After performing the sealing techniques, the lungs were submerged in water, inflated with oxygen at positive ventilatory pressures at physiological (20 cmH2O) and supraphysiological levels (above 20 cmH2O) to evaluate the performance of the sealing methods and to asses the level of ventilatory pressures at which air leakage occur. Results: At physiological ventilatory pressure levels there was no difference between groups. However, when evaluating such methods at ventilation pressure levels above 20 cmH2O, it was found a superiority of G5 over G3 and G4. Conclusion: Manual sutures, as well as staples and synthetic tissue glue were able to promote aerostasis after partial lobectomy of the RCLL at physiological ventilatory pressures. Sealing with surgical glue was superior to Ford interlocking suture and stapling device at supraphysiological levels of ventilatory pressure. This study supports the efficay of all manual, mechanical sutures and synthetic glue sealant when used after partial lobectomy in dogs.
Canine hemangiosarcoma (HSA) is a relatively common neoplasia, occurring mainly in the skin, spleen, liver and right atrium. Despite the numerous studies investigating the treatment of canine HSA, no significant improvement in survival has been achieved in the last 20 years. Advancements in genetic and molecular profiling presented molecular similarities of canine HSA with human angiosarcoma. It could therefore serve as a valuable model for investigating new and more effective treatments in people and dogs. The most common genetic abnormalities in canine HSA have been found in the phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) and neuroblastoma RAS viral oncogene homolog (NRAS) pathways. Mutations are also found in tumor protein p53 (TP53), phosphatase and tensin homolog (PTEN) and cyclin dependent kinase inhibitor 2A (CDKN2A). Known abnormal protein expression could be exploited to trial new target treatments that could be beneficial for both canine and human patients. Despite the high expression of vascular endothelial growth factor (VEGF) and its receptor (VEGFR), no correlation with overall survival time has ever been found. In this review, we explore the most recent developments in molecular profiling in canine HSA and discuss their possible applications in the prognosis and treatment of this fatal disease.
Canine hemangiosarcoma (HSA) is a relatively common neoplasia, occurring mainly in the skin, spleen, liver and right atrium. Despite the numerous studies investigating the treatment of canine HSA, no significant improvement in survival has been achieved in the last 20 years. Advancements in genetic and molecular profiling presented molecular similarities between canine HSA and human angiosarcoma. It could therefore serve as a valuable model for investigating new and more effective treatments in people and dogs. The most common genetic abnormalities in canine HSA have been found in the phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) and neuroblastoma RAS viral oncogene homolog (NRAS) pathways. Mutations are also found in tumor protein p53 (TP53), phosphatase and tensin homolog (PTEN) and cyclin dependent kinase inhibitor 2A (CDKN2A). Known abnormal protein expression could be exploited to trial new target treatments that could be beneficial for both canine and human patients. Despite the high expression of vascular endothelial growth factor (VEGF) and its receptor (VEGFR), no correlation with overall survival time has ever been found. In this review, we explore the most recent developments in molecular profiling in canine HSA and discuss their possible applications in the prognosis and treatment of this fatal disease.
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