Entity

Time filter

Source Type

Porto Alegre, Brazil

Forgiarini L.A.,University of Porto | Grun G.,Hospital de Clinicas de Porto Alegre | Kretzmann N.A.,Hospital de Clinicas de Porto Alegre | De Munoz G.A.O.,Hospital de Clinicas de Porto Alegre | And 3 more authors.
Journal of Surgical Research | Year: 2013

Objective: To verify the impact of ischemic time on lung cell viability in an experimental model of lung ischemia-reperfusion (IR) injury and its repercussion on lung performance after reperfusion. Methods: Twenty-four animals were subjected to selective clamping of the left pulmonary artery and divided into four groups (n = 6) according to ischemic time: 15 (IR15), 30 (IR30), 45 (IR45), and 60 min (IR60). All animals were observed for 120 min after reperfusion. The hemodynamics, arterial blood gases measurements, and histologic changes were analyzed. Immunofluorescence assays for caspase 3 and annexin V were performed. Lipid peroxidation was assessed by thiobarbituric acid-reactive substances, and caspase 3 activity was assessed by colorimetric extract. Results: The partial pressure of arterial oxygen significantly decreased at the end of the observation period in the IR30, IR45, and IR60 groups (P < 0.05). The final mean arterial pressure significantly decreased in the IR60 group (P < 0.05). We observed a significant increase in caspase 3 activity and caspase 3-positive cells by immunofluorescence in the IR45 group compared with the other groups (P < 0.05). Additionally, there was an increase in necrotic cells assessed by annexin V in the IR60 group. The histologic score did not show differences among the different groups. Conclusions: The degree of cell damage had a negative impact on lung performance. Sixty minutes of lung ischemia and posterior reperfusion resulted in an increased number of necrotic cells, suggesting that these cells may not be able to reverse the effects of the IR injury because of the lack of viable cells. © 2013 Elsevier Inc. All rights reserved.


Ferrari R.S.,Laboratory of Airways and Lung | Ferrari R.S.,Federal University of Rio Grande do Sul | Andrade C.F.,Laboratory of Airways and Lung | Andrade C.F.,Federal University of Rio Grande do Sul
Oxidative Medicine and Cellular Longevity | Year: 2015

Ischemia-reperfusion (IR) injury is directly related to the formation of reactive oxygen species (ROS), endothelial cell injury, increased vascular permeability, and the activation of neutrophils and platelets, cytokines, and the complement system. Several studies have confirmed the destructiveness of the toxic oxygen metabolites produced and their role in the pathophysiology of different processes, such as oxygen poisoning, inflammation, and ischemic injury. Due to the different degrees of tissue damage resulting from the process of ischemia and subsequent reperfusion, several studies in animal models have focused on the prevention of IR injury and methods of lung protection. Lung IR injury has clinical relevance in the setting of lung transplantation and cardiopulmonary bypass, for which the consequences of IR injury may be devastating in critically ill patients. © 2015 Renata Salatti Ferrari and Cristiano Feijó Andrade.


Forgiarini Junior L.A.,Federal University of Rio Grande do Sul | Forgiarini Junior L.A.,University of Porto | Forgiarini Junior L.A.,Laboratory of Airways and Lung | Holand A.R.R.,Laboratory of Airways and Lung | And 6 more authors.
Mediators of Inflammation | Year: 2013

Background. The aim of this study was to evaluate the use of liquid perfluorocarbon (PFC) as an adjuvant substance for lung preservation and assess its role in pulmonary protection after transplantation. Methods. Seventy-two rat lungs were flushed with low-potassium dextran (LPD) solution and randomized into three main groups: control with LPD alone and experimental with 3 (PFC3) and 7 mL/kg (PFC7) of endobronchial PFC instilled just after harvest. Each group was divided into four subgroups according to preservation time (3, 6, 12, and 24 hours). Afterwards, we performed lung transplantation using rat lungs preserved for 12 hours with LPD alone or with 7 mL/kg of endobronchial PFC. Results. There was a significant increase in oxidative stress in the control group at 6 h of cold ischemic time compared with the PFC3 and PFC7 groups. The apoptotic activity and NF- B expression were significantly higher in the control group compared with the PFC groups at 3, 12, and 24 h of cold preservation. After transplantation, the NF- B, iNOS, and nitrotyrosine expression as well as caspase 3 activity were significantly lower in the PFC groups. Conclusion. The use of endobronchial PFC as an adjuvant to the current preservation strategy improved graft viability. © 2013 Luiz Alberto Forgiarini Junior et al.

Discover hidden collaborations