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.
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.
Authors: Vera L Oliveira-Freitas; Leonardo Dalla Giacomassa Rocha Thomaz; Lucas Elias Lise Simoneti; Christiane Malfitano; Kátia De Angelis; Jane Maria Ulbrich; Gilberto Schwartsmann; Cristiano Feijó Andrade Journal: Biomed Res Int Date: 2015-03-29 Impact factor: 3.411
Authors: Marcus da Matta Abreu; Francine Maria de Almeida; Kelli Borges Dos Santos; Emílio Augusto Campos Pereira de Assis; Rafael Kenji Fonseca Hamada; Fabio Biscegli Jatene; Paulo Manuel Pêgo-Fernandes; Rogerio Pazetti Journal: J Bras Pneumol Date: 2018 Sep-Oct Impact factor: 2.624