When is injury potentially reversible in a lung ischemia–reperfusion model?

Holand

Mediators of Inflammation

et al. 2013

Self Cite

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-κB 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-κB, 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.

Section: Discussionmentioning

confidence: 99%

“…Caspase 3 activity was analyzed as described by Forgiarini et al [32] and TUNEL studies as described by Fischer et al [13]. …”

Section: Methodsmentioning

confidence: 99%

Endobronchial Perfluorocarbon Reduces Inflammatory Activity before and after Lung Transplantation in an Animal Experimental Model

Holand

Mediators of Inflammation

et al. 2013

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BioMed Research International

“…Interestingly, the RC-Pre group did not show these alterations, suggesting that its administration prior to reperfusion might have a beneficial effect or at least did not induce an increase in caspase-9 activity. Additionally, in a previous study conducted by our group, we observed an increase in the activity of caspase-3 after 45 min of ischemia, which was associated with a higher number of apoptotic cells [ 21 ].…”

Section: Discussionmentioning

confidence: 92%

“…A rodent model for LIRI was selected for the present study because this has been extensively used in the previous reports [ 16 , 21 ]. This animal model mimics several features of LIRI such as the inflammatory changes and structural damage to the lungs [ 20 , 21 ]. Furthermore, the differences in mean arterial pressure prior to and after reperfusion among the groups were similar compared to those described in the literature [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

RC-3095, a Selective Gastrin-Releasing Peptide Receptor Antagonist, Does Not Protect the Lungs in an Experimental Model of Lung Ischemia-Reperfusion Injury

Oliveira-Freitas

Thomaz

Simoneti

et al. 2015

Self Cite

RC-3095, a selective GRPR antagonist, has been shown to have anti-inflammatory properties in different models of inflammation. However, its protective effect on lungs submitted to lung ischemia-reperfusion injury has not been addressed before. Then, we administrated RC-3095 intravenously before and after lung reperfusion using an animal model of lung ischemia-reperfusion injury (LIRI) by clamping the pulmonary hilum. Twenty Wistar rats were subjected to an experimental model in four groups: SHAM, ischemia-reperfusion (IR), RC-Pre, and RC-Post. The final mean arterial pressure significantly decreased in IR and RC-Pre compared to their values before reperfusion (P < 0.001). The RC-Post group showed significant decrease of partial pressure of arterial oxygen at the end of the observation when compared to baseline (P = 0.005). Caspase-9 activity was significantly higher in the RC-Post as compared to the other groups (P < 0.013). No significant differences were observed in eNOS activity among the groups. The groups RC-Pre and RC-Post did not show any significant decrease in IL-1β (P = 0.159) and TNF-α (P = 0.260), as compared to IR. The histological score showed no significant differences among the groups. In conclusion, RC-3095 does not demonstrate a protective effect in our LIRI model. Additionally, its use after reperfusion seems to potentiate cell damage, stimulating apoptosis.

“…The result is the apoptosis of the cell. Forgiarini et al [23] determined that an ischaemia period longer than 45 minutes increased the caspase cascade activation and the apoptosis. Wang et al [24] confirmed that caspase-9 and Apaf levels were increased and apoptosis occurred in acute myocardial infarction.…”

Section: Discussionmentioning

confidence: 99%

Apoptosis biomarkers (Apaf-1, sFa s, sFa s-L, and caspase-9), albumin, and fetuin-A levels in pulmonary thromboembolic patients

Aydın

Tekin

Korkmaz

et al. 2020

Disaster Emerg Med J

INTRODUCTION: Pulmonary thromboembolism (PE) is the third most common medical emergency with mortality due to ischemia and reperfusion lung injury. Lung ischaemia-reperfusion injury. Lung reperfusion damage is believed to cause cellular damage and apoptosis. The aim of the present study was to evaluate the levels of fetuin-A, albumin, and apoptosis biomarkers (Apaf-1, sFas, and sFasL) among pulmonary thromboembolic patients. MATERIAL AND METHODS: Blood samples were collected from 45 volunteer patients and 40 healthy control volunteers. Human apoptosis biomarkers (Apaf-1, sFas, sFasL, and caspase-9) and fetuin-A values were measured by ELISA device. Student's t-test or Mann-Whitney U test were used for continuous variables, and categorical variables were compared with the chi-square test to assess the significance of intergroup differences. The mean values of apoptosis biomarkers and acute phase reactants between dead and survival patients were also compared. RESULTS: While the apoptosis mean values of Apaf-1, sFas, sFasL, and caspase-9 for the control group were