Investigating Pulmonary Edema Development and the Affect Following Cardiopulmonary Resuscitation
Session Number
1
Advisor(s)
Dr. Willard Sharp and Dr. Lin Piao, University of Chicago
Location
B116
Discipline
Medical and Health Sciences
Start Date
15-4-2026 10:15 AM
End Date
15-4-2026 11:00 AM
Abstract
Sudden Cardiac arrest (CA) is a major cause of death and is often succeeded by complications: cardiac dysfunction and neurological injury. Although oxygen therapy is commonly administered after resuscitation, evidence suggests that early oxygen supplementation may worsen physiological outcomes and tissue injury. This study investigated post–CA and tested the hypothesis that oxygen supplementation increases vascular permeability, connecting pulmonary edema. To test this hypothesis, a CA mouse model underwent 12 minutes of KCl-induced asystole followed by cardiopulmonary resuscitation (CPR). Mice received 2 hours of hypoxia (30% oxygen), and organs were collected. Sham-operated animals served as controls, receiving 2 hours 30% oxygen. Evans Blue dye was injected 20 minutes prior to organ collection to assess vascular permeability, and wet weights measured edema in heart, lungs, brain, liver, and kidneys. Lungs after CA mice demonstrated increased Evans Blue leakage (47.94 ± 3.57 nm/mg) and higher wet weights (0.2 ± 0.01 g) compared to sham. Evans blue leakage strongly correlated with increased lung wet weight in CA mice treated with 30% O2 (P< 0.05). These findings suggest oxygen after CA promotes vascular permeability and pulmonary edema. Future studies will evaluate therapeutic strategies to reduce organ injury post-cardiac arrest.
Investigating Pulmonary Edema Development and the Affect Following Cardiopulmonary Resuscitation
B116
Sudden Cardiac arrest (CA) is a major cause of death and is often succeeded by complications: cardiac dysfunction and neurological injury. Although oxygen therapy is commonly administered after resuscitation, evidence suggests that early oxygen supplementation may worsen physiological outcomes and tissue injury. This study investigated post–CA and tested the hypothesis that oxygen supplementation increases vascular permeability, connecting pulmonary edema. To test this hypothesis, a CA mouse model underwent 12 minutes of KCl-induced asystole followed by cardiopulmonary resuscitation (CPR). Mice received 2 hours of hypoxia (30% oxygen), and organs were collected. Sham-operated animals served as controls, receiving 2 hours 30% oxygen. Evans Blue dye was injected 20 minutes prior to organ collection to assess vascular permeability, and wet weights measured edema in heart, lungs, brain, liver, and kidneys. Lungs after CA mice demonstrated increased Evans Blue leakage (47.94 ± 3.57 nm/mg) and higher wet weights (0.2 ± 0.01 g) compared to sham. Evans blue leakage strongly correlated with increased lung wet weight in CA mice treated with 30% O2 (P< 0.05). These findings suggest oxygen after CA promotes vascular permeability and pulmonary edema. Future studies will evaluate therapeutic strategies to reduce organ injury post-cardiac arrest.