Effects and mechanisms of NAD + on lung injury after cardiac arrest and cardiopulmonary resuscitation in swine.

Figures

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  Fig. 1.. Analysis of cardiopulmonary resuscitation outcomes. CPR, cardiopulmonary resuscitation; NAD+, nicotinamide adenine dinucleotide; CPP, coronary perfusion pressure. *P < 0.05 vs. Sham group; #P < 0.05 vs. CPR group. Data are expressed as mean ± SD, intergroup comparisons were conducted using the Student t test. CPR, cardiopulmonary resuscitation; NAD+, nicotinamide adenine dinucleotide; Sham, sham-operated.

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  Fig. 2.. Analysis of arterial blood gas parameters. A, Potential of hydrogen (pH). B, Arterial partial pressure of oxygen (PaO2). C, Arterial partial pressure of carbon dioxide (PaCO2). D, Lactate (LAC). E, Bicarbonate (HCO3−). F, Base excess (BE). *P < 0.05 vs. Sham group; #P < 0.05 vs. CPR group. Data are presented as mean ± SD, intergroup comparisons were performed using ANOVA and Bonferroni test. ANOVA, analysis of variance; BL, baseline; CPR, cardiopulmonary resuscitation; NAD+, nicotinamide adenine dinucleotide; Sham, sham-operated.

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  Fig. 3.. Analysis of lung function injury markers. A, Extravascular lung water index (ELWI). B, Pulmonary vascular permeability index (PVPI). C, Oxygenation index (OI). D, Serum surfactant protein D (SP-D) levels. E, Lung tissue SP-D levels. *P < 0.05 vs. Sham group; #P < 0.05 vs. CPR group. Data are presented as mean ± SD, intergroup comparisons were performed using ANOVA and Bonferroni test. ANOVA, analysis of variance; BL, baseline; CPR, cardiopulmonary resuscitation; NAD+, nicotinamide adenine dinucleotide; Sham, sham-operated.

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  Fig. 4.. Histopathological lung injury and injury scores. A, Representative hematoxylin and eosin (H&E)–stained lung tissue sections (original magnification ×200). B, Histopathological lung injury scores. *P < 0.05 vs. Sham group; #P < 0.05 vs. CPR group. Data are presented as mean ± SD, intergroup comparisons were performed using ANOVA and Bonferroni test. ANOVA, analysis of variance; CPR, cardiopulmonary resuscitation; NAD+, nicotinamide adenine dinucleotide; Sham, sham-operated.

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  Fig. 5.. Changes in lung tissue apoptosis. Lung tissue apoptosis was assessed 24 hours after model induction. A, Representative images of terminal deoxynucleotidyl transferase–mediated dUTP nick-end labeling (TUNEL) staining in lung tissue (original magnification ×200). B, Percentage of TUNEL-positive cells in lung tissue. *P < 0.05 vs. Sham group; #P < 0.05 vs. CPR group. Data are presented as mean ± SD, intergroup comparisons were performed using ANOVA and Bonferroni test. ANOVA, analysis of variance; CPR, cardiopulmonary resuscitation; NAD+, nicotinamide adenine dinucleotide; Sham, sham-operated.

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  Fig. 6.. Analysis of ferroptosis-related products in lung tissue. A, Representative immunofluorescence images of reactive oxygen species (ROS) in lung tissue (original magnification ×200). B, Quantification of fluorescence intensity. C, Ferrous iron (Fe2+). D, Malondialdehyde (MDA). E, 4-hydroxynonenal (4-HNE). F, Glutathione (GSH). *P < 0.05 vs. Sham group; #P < 0.05 vs. CPR group. Data are presented as mean ± SD, intergroup comparisons were performed using ANOVA and Bonferroni test. ANOVA, analysis of variance; CPR, cardiopulmonary resuscitation; NAD+, nicotinamide adenine dinucleotide; Sham, sham-operated.

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  Fig. 7.. Analysis of ferroptosis-regulatory proteins in lung tissue. A, Representative western blot bands of Yes-associated protein (YAP) and acyl-CoA synthetase long-chain family member 4 (ACSL4). B, Relative protein expression levels of YAP. C, Relative protein expression levels of ACSL4. *P < 0.05 vs. Sham group; #P < 0.05 vs. CPR group. Data are presented as mean ± SD, intergroup comparisons were performed using ANOVA and Bonferroni test. ANOVA, analysis of variance; CPR, cardiopulmonary resuscitation; NAD+, nicotinamide adenine dinucleotide; Sham, sham-operated.