Epinephrine Exacerbates Myocyte Injury in a Porcine Model of Cardiac Arrest

Introduction: Systemic ischemia-reperfusion injury produced by CA and resuscitation can result in severe post-cardiac arrest syndrome; which includes systemic inflammatory response and multiple organ dysfunction syndrome such as acute pulmonary edema. We previously demonstrated that remote ischemic post-conditioning (RIpostC) improved post-resuscitation myocardial and cerebral function in a rat model of CA. In this study, we investigated the effects of RIpostC on inflammatory response and pulmonary edema after CPR in a porcine model. Hypothesis: RIpostC would alleviate post-resuscitation inflammatory response and pulmonary edema in a porcine model of CA. Methods: Fourteen male domestic pigs weighing 37 ± 2 kg were utilized. Ventricular fibrillation was electrically induced and untreated for 10 mins. The animals were then randomized to receive RIpostC or control. Coincident with the start of CPR, RIpostC was induced by four cycles of 5 mins of limb ischemia and then 5 mins of reperfusion. Defibrillation was attempted after 5 mins of CPR. The resuscitated animals were monitored for 4 hrs and observed for an additional 68 hrs. Results: Six of the seven animals in each group were successfully resuscitated. After resuscitation, significantly lower levels of tumor necrosis factor-α and interleukin-6 were measured in the animals that received RIpostC when compared with the control group. Post-resuscitation extra-vascular lung water index was lower in the RIpostC group than in the control group; in which the differences were significant at 2,3 and 4 hrs (Table). Conclusion: In a porcine model of CA, RIpostC significantly alleviates post-resuscitation inflammatory response and pulmonary edema.

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Association between ACE2/ACE balance and pneumocyte apoptosis in a porcine model of acute pulmonary thromboembolism with cardiac arrest

Molecular Medicine Reports ◽

10.3892/mmr.2018.8426 ◽

2018 ◽

Author(s):

Hong‑Li Xiao ◽

Lian‑Xing Zhao ◽

Jun Yang ◽

Nan Tong ◽

Le An ◽

...

Keyword(s):

Cardiac Arrest ◽

Porcine Model ◽

Pulmonary Thromboembolism ◽

Acute Pulmonary Thromboembolism

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Effects of Add-On Left Ventricular Assist Device to Extracorporeal Membrane Oxygenation During Refractory Cardiac Arrest in a Porcine Model

ASAIO Journal ◽

10.1097/mat.0000000000001528 ◽

2021 ◽

Vol Publish Ahead of Print ◽

Author(s):

Erik J. S. Packer ◽

Atle Solholm ◽

Tom Roar Omdal ◽

Lodve Stangeland ◽

Liqun Zhang ◽

...

Keyword(s):

Cardiac Arrest ◽

Extracorporeal Membrane Oxygenation ◽

Left Ventricular Assist Device ◽

Ventricular Assist Device ◽

Porcine Model ◽

Left Ventricular ◽

Assist Device ◽

Ventricular Assist ◽

Left Ventricular Assist ◽

Refractory Cardiac Arrest

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Abstract 122: Effects of Early Administration of Argatroban on CPR Quality in Porcine Model of Prolonged Out-of-Hospital Cardiac Arrest

Circulation ◽

10.1161/circ.142.suppl_4.122 ◽

2020 ◽

Vol 142 (Suppl_4) ◽

Author(s):

Jensyn J VanZalen ◽

Annie G Phillips ◽

Stephen L Harvey ◽

Joseph E Hill ◽

Olivia L Pak ◽

...

Keyword(s):

Cardiac Arrest ◽

Porcine Model ◽

Diastolic Pressure ◽

Randomized Study ◽

Coronary Perfusion ◽

Hemodynamic Parameters ◽

Early Administration ◽

Intravascular Thrombosis ◽

Arterial Blood ◽

The Impact

Background: The effectiveness of CPR declines over time during prolonged cardiac arrest (CA). Intravascular thrombosis may be a contributing factor. As part of a larger study examining antithrombotic therapy in a porcine model of prolonged CA, the impact of early administration of argatroban on CPR hemodynamics is reported. Hypothesis: Early administration of argatroban during CPR improves the quality of goal-directed CPR (gdCPR). Methods: In a blinded and randomized study, 48 swine (40±5kg) underwent an 8min untreated period of ventricular fibrillation CA followed by a gdCPR protocol for 30min (total arrest time 38min). Manual and mechanical chest compressions with the use of an impedance threshold device (ITD) were introduced to maintain end-tidal CO 2 (Et-CO 2 ) >20mmHg. Argatroban (350mg/kg) or placebo (20mL NSS) were administered to respective groups (n=24 per group) 12mins after initiation of CA. Et-CO 2 , coronary perfusion pressure (CPP), end-diastolic pressure (EDP), and intracranial pressure (ICP) were monitored continuously. Averages were taken over the course of gdCPR for hemodynamic parameters. Arterial blood gases (ABGs) were obtained at the end of gdCPR. Analysis between groups was performed using an unpaired t-test (significance = p <0.05). Results: Average hemodynamic parameters were not statistically different between argatroban vs. placebo groups (Et-CO 2 22.6±6.7 vs. 21.5±5.9 mmHg; EDP 25.6±10.7 vs. 23.7±9.6 mmHg; ICP 25.7±2.0 vs.20.9±2.7 cmH 2 O; CPP 8.7±11.2 vs. 7.0±11.2 mmHg). Final ABG values were also not statistically different between argatroban vs. placebo groups (pH 7.23±0.1 vs. 7.23±0.2; PaO 2 187.4±146.3 vs. 132.2±187.4 mmHg; PaCO 2 38.8±16.6 vs. 43.0±26.1 mmHg; lactate 8.5±1.7 vs. 8.8±1.4 mmol/L). Conclusion: These results demonstrate that early administration of argatroban during CPR did not have a significant effect on gdCPR quality in a porcine model of prolonged CA.

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Extracorporeal resuscitation with carbon monoxide improves renal function by targeting inflammatory pathways in cardiac arrest in pigs

AJP Renal Physiology ◽

10.1152/ajprenal.00241.2019 ◽

2019 ◽

Vol 317 (6) ◽

pp. F1572-F1581 ◽

Cited By ~ 1

Author(s):

Jakob Wollborn ◽

Bjoern Schlueter ◽

Christoph Steiger ◽

Cornelius Hermann ◽

Christian Wunder ◽

...

Keyword(s):

Carbon Monoxide ◽

Renal Function ◽

Cardiac Arrest ◽

Renal Injury ◽

Porcine Model ◽

Life Support ◽

Apoptotic Cell ◽

Extracorporeal Life Support ◽

Successful Resuscitation ◽

Extracorporeal Resuscitation

Deleterious consequences like acute kidney injury frequently occur upon successful resuscitation from cardiac arrest. Extracorporeal life support is increasingly used to overcome high cardiac arrest mortality. Carbon monoxide (CO) is an endogenous gasotransmitter, capable of reducing renal injury. In our study, we hypothesized that addition of CO to extracorporeal resuscitation hampers severity of renal injury in a porcine model of cardiac arrest. Hypoxic cardiac arrest was induced in pigs. Animals were resuscitated using a conventional [cardiopulmonary resuscitation (CPR)], an extracorporeal (E-CPR), or a CO-assisted extracorporeal (CO-E-CPR) protocol. CO was applied using a membrane-controlled releasing system. Markers of renal injury were measured, and histopathological analyses were carried out. We investigated renal pathways involving inflammation as well as apoptotic cell death. No differences in serum neutrophil gelatinase-associated lipocalin (NGAL) were detected after CO treatment compared with Sham animals (Sham 71 ± 7 and CO-E-CPR 95 ± 6 ng/mL), while NGAL was increased in CPR and E-CPR groups (CPR 135 ± 11 and E-CPR 124 ± 5 ng/mL; P < 0.05). Evidence for histopathological damage was abrogated after CO application. CO increased renal heat shock protein 70 expression and reduced inducible cyclooxygenase 2 (CPR: 60 ± 8; E-CPR 56 ± 8; CO-E-CPR 31 ± 3 µg/mL; P < 0.05). Caspase 3 activity was decreased (CPR 1,469 ± 276; E-CPR 1,670 ± 225; CO-E-CPR 755 ± 83 pg/mL; P < 0.05). Furthermore, we found a reduction in renal inflammatory signaling upon CO treatment. Our data demonstrate improved renal function by extracorporeal CO treatment in a porcine model of cardiac arrest. CO reduced proinflammatory and proapoptotic signaling, characterizing beneficial aspects of a novel treatment option to overcome high mortality.

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