Duration of Untreated Cardiac Arrest and Clinical Relevance of Animal Experiments: The Relationship Between the “No-Flow” Duration and the Severity of Post-Cardiac Arrest Syndrome in a Porcine Model

Babini, G; Grassi, Luigi; Russo, Ilaria; Novelli, Deborah; Boccardo, Antonio; Luciani, Anita; Fumagalli, Francesca; Staszewsky, Lidia; Fiordaliso, Fabio; Maglie, Marcella De; Salio, Monica; Zani, Davide Danilo; Letizia, Teresa; Masson, Serge; Luini, M.; Pravettoni, D.; Scanziani, Eugenio; Latini, Roberto; Ristagno, Giuseppe

doi:10.1097/shk.0000000000000914

Cited by 25 publications

(31 citation statements)

References 33 publications

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“…A cuffed tracheal tube was placed, and animals were mechanically ventilated with a tidal volume of 15 mL/kg and FiO 2 of 0.21. Respiratory frequency was adjusted to maintain the end-tidal partial pressure of carbon dioxide (EtCO 2 ) between 35 and 40 mmHg, monitored with an infrared capnometer 18 – 20 . To measure aortic pressure, a fluid-filled 7F catheter was advanced from the right femoral artery into the thoracic aorta.…”

Section: Methodsmentioning

confidence: 99%

“…Conventional pressure transducers were used (MedexTransStar, Monsey, NY). Myocardial infarction was induced in a closed-chest preparation by intraluminal occlusion of the left anterior descending (LAD) coronary artery 18 – 20 . Briefly, a 6F balloon-tipped catheter was inserted from the right common carotid artery and advanced into the aorta and then into the LAD, beyond the first diagonal branch, with the aid of image intensification and confirmed by injection of radiographic contrast media.…”

Section: Methodsmentioning

confidence: 99%

“…After baseline measurements, the LAD catheter balloon was then inflated with 0.7 mL of air to occlude the flow, as previously described 18 – 20 . If VF did not occur spontaneously after 10 min, CA was induced with 1 to 2 mA AC current delivered to the right ventricle endocardium.…”

Section: Methodsmentioning

confidence: 99%

“…After that, if VF reoccurred, it was treated by immediate defibrillation. Immediately after resuscitation, the LAD catheter correct placement was reconfirmed by fluoroscopy 20 . After successful resuscitation, anesthesia was maintained, and animals were invasively monitored for 4 h. Forty-five minutes after resuscitation, the LAD catheter was withdrawn.…”

Section: Methodsmentioning

confidence: 99%

“…due to acute myocardial infarction (AMI). The aim of this study was to investigate the effects of a single dose of esmolol, compared to placebo, in addition to epinephrine during CPR in a preclinical porcine model of CA with an underlying AMI 18 – 20 . A decrease in the total number of defibrillations needed to terminate VF with esmolol compared with placebo was hypothesized.…”

Section: Introductionmentioning

confidence: 99%

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Esmolol during cardiopulmonary resuscitation reduces neurological injury in a porcine model of cardiac arrest

Ruggeri

Nespoli

Ristagno

et al. 2021

Sci Rep

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Primary vasopressor efficacy of epinephrine during cardiopulmonary resuscitation (CPR) is due to its α-adrenergic effects. However, epinephrine plays β1-adrenergic actions, which increasing myocardial oxygen consumption may lead to refractory ventricular fibrillation (VF) and poor outcome. Effects of a single dose of esmolol in addition to epinephrine during CPR were investigated in a porcine model of VF with an underlying acute myocardial infarction. VF was ischemically induced in 16 pigs and left untreated for 12 min. During CPR, animals were randomized to receive epinephrine (30 µg/kg) with either esmolol (0.5 mg/kg) or saline (control). Pigs were then observed up to 96 h. Coronary perfusion pressure increased during CPR in the esmolol group compared to control (47 ± 21 vs. 24 ± 10 mmHg at min 5, p < 0.05). In both groups, 7 animals were successfully resuscitated and 4 survived up to 96 h. No significant differences were observed between groups in the total number of defibrillations delivered prior to final resuscitation. Brain histology demonstrated reductions in cortical neuronal degeneration/necrosis (score 0.3 ± 0.5 vs. 1.3 ± 0.5, p < 0.05) and hippocampal microglial activation (6 ± 3 vs. 22 ± 4%, p < 0.01) in the esmolol group compared to control. Lower circulating levels of neuron specific enolase were measured in esmolol animals compared to controls (2[1–3] vs. 21[16–52] ng/mL, p < 0.01). In this preclinical model, β1-blockade during CPR did not facilitate VF termination but provided neuroprotection.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Esmolol during cardiopulmonary resuscitation reduces neurological injury in a porcine model of cardiac arrest

Ruggeri

Nespoli

Ristagno

et al. 2021

Sci Rep

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A comprehensive neuromonitoring approach in a large animal model of cardiac arrest

Annoni

Peluso

Hirai

et al. 2022

Anim Models and Exp Med

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CA remains a leading cause of death and morbidity worldwide 1 and brain injurie remains responsible for most deaths among survivors. 2 Many treatments have been proposed, 3,4 but the discrepancies between experimental results and their translation into clinical practice reinforce the necessity for better preclinical models. 5 Pigs are appropriate as CA models because of anatomic similarity between cardiovascular systems, the possibility of applying standardized resuscitation maneuvers, and their tolerability for invasive procedures and frequent blood sampling. [6][7][8] Similarly, they possess a gyrencephalic brain with regional susceptibility to ischemiareperfusion comparable to humans. Also, their brain is large enough to allow the placement of multiple human monitoring devices.

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Searching for Preclinical Models of Acute Decompensated Heart Failure: a Concise Narrative Overview and a Novel Swine Model

Olivari

Giorgio

Staszewsky

et al. 2020

Cardiovasc Drugs Ther

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Purpose Available animal models of acute heart failure (AHF) and their limitations are discussed herein. A novel and preclinically relevant porcine model of decompensated AHF (ADHF) is then presented. Methods Myocardial infarction (MI) was induced by occlusion of left anterior descending coronary artery in 17 male pigs (34 ± 4 kg). Two weeks later, ADHF was induced in the survived animals (n = 15) by occlusion of the circumflex coronary artery, associated with acute volume overload and increases in arterial blood pressure by vasoconstrictor infusion. After onset of ADHF, animals received 48-h iv infusion of either serelaxin (n = 9) or placebo (n = 6). The pathophysiology and progression of ADHF were described by combining evaluation of hemodynamics, echocardiography, bioimpedance, blood gasses, circulating biomarkers, and histology. Results During ADHF, animals showed reduced left ventricle (LV) ejection fraction < 30%, increased thoracic fluid content > 35%, pulmonary edema, and high pulmonary capillary wedge pressure ~ 30 mmHg (p < 0.01 vs. baseline). Other ADHF-induced alterations in hemodynamics, i.e., increased central venous and pulmonary arterial pressures; respiratory gas exchanges, i.e., respiratory acidosis with low arterial PO2 and high PCO2; and LV dysfunction, i.e., increased LV end-diastolic/systolic volumes, were observed (p < 0.01 vs. baseline). Representative increases in circulating cardiac biomarkers, i.e., troponin T, natriuretic peptide, and bio-adrenomedullin, occurred (p < 0.01 vs. baseline). Finally, elevated renal and liver biomarkers were observed 48 h after onset of ADHF. Mortality was ~ 50%. Serelaxin showed beneficial effects on congestion, but none on mortality. Conclusion This new model, resulting from a combination of chronic and acute MI, and volume and pressure overload, was able to reproduce all the typical clinical signs occurring during ADHF in a consistent and reproducible manner.

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Duration of Untreated Cardiac Arrest and Clinical Relevance of Animal Experiments: The Relationship Between the “No-Flow” Duration and the Severity of Post-Cardiac Arrest Syndrome in a Porcine Model

Abstract: Longer no-flow durations caused greater postresuscitation myocardial and neurological dysfunction and reduced survival. An untreated CA of 12-13 min may be an optimal choice for a clinically relevant model.

Cited by 25 publications

References 33 publications

Esmolol during cardiopulmonary resuscitation reduces neurological injury in a porcine model of cardiac arrest

Esmolol during cardiopulmonary resuscitation reduces neurological injury in a porcine model of cardiac arrest

A comprehensive neuromonitoring approach in a large animal model of cardiac arrest

Searching for Preclinical Models of Acute Decompensated Heart Failure: a Concise Narrative Overview and a Novel Swine Model

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