scholarly journals Mild Hypothermia Inhibits Systemic and Cerebral Complement Activation in a Swine Model of Cardiac Arrest

2015 ◽  
Vol 35 (8) ◽  
pp. 1289-1295 ◽  
Author(s):  
Ping Gong ◽  
g Zhao ◽  
Rong Hua ◽  
Mingyue Zhang ◽  
Ziren Tang ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Complement Activation ◽  
Ischemia Reperfusion Injury ◽  
Mild Hypothermia ◽  
Ischemia Reperfusion ◽  
Spontaneous Circulation ◽  
Enzyme Linked Immunosorbent Assay ◽  
Swine Model ◽  
Factor Α ◽  
Necrosis Factor

Complement activation has been implicated in ischemia/reperfusion injury. This study aimed to determine whether mild hypothermia (HT) inhibits systemic and cerebral complement activation after resuscitation from cardiac arrest. Sixteen minipigs resuscitated from 8 minutes of untreated ventricular fibrillation were randomized into two groups: HT group ( n = 8), treated with HT (33 °C) for 12 hours; and normothermia group ( n = 8), treated similarly as HT group except for cooling. Blood samples were collected at baseline and 0.5, 6, 12, and 24 hours after return of spontaneous circulation (ROSC). The brain cortex was harvested 24 hours after ROSC. Complement and pro-inflammatory markers were detected using enzyme-linked immunosorbent assay. Neurologic deficit scores were evaluated 24 hours after ROSC. C1q, Bb, mannose-binding lectin (MBL), C3b, C3a, C5a, interleukin-6, and tumor necrosis factor- α levels were significantly increased under normothermia within 24 hours after ROSC. However, these increases were significantly reduced by HT. Hypothermia decreased brain C1q, MBL, C3b, and C5a contents 24 hours after ROSC. Hypothermic pigs had a better neurologic outcome than normothermic pigs. In conclusion, complement is activated through classic, alternative, and MBL pathways after ROSC. Hypothermia inhibits systemic and cerebral complement activation, which may provide an additional mechanism of cerebral protection.

Abstract 296: Adult Swine Model of Ventricular Fibrillation Arrest for Resuscitation with Perfluorocarbon Emulsions

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_4) ◽  
Author(s):  
Travis W Murphy ◽  
Jiepei Zhu ◽  
Travis Parsons ◽  
Bruce D Spiess ◽  
Torben K Becker
Keyword(s):  
Cardiac Arrest ◽  
Ventricular Fibrillation ◽  
Minimally Invasive ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Circulatory Arrest ◽  
Spontaneous Circulation ◽  
Blood Levels ◽  
Swine Model ◽  
Initial Attempt

Background: The purpose of this study was to develop a model of ventricular fibrillation arrest with reliable outcomes and minimally invasive methods to study the use of perfluorocarbon emulsions (PFC) as agents to prevent ischemia-reperfusion injury after cardiac arrest as quantified by known biomarkers. Methods: Female Yorkshire swine underwent anesthesia and minimally invasive instrumentation for monitoring under ultrasound. Cardiac arrest was induced with spinal needle insertion at the apex and right parasternal space. Ventricular fibrillation was reliably obtained in all animals on initial attempts. A three-minute circulatory arrest state was observed. Administration of PFC was concurrent with resuscitation including closed chest compressions, epinephrine, amiodarone, and defibrillation at 1J/kg. Primary endpoint was induction of cardiac arrest and tolerance of PFC with return of spontaneous circulation. Blood levels of glial fibrillary acidic protein (GFAP) and ubiquitin C-Terminal Hydrolase-L1 (UCLH1) were secondary end points for three animals. Results: Six of six animals were induced into ventricular fibrillation on initial attempt and two of three survival experiments were able to obtain spontaneous circulation. PFC with pretreatment was tolerated well and no signs of increased pulmonary pressures. GFAP, UCHL1 were significantly lower in intervention animals compared to controls. Conclusions: The results obtained from this preliminary study and technical refinements via additional donated animals have allowed us to make modifications in the choice of PFC, vascular access, and anticoagulation plan. This model provides a consistent method for inducing ventricular fibrillation with minimally invasive techniques. The PFC tested was well tolerated. More robust evaluation of PFC as resuscitative agents is needed with appropriately powered studies.

Abstract P15: Periodic Acceleration (pGz) Preconditioning in Swine Increases Endothelial Derived NO and Phosphorylated eNOS via Akt Pathway

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Jose A Adams ◽  
Jaqueline Arias ◽  
Jorge Bassuk ◽  
Heng Wu ◽  
Arkady Uryash ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Myocardial Stunning ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Spontaneous Circulation ◽  
Akt Pathway ◽  
Phosphorylated Akt ◽  
Manual Chest Compression ◽  
Periodic Acceleration ◽  
Pulsatile Shear Stress

Periodic acceleration (pGz) is the motion of the supine body using a motorized platform (3Hz & ±0.4G). pGz produces pulsatile shear stress increasing release of endothelial derived NO (eNO) which, also decreases myocardial stunning and improves outcomes from ventricular fibrillation (VF) cardiac arrest. Preconditioning with pGz (PRE-pGz) prior to VF cardiac arrest ameliorates global post resuscitation cardiac dysfunction and reduces arrhythmias. To test whether pGz and PRE-pGz increase eNOS and phosphorylated eNOS (p-eNOS) via the PI3-kinase-Akt pathway, anesthetized, intubated male swine (40 –50lbs) were studied. Five animals had no intervention (BL) and 5 received 1 hr pGz preconditioning (pGz) followed by Western Blot of myocardial tissue. Additional animals (10 per group) received 1 hr pGz (PRE-pGz) or no treatment (CPR-CONT). In the latter groups VF was electrically induced and unsupported for 8 min followed by continuous manual chest compression and defibrillation for 10 min or until return of spontaneous circulation (ROSC). PRE-pGz animals showed less hemodynamically significant arrhythmias after ROSC than CPR-CONT (35 vs 7; p<0.05) and less myocardial stunning. eNOS and phosphorylated-eNOS (p-eNOS) significantly increased after pGz and after CPR but were significantly higher in pGz preconditioned animals along with increased phosphorylated Akt (p-Akt). The graph below shows % changes relative to BL (M±SD). *p < 0.01 PRE-pGz vs CPR-CONT. Conclusion: pGz applied prior to ischemia reperfusion injury increases eNOS and p-eNOS expression and increased p-Akt. Thus, pGz preconditioning protects myocardium during I-R in part by activating eNOS through p-Akt

The Role of Tumor Necrosis Factor-α and Interleukin-1β in Ischemia-Reperfusion Injury of the Rat Small Intestine

2001 ◽  
Vol 99 (1) ◽  
pp. 134-141 ◽  
Author(s):  
Seiichiro Yamamoto ◽  
Minoru Tanabe ◽  
Go Wakabayashi ◽  
Motohide Shimazu ◽  
Koshi Matsumoto ◽  
...  
Keyword(s):  
Small Intestine ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Rat Small Intestine ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Elevated Plasma Soluble PD-L1 Levels in Out-of-Hospital Cardiac Arrest Patients

2021 ◽  
Vol 10 (18) ◽  
pp. 4188
Author(s):  
Miho Sumiyoshi ◽  
Eiji Kawamoto ◽  
Yuki Nakamori ◽  
Ryo Esumi ◽  
Kaoru Ikejiri ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Ischemia Reperfusion ◽  
Plasma Concentrations ◽  
Spontaneous Circulation ◽  
University Hospital ◽  
Soluble Form ◽  
Enzyme Linked Immunosorbent Assay ◽  
Immune Functions ◽  
Protein Levels ◽  
Hospital Cardiac Arrest

Background: A deregulated immune system has been implicated in the pathogenesis of post-cardiac arrest syndrome (PCAS). A soluble form of programmed cell death-1 (PD-1) ligand (sPD-L1) has been found at increased levels in cancer and sustained inflammation, thereby deregulating immune functions. Here, we aim to study the possible involvement of sPD-L1 in PCAS. Methods: Thirty out-of-hospital cardiac arrest (OHCA) patients consecutively admitted to the ER of Mie University Hospital were prospectively enrolled. Plasma concentrations of sPD-L1 were measured by an enzyme-linked immunosorbent assay in blood samples of all 30 OHCA patients obtained during cardiopulmonary resuscitation (CPR). In 13 patients who achieved return-of-spontaneous-circulation (ROSC), sPD-L1 levels were also measured daily in the ICU. Results: The plasma concentrations of sPD-L1 in OHCA were significantly increased; in fact, to levels as high as those observed in sepsis. sPD-L1 levels during CPR correlated with reduced peripheral lymphocyte counts and increased C-reactive protein levels. Of 13 ROSC patients, 7 cases survived in the ICU for more than 4 days. A longitudinal analysis of sPD-L1 levels in the 7 ROSC cases revealed that sPD-L1 levels occurred in parallel with organ failure. Conclusions: This study suggests that ischemia- reperfusion during CPR may aberrantly activate immune and endothelial cells to release sPD-L1 into circulation, which may play a role in the pathogenesis of immune exhaustion and organ failures associated with PCAS.

scholarly journals Pentraxin-3-mediated complement activation in a swine model of renal ischemia/reperfusion injury

Aging ◽  
2021 ◽  
Author(s):  
Chiara Divella ◽  
Alessandra Stasi ◽  
Rossana Franzin ◽  
Michele Rossini ◽  
Paola Pontrelli ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Complement Activation ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Swine Model ◽  
Pentraxin 3 ◽  
Renal Ischemia Reperfusion Injury
Sign in / Sign up

Export Citation Format

Share Document