Abstract 266: The Effect of Different Kinds of Chest Compression Waveforms on the Heart Ischemia-Reperfusion Injury After Cardiac Arrest

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Tang Songling ◽  
Yarong He ◽  
Peng Yao ◽  
Yu Cao
Keyword(s):  
Cardiac Arrest ◽  
Reperfusion Injury ◽  
Chest Compression ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Sine Wave ◽  
The Other ◽  
Wave Group ◽  
Heart Ischemia ◽  
Manual Group

Purpose: This study was aimed to compare the effect of different kinds of chest compression waveforms on the heart ischemia-reperfusion injury after cardiac arrest (CA) in a rat model. Materials and methods: After the CA model was successfully established with continuous electrical stimulation of ventricular fibrillation, rats were divided into four different chest compression groups randomly, including manual group, triangular wave group, sine wave group and trapezoidal wave group. The success rates of return of spontaneous circulation (ROSC) of those four groups were calculated, and all ROSC rats were executed 30 minutes after ROSC. Further comparisons were made among those four groups, including pathological changes, superoxide dismutase (SOD) activities, malondialdehyde (MDA) and superoxide (O 2 - ) content. Results: The success ROSC rates for those four groups (manual group, triangular wave group, sine wave group and trapezoidal wave group) were 30%, 40%, 40% and 90% respectively. There were inflammatory cell infiltration and edema in the heart tissue of those four groups. The activities of SOD in trapezoidal wave group were 85.91±1.91 U/mg, much higher than those of the other three groups (P <0.05). On the other hand, the MDA and O 2 - levels of trapezoidal wave group were much lower than those of the other three groups (p<0.05). Conclusion: Our study demonstrated that trapezoidal wave chest compression may be beneficial in improving the success rate of ROSC and alleviate heart injury. Its possible mechanism might lie in its anti-oxidative stress capability during the chest compression.

Cardiolipin alterations and mitochondrial dysfunction in heart ischemia/reperfusion injury

2015 ◽  
Vol 10 (5) ◽  
pp. 415-429 ◽  
Author(s):  
Giuseppe Paradies ◽  
Valeria Paradies ◽  
Francesca M Ruggiero ◽  
Giuseppe Petrosillo
Keyword(s):  
Mitochondrial Dysfunction ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Heart Ischemia

Abstract 14456: Rethinking The Treatment Of Cardiac Arrest To Include Non-oxygen Metabolite Supplementation: Plasma Lysophosphatidylcholine Level Maintenance After Cardiac Arrest Is Critical For Survival

Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Muhammad Shoaib ◽  
Mitsuaki Nishikimi ◽  
Rishabh Choudhary ◽  
Tai Yin ◽  
Kei Hayashida ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Therapeutic Potential ◽  
Ischemia Reperfusion ◽  
Membrane Integrity ◽  
Whole Body ◽  
Strongly Correlated ◽  
Oxygen Metabolites ◽  
Subsequent Resuscitation

Cardiac arrest (CA) is a loss of circulation that curtails the supply of oxygen and non-oxygen metabolites to the whole body resulting in ischemia and death. Subsequent resuscitation is vital for survival, but also causes reperfusion injury. Oxygen deprivation as one arm of ischemia-reperfusion injury and its relationship with death is well-established, but its counterpart, metabolite dysfunction, is overlooked and poorly understood. We have previously shown that many metabolites are not normalized as efficiently or rapidly after resuscitation especially, particularly those that are severely decreased after CA. As such, we hypothesize that appropriate replenishment of certain metabolites is essential for survival. Lysophosphatidylcholine (LPC), an important family of phospholipids, is an example of such non-oxygen metabolites required post-CA. With multifactorial roles for maintaining homeostasis, such as acting as an energy substrate, maintaining membrane integrity, and functioning in inter- and intra-cellular signaling, decreased levels of LPC post-CA disrupts the various physiologic responsibilities resulting in profound systemic effects causing cellular and organ system injury. In this analysis, 1) phospholipid screening using HPLS-MS on plasma samples obtained from asphyxial-CA rats and human CA patients shows that LPC significantly decreases post-CA, especially during the reperfusion phase, and is strongly correlated with the duration of preceding CA and poor neurological/survival outcomes, and 2) individual supplementation of three species of LPC (LPC 18:0, LPC 18:1, and LPC 22:6) following resuscitation after 10 and 12 min rat CA helps improve survival and brain function as compared with vehicle. Overall, our study highlights that LPC is an essential, non-oxygen metabolite that is necessary to help promote survival after CA in rats that has therapeutic potential for human translation.

scholarly journals Comparing anesthesia with isoflurane and fentanyl/fluanisone/midazolam in a rat model of cardiac arrest

2017 ◽  
Vol 123 (4) ◽  
pp. 867-875 ◽  
Author(s):  
Niels Secher ◽  
Christian Lind Malte ◽  
Else Tønnesen ◽  
Leif Østergaard ◽  
Asger Granfeldt
Keyword(s):  
Cardiac Arrest ◽  
Reperfusion Injury ◽  
Perfusion Pressure ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Coronary Perfusion Pressure ◽  
Spontaneous Circulation ◽  
Coronary Perfusion ◽  
Return Of Spontaneous Circulation ◽  
Arterial Blood

Only one in ten patients survives cardiac arrest (CA), underscoring the need to improve CA management. Isoflurane has shown cardio- and neuroprotective effects in animal models of ischemia-reperfusion injury. Therefore, the beneficial effect of isoflurane should be tested in an experimental CA model. We hypothesize that isoflurane anesthesia improves short-term outcome following resuscitation from CA compared with a subcutaneous fentanyl/fluanisone/midazolam anesthesia. Male Sprague-Dawley rats were randomized to anesthesia with isoflurane ( n = 11) or fentanyl/fluanisone/midazolam ( n = 11). After 10 min of asphyxial CA, animals were resuscitated by mechanical chest compressions, ventilations, and epinephrine and observed for 30 min. Hemodynamics, including coronary perfusion pressure, systemic O2 consumption, and arterial blood gases, were recorded throughout the study. Plasma samples for endothelin-1 and cathecolamines were drawn before and after CA. Compared with fentanyl/fluanisone/midazolam anesthesia, isoflurane resulted in a shorter time to return of spontaneous circulation (ROSC), less use of epinephrine, increased coronary perfusion pressure during cardiopulmonary resusitation, higher mean arterial pressure post-ROSC, increased plasma levels of endothelin-1, and decreased levels of epinephrine. The choice of anesthesia did not affect ROSC rate or systemic O2 consumption. Isoflurane reduces time to ROSC, increases coronary perfusion pressure, and improves hemodynamic function, all of which are important parameters in CA models. NEW & NOTEWORTHY The preconditioning effect of volatile anesthetics in studies of ischemia-reperfusion injury has been demonstrated in several studies. This study shows the importance of anesthesia in experimental cardiac arrest studies as isoflurane raised coronary perfusion pressure during resuscitation, reduced time to return of spontaneous circulation, and increased arterial blood pressure in the post-cardiac arrest period. These effects on key outcome measures in cardiac arrest research are important in the interpretation of results from animal studies.

scholarly journals Brain Protection after Anoxic Brain Injury: Is Lactate Supplementation Helpful?

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1714
Author(s):  
Filippo Annoni ◽  
Lorenzo Peluso ◽  
Elisa Gouvêa Bogossian ◽  
Jacques Creteur ◽  
Elisa R. Zanier ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Brain Perfusion ◽  
Current Evidence ◽  
Anoxic Injury ◽  
Tissue Oxygen Delivery ◽  
Resuscitated Patients ◽  
Key Aspects

While sudden loss of perfusion is responsible for ischemia, failure to supply the required amount of oxygen to the tissues is defined as hypoxia. Among several pathological conditions that can impair brain perfusion and oxygenation, cardiocirculatory arrest is characterized by a complete loss of perfusion to the brain, determining a whole brain ischemic-anoxic injury. Differently from other threatening situations of reduced cerebral perfusion, i.e., caused by increased intracranial pressure or circulatory shock, resuscitated patients after a cardiac arrest experience a sudden restoration of cerebral blood flow and are exposed to a massive reperfusion injury, which could significantly alter cellular metabolism. Current evidence suggests that cell populations in the central nervous system might use alternative metabolic pathways to glucose and that neurons may rely on a lactate-centered metabolism. Indeed, lactate does not require adenosine triphosphate (ATP) to be oxidated and it could therefore serve as an alternative substrate in condition of depleted energy reserves, i.e., reperfusion injury, even in presence of adequate tissue oxygen delivery. Lactate enriched solutions were studied in recent years in healthy subjects, acute heart failure, and severe traumatic brain injured patients, showing possible benefits that extend beyond the role as alternative energetic substrates. In this manuscript, we addressed some key aspects of the cellular metabolic derangements occurring after cerebral ischemia-reperfusion injury and examined the possible rationale for the administration of lactate enriched solutions in resuscitated patients after cardiac arrest.

Sign in / Sign up

Export Citation Format

Share Document