Salutary effects of moderate hypothermia on the circulatory and myocardial consequences of acute coronary occlusion in dogs

Bergmann, Steven R.; Angelakos, E. T.; Torres, Joseph Charles

doi:10.1016/0011-2240(85)90032-x

Cited by 9 publications

(4 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In some ex vivo studies of hypothermia, 49 , 50 hypothermia increased cardiac contractility, and our study showed similar results that miR‐483‐3p also significantly increased cardiac contractility. Moreover, hypothermia led to a decrease in stroke volume or cardiac output 51 , 52 in in vivo studies, but overexpression of miR‐483‐3p promoted stroke volume or cardiac output. Together, these data indicated that miR‐483‐3p partially simulated therapeutic hypothermia and improved some adverse effects of therapeutic hypothermia.…”

Section: Discussionmentioning

confidence: 95%

Therapeutic Hypothermia Inhibits Hypoxia‐Induced Cardiomyocyte Apoptosis Via the MiR‐483‐3p/Cdk9 Axis

Xue

Zhang

Guo

et al. 2023

JAHA

View full text Add to dashboard Cite

Background Therapeutic hypothermia has a beneficial effect on cardiac function after acute myocardial infarction, but the exact mechanism is still unclear. Recent research has suggested that microRNAs participate in acute myocardial infarction to regulate cardiomyocyte survival. This study aimed to explore the ability of hypothermia‐regulated microRNA‐483‐3p (miR‐483‐3p) to inhibit hypoxia‐induced myocardial infarction. Methods and Results Primary cardiomyocytes were cultured under hypoxia at 32 °C to mimic therapeutic hypothermia, and the differentially expressed microRNAs were determined by RNA sequencing. Therapeutic hypothermia recovered hypoxia‐induced increases in apoptosis, decreases in ATP levels, and decreases in miR‐483‐3p expression. Overexpression of miR‐483‐3p exhibited effects similar to those of therapeutic hypothermia on hypoxia in the treatment of cardiomyocytes to associate with maintaining the mitochondrial membrane potential, and cyclin‐dependent kinase 9 (Cdk9) was identified as a target gene with downregulated expression by miR‐483‐3p. Knockdown of Cdk9 also promoted cardiac survival, ATP production, and mitochondrial membrane potential stability under hypoxia. In vivo, the expression of miR‐483‐3p and Cdk9 was tested in the cardiac tissue of the mice with acute myocardial infarction, and the expression of miR‐483‐3p decreased and Cdk9 increased in the region of myocardial infarction. However, miR‐483‐3p was overexpressed with lentivirus, which suppressed apoptosis, infarct size (miR‐483‐3p, 22.00±4.04% versus negative control, 28.57±5.44%, P <0.05), and Cdk9 expression to improve cardiac contractility. Conclusions MiR‐483‐3p antagonizes hypoxia, leading to cardiomyocyte injury by targeting Cdk9, which is a new mechanism of therapeutic hypothermia.

show abstract

Section: Discussionmentioning

confidence: 95%

Therapeutic Hypothermia Inhibits Hypoxia‐Induced Cardiomyocyte Apoptosis Via the MiR‐483‐3p/Cdk9 Axis

Xue

Zhang

Guo

et al. 2023

JAHA

View full text Add to dashboard Cite

show abstract

“…TTM (targeted temperature management) has been used to reduce systemic low-flow and no-flow reperfusion injury after cardiac arrest [ 82 – 86 ]. In the ischemic heart, TTM has shown infarct size reduction in several preclinical models with a variety of animal species, ischemia durations, cooling methods, cooling durations, magnitudes of cooling, and timings of cooling initiation [ 87 , 88 ]. A study in rabbits identified a linear relationship between the myocardial infarct area and temperature when heart rate was controlled and body temperature was maintained at 35–42 °C.…”

Section: Cardiac Protection Strategiesmentioning

confidence: 99%

Cardioprotective Strategies After Ischemia–Reperfusion Injury

Zhang,

Hu,

Zhai

et al. 2023

Am J Cardiovasc Drugs

View full text Add to dashboard Cite

Acute myocardial infarction (AMI) is associated with high morbidity and mortality worldwide. Although early reperfusion is the most effective strategy to salvage ischemic myocardium, reperfusion injury can develop with the restoration of blood flow. Therefore, it is important to identify protection mechanisms and strategies for the heart after myocardial infarction. Recent studies have shown that multiple intracellular molecules and signaling pathways are involved in cardioprotection. Meanwhile, device-based cardioprotective modalities such as cardiac left ventricular unloading, hypothermia, coronary sinus intervention, supersaturated oxygen (SSO 2 ), and remote ischemic conditioning (RIC) have become important areas of research. Herein, we review the molecular mechanisms of cardioprotection and cardioprotective modalities after ischemia–reperfusion injury (IRI) to identify potential approaches to reduce mortality and improve prognosis in patients with AMI.

show abstract

“… 56 In the ischemic heart, TTM has shown IS reduction in several preclinical models with a variety of animal species, ischemia duration, cooling methods, cooling duration, magnitude of cooling, and timing of cooling initiation. 57 , 58 Most of these studies used target temperature between 32 °C and 35 °C. Meanwhile, experimental data suggest that even small changes of temperature within normothermic range can affect IS significantly.…”

Section: Myocardial Coolingmentioning

confidence: 99%

Device‐Based Approaches Targeting Cardioprotection in Myocardial Infarction: The Expanding Armamentarium of Innovative Strategies

Romeo

Mazurek

Sakata

et al. 2022

JAHA

View full text Add to dashboard Cite

Coronary reperfusion therapy has played a pivotal role for reducing mortality and heart failure after acute myocardial infarction. Although several adjunctive approaches have been studied for reducing infarct size further, both ischemia–reperfusion injury and microvascular obstruction are still major contributors to both early and late clinical events after acute myocardial infarction. The progress in the field of cardioprotection has found several promising proof‐of‐concept preclinical studies. However, translation from bench to bedside has not been very successful. This comprehensive review discusses the importance of infarct size as a driver of clinical outcomes post‐acute myocardial infarction and summarizes recent novel device‐based approaches for infarct size reduction. Device‐based interventions including mechanical cardiac unloading, myocardial cooling, coronary sinus interventions, supersaturated oxygen therapy, and vagal stimulation are discussed. Many of these approaches can modify ischemic myocardial biology before reperfusion and offer unique opportunities to target ischemia–reperfusion injury.

show abstract

Salutary effects of moderate hypothermia on the circulatory and myocardial consequences of acute coronary occlusion in dogs

Cited by 9 publications

References 31 publications

Therapeutic Hypothermia Inhibits Hypoxia‐Induced Cardiomyocyte Apoptosis Via the MiR‐483‐3p/Cdk9 Axis

Therapeutic Hypothermia Inhibits Hypoxia‐Induced Cardiomyocyte Apoptosis Via the MiR‐483‐3p/Cdk9 Axis

Cardioprotective Strategies After Ischemia–Reperfusion Injury

Device‐Based Approaches Targeting Cardioprotection in Myocardial Infarction: The Expanding Armamentarium of Innovative Strategies

Contact Info

Product

Resources

About