Mild hypothermia in rat with acute myocardial ischaemia‐reperfusion injury complicating severe sepsis

Abstract

Myocardial ischemia‐reperfusion injury (MIRI) with concurrent severe sepsis has led to substantial mortality. Mild hypothermia (MHT) has been proved to have a therapeutic effect in either MIRI or severe sepsis, which suggests it might be beneficial for MIRI complicating severe sepsis. In this study, Sprague‐Dawley rats with MIRI complicating severe sepsis were allotted in either MHT (33 ± 0.5°C) group or normothermia (NT, 37 ± 0.5°C) group; as control, rats receiving sham surgery and normal saline were kept at NT. After 2h of temperature maintenance, blood and heart tissue were acquired for detections. Lactate dehydrogenase (LDH) and MB isoenzyme of creatine kinase (CK‐MB) in blood, triphenyl tetrazolium chloride and Evans blue staining, hematoxylin and eosin staining for myocardium were employed to detect myocardial damage. Tumor necrosis factor (TNF)‐α and caspase‐3 was performed by immunohistochemistry to exam myocardial inflammation and apoptosis. Detection of NADPH oxidase (NOX) 2 was for myocardial oxidative stress. In MHT group, systolic blood pressure was improved significantly compared with NT group. Myocardial infarct size, morphological change, LDH and CK‐MB levels were attenuated compared to NT group. Moreover, less expressions of TNF‐α, caspase‐3 and NOX2 in MHT group were presented compared with NT group. MHT showed cardioprotection by improving cardiac dysfunction, reducing myocardial infarct size and attenuating myocardial injury, inflammation, apoptosis and oxidative stress.

Interleukin 32 participates in cardiomyocyte‑induced oxidative stress, inflammation and apoptosis during hypoxia/reoxygenation via the NOD2/NOX2/MAPK signaling pathway

“…It is considered that the investigation of the disease mechanism of MIRI can provide a novel concept for the development of therapeutic strategies for the treatment of this condition. Myocardial membrane permeability is increased in patients with MIRI, resulting in a rapid rise in LDH levels in the body ( 23 ). The results of the present study demonstrated that IL-32 levels were increased following H/R, whereas increased IL-32 levels promoted a cascade reaction in cardiomyocytes, which was accompanied by increased LDH release, inflammatory response, oxidative stress and apoptosis.…”

Contractility detection of isolated mouse papillary muscle using myotronic Myostation‐Intact device

“…CS should be preheated to the desired temperature before being perfused into the cuvette to save time at later stages. Previous studies showed that mild hyperthermia (32–35°C) can protect myocardial tissue by increasing myocardial contractility and decreasing body metabolism 18–20 . Though these studies were conducted in vivo, lower temperature can also be applied on ex vivo myocardial tissues.…”