心肌损伤的即时检测,临床前研究

Ida Maiorov, A. Livneh, Roy Efraim, A. Landesberg
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摘要

心肌功能评估对于心肌炎、COVID-19和败血症等严重炎症至关重要,因为它可能导致器官衰竭和死亡。心肌损伤的即时检测可以改善这些危重患者的治疗。本研究旨在开发评估全身性炎症动物模型收缩期和舒张期心功能的护理点技术。连续记录Langendorff灌注离体成年大鼠心脏超声和心室压。由计算机控制的系统控制心室负荷条件。两个心室的预负荷在目标值2和22 mmHg之间呈正弦曲线摆动。在基线记录后,将胶原酶(MMP8)添加到Krebs-Henseleit溶液中,以模拟活化的白细胞和巨噬细胞释放MMPs。胶原酶灌注导致心肌收缩压峰值逐渐下降,舒张末期体积(EDV)逐渐减小,与心壁同心增厚有关。胶原酶降解细胞外基质引起严重的舒张功能障碍,舒张末期容积明显向低容积移动,心外膜直径无明显变化。早期发现这些症状有助于评估心肌损伤的严重程度,并及时进行适当的治疗。
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Point-of-care detection of myocardial injury, a pre-clinical study
Evaluation of myocardial function is critical in severe inflammations as myocarditis, COVID-19 and sepsis, since it can lead to organ failure and death. Point-of-care detection of myocardial injury may improve the treatment of these critically ill patients. The study aimed to develop point of care technology for assessing the systolic and diastolic cardiac functions in animal model of systemic inflammation. Ultrasound and ventricular pressure were continuously recorded in Langendorff perfused isolated adult rat hearts. A computer controlled system controlled the ventricle loading conditions. The preload of both ventricles swung in a sinusoidal manner between target values of 2 and 22 mmHg. Collagenase (MMP8) was added to the Krebs-Henseleit solution following baseline recordings, to emulate the release of MMPs from activated leukocytes and macrophages. Collagenase perfusion led to gradual decline in peak systolic pressure and decrease in the end-diastolic volume (EDV), that were associated with concentric myocardial wall thickening. Extracellular matrix degradation by collagenases caused sever diastolic dysfunction with overt shift of the end-diastolic volume toward lower volumes, without significant changes in the epicardial diameter. Early detection of these signs may assist in assessing the severity of the myocardial injury and prompt the adequate treatment.
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