Original Research: Establishment of an early embolus-related cerebral injury model after cardiopulmonary bypass in miniature pigs

Abstract

Embolus-related cerebral injury is still a serious adverse event after cardiopulmonary bypass (CPB). But there is no stable animal model for basic and clinical research purposes. We chose miniature pig to establish a stable animal model of embolus-related cerebral injury after CPB and verified the validity of results by correlating the histopathological findings with those of diffusionweighted magnetic resonance imaging (DW-MRI). Based on different treatment regimens, 24 male miniature pigs were randomly assigned into four groups: Control, CPB, embolus, and CPB-embolus groups. DW-MRI was performed before and after surgery to diagnose and locate the brain lesions. Histopathological changes in brain tissues were examined using H&E and Nissl staining. All surgical procedures were uneventful with 100% postoperative survival of pigs. Two animals in the Embolus group and six animals in the CPB-embolus group showed signs of ischemic penumbra on DW-MRI performed 6 h after surgery. Consistent with the results of DW-MRI, histopathological examination showed necrosis and ischemic lesions. In this paper, we demonstrate the feasibility and validity of a pig model of embolus-related cerebral injury associated with CPB. This model may be used in the future for basic and translational research.

Cardiopulmonary bypass duration is an independent predictor of adverse outcome in surgical repair for acute type A aortic dissection

“…The mechanism of brain injury after CPB is complex with major causes that include cerebral emboli (gas, liquid, or solid), cerebral ischaemic injury (e.g., vascular embolism, hypoperfusion, and hypoxia), and inflammatory responses. 3 , 21 During CPB, stimulation by surgical trauma, blood contact with foreign bodies, body endotoxins, and a low temperature activate non-infectious systemic inflammatory response syndromes. 4 Therefore, a large number of inflammatory cytokines enter the brain, leading to brain damage.…”

Dexmedetomidine reduces the neuronal apoptosis related to cardiopulmonary bypass by inhibiting activation of the JAK2–STAT3 pathway

“… 6 Several studies have shown that CPB-mediated brain injury is associated with embolism, hypoperfusion, arrhythmias, rapid rewarming, and inflammation. 3 , 4 , 7 Moreover, a substantial amount of research has been conducted into brain injury associated with CPB in relation to different cell factors and signal pathways. 5 , 8 …”

Cardiopulmonary bypass duration is an independent predictor of adverse outcome in surgical repair for acute type A aortic dissection

“…However, the incidence of complications related to the nervous system has remained consistent. The mechanism of brain injury after CPB is complex, with major causes including cerebral emboli (gas, liquid, or solid), cerebral ischaemic injury (such as vascular embolism, hypo perfusion, and hypoxia), and inflammatory responses [19,20]. During CPB, stimulation by surgical trauma, blood contact with foreign bodies, body endotoxins, and a low temperature activate non-infectious systemic inflammatory response syndromes [21].…”