Microglia activation in the hypothalamic PVN following myocardial infarction

Aims: The development of neuroinflammation deteriorates the prognosis of myocardial infarction (MI). We aimed to investigate the effect of renal denervation (RDN) on post-MI neuroinflammation in rats and the related mechanisms.Methods and Results: Male adult Sprague-Dawley rats were subjected to sham or ligation of the left anterior descending coronary artery to induce MI. One week later, the MI rats received a sham or RDN procedure. Their cardiac functions were analyzed by echocardiography, and their intestinal structures, permeability, and inflammatory cytokines were tested. The intestinal microbiota were characterized by 16S rDNA sequencing. The degrees of neuroinflammation in the brains of rats were analyzed for microglia activation, inflammatory cytokines, and inflammation-related signal pathways. In comparison with the Control rats, the MI rats exhibited impaired cardiac functions, intestinal injury, increased intestinal barrier permeability, and microbial dysbiosis, accompanied by increased microglia activation and pro-inflammatory cytokine levels in the brain. A RDN procedure dramatically decreased the levels of renal and intestinal sympathetic nerve activity, improved cardiac functions, and mitigated the MI-related intestinal injury and neuroinflammation in the brain of MI rats. Interestingly, the RDN procedure mitigated the MI-increased intestinal barrier permeability and pro-inflammatory cytokines and plasma LPS as well as ameliorated the gut microbial dysbiosis in MI rats. The protective effect of RDN was not significantly affected by treatment with intestinal alkaline phosphatase but significantly reduced by L-phenylalanine treatment in MI rats.Conclusions: RDN attenuated the neuroinflammation in the brain of MI rats, associated with mitigating the MI-related intestinal injury.

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GW29-e1962 LED therapy might reduce ventricular arrhythmia by attenuating microglia activation and sympathetic hyperactivity in a myocardial infarction rat model

Journal of the American College of Cardiology ◽

10.1016/j.jacc.2018.08.246 ◽

2018 ◽

Vol 72 (16) ◽

pp. C68

Author(s):

Songyun Wang ◽

Jiang Hong

Keyword(s):

Myocardial Infarction ◽

Ventricular Arrhythmia ◽

Rat Model ◽

Microglia Activation ◽

Sympathetic Hyperactivity ◽

Led Therapy

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An electron microscopic study of the intra-myocardial lesions in cases of acute myocardial infarction

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s042482010008328x ◽

1978 ◽

Vol 36 (2) ◽

pp. 484-485

Author(s):

Masahiro Ono ◽

Kaoru Aihara ◽

Gompachi Yajima

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Coronary Vessels ◽

Vascular Wall ◽

Vascular Changes ◽

Electron Microscopic ◽

Main Trunk ◽

Mechanical Destruction ◽

Transmission Electron ◽

Myocardial Lesions

The pathogenesis of the arteriosclerosis in the acute myocardial infarction is the matter of the extensive survey with the transmission electron microscopy in experimental and clinical materials. In the previous communication,the authors have clarified that the two types of the coronary vascular changes could exist. The first category is the case in which we had failed to observe no occlusive changes of the coronary vessels which eventually form the myocardial infarction. The next category is the case in which occlusive -thrombotic changes are observed in which the myocardial infarction will be taken placed as the final event. The authors incline to designate the former category as the non-occlusive-non thrombotic lesions. The most important findings in both cases are the “mechanical destruction of the vascular wall and imbibition of the serous component” which are most frequently observed at the proximal portion of the coronary main trunk.

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