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多巴胺、多巴酚丁胺與心臟 (xīnz224。ng)循環(huán)系統(tǒng)( MAP\CI\SVRI\LVSWI/PAOP)密切相關。? Immunol Invest2024。39(8):84962第十六 頁 ,共四十一 頁 。? 其次,免疫效應細胞引起的 促炎性信號和抗炎的信號之間 失平衡 。 過度的全身炎癥反應可能有利于器官衰竭,過量抗炎介質的發(fā)展 (fāzhǎn), 也 會危及 各臟器功能。 *Pinsky MR: Dysregulation of the immune response in severe J Med Sci 2024, 328:220229.四、 SIC的發(fā)病機制 (jīzh236。)免疫炎癥失調(diào)第十七 頁 ,共四十一 頁 。四、 SIC的發(fā)病機制 (jīzh236。)循環(huán)代謝系統(tǒng) Sepsisinduced cardiac dysfunction. Cardiac performance during sepsis is impaired due to changes in the macro and microcirculation, autonomic dysfunction, and inflammationinduced intrinsic myocardial depression. The mechanisms of myocardial depression include downregulation of adrenergic pathways, disturbed intracellular calcium (Ca 2?) trafficking, and impaired electromechanical coupling at the myofibrillar level. Mitochondrial dysfunction seems to plays a central role in this sepsisinduced an dysfunction. 大、微循環(huán)改變,自主神經(jīng)功能紊亂,炎性介導的內(nèi)源性心肌抑制共同(g242。ngt243。ng)作用誘導腎上腺素下調(diào),干擾 Ca輸送,肌原纖維受損。線粒體功能障礙起到核心作用,其抑制 ATP的產(chǎn)生,引起心肌細胞凋亡。 Crit Care Med 2024 Vol. 35, No. 6第十八 頁 ,共四十一 頁 。四、 SIC的發(fā)病機制 (jīzh236。)循環(huán)代謝系統(tǒng)Effects of esmolol on systemic and pulmonary hemodynamics and on oxygenation in pigs with hypodynamic endotoxin shock.第十九 頁 ,共四十一 頁 。四、 SIC的發(fā)病 (fā b236。ng)機制 兒茶酚胺系統(tǒng)? Shortterm?βadrenergic stimulation with catecholamines increases cardiac contractility and heart rate. However, prolonged and excess stimulation can lead to myocardial damage by calcium overload and consequent cell necrosis 。? 短期的 β腎上腺素能刺激兒茶酚胺增加心肌收縮力和心臟速率 (s249。lǜ)。然而,長期和過量的刺激可通過鈣超載和隨之而來的細胞壞死 引起 心肌損傷 。Opie LH: Receptors and signal transduction. In: Heart Physiology: From Cell to Circulation. Fourth Edition. Opie LH (Ed).London, Lippincott Williams Wilkins,2024, pp 186 –220第二十 頁 ,共四十一 頁 。四、 SIC的發(fā)病 (fā b236。ng)機制 兒茶酚胺系統(tǒng) AM J RESPIR CRIT CARE MED 1999。160:458–465.第二十一 頁 ,共四十一 頁 。四、 SIC的發(fā)病機制 (jīzh236。)兒茶酚胺系統(tǒng) 在皮下注射 20mmol/kg兒茶酚胺類藥藥物后,心肌凋亡(淺灰色)和壞死 (hu224。i sǐ)(深灰色)矩形圖(左);運用異丙腎上腺素不同劑量后,心肌心肌凋亡(淺灰色)和壞死(深