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离体心脏标本:循环性休克中心肌内在功能障碍的模型

Isolated cardiac preparations: models of intrinsic myocardial dysfunction in circulatory shock.

作者信息

Parker J L, Adams H R

出版信息

Circ Shock. 1985;15(4):227-45.

PMID:3995693
Abstract

Isolated cardiac preparations have been adapted for modeling intrinsic myocardial responses to circulatory shock syndromes independently of immediate influence from depressive or supportive constraints operative in the intact host. Left atrial and left ventricular (LV) papillary muscles and coronary-perfused hearts were removed from guinea pigs during development of Escherichia coli endotoxin shock. Preparations were then subjected to a battery of functional analyses under conditions of constant perfusate pH, pO2, pCO2, electrolyte and substrate concentrations, osmolality, and temperature. Evidence for contractile depression intrinsic to the myocardium itself was a consistent and reproducible finding in all three tissue models. The LV mechanical disadvantage of shock hearts was not correlated with changes in cardiac cycle length (beating frequency), active state duration (contraction-relaxation intervals), or tissue water content; neither was it surmounted by maximally effective increments in coronary flow, [Ca2+]o, or diastolic fiber length. Taken in concert, studies to date suggest that gram-negative endotoxin leads in some way to a reduction of intrinsic contractile reserves of the myocardium, and we have postulated that this change underlies the circulatory shock phase of endotoxicosis. The experimental approach embodied in these models may yield unique cardiodynamic interpretations that will allow the formulation of testable hypotheses about the pathogenesis and prevention of intrinsic cardiac complications of endotoxin and related shock forms.

摘要

已对离体心脏标本进行了调整,以模拟心肌对循环休克综合征的内在反应,而不受完整宿主中起作用的抑制性或支持性因素的直接影响。在大肠杆菌内毒素休克发展过程中,从豚鼠身上取出左心房和左心室(LV)乳头肌以及冠状动脉灌注心脏。然后在灌注液pH值、pO2、pCO2、电解质和底物浓度、渗透压及温度恒定的条件下,对标本进行一系列功能分析。心肌自身收缩抑制的证据在所有三种组织模型中都是一致且可重复的发现。休克心脏的左心室机械劣势与心动周期长度(搏动频率)、活动状态持续时间(收缩 - 舒张间隔)或组织含水量的变化无关;冠状动脉流量、[Ca2 +]o或舒张期纤维长度的最大有效增加也无法克服这一劣势。综合来看,迄今为止的研究表明,革兰氏阴性内毒素以某种方式导致心肌内在收缩储备减少,并且我们推测这种变化是内毒素血症循环休克阶段的基础。这些模型所采用的实验方法可能会产生独特的心脏动力学解释,这将有助于形成关于内毒素及相关休克形式的内在心脏并发症的发病机制和预防的可验证假设。

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