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肺动脉高压因充盈不足导致大鼠左心室收缩性指标出现代偿性增加。

Pulmonary Arterial Hypertension Induces Compensatory Increase of Left Ventricular Contractility Indexes in Rats in Response to Its Filling Insufficiency.

作者信息

Abramov A A, Lakomkin V L, Prosvirnin A V, Kuzmin V S

机构信息

National Medical Research Centre of Cardiology named after academician E. I. Chazov, Ministry of Health of the Russian Federation, Moscow, Russia.

Biological Faculty, Lomonosov Moscow State University, Moscow, Russia.

出版信息

Bull Exp Biol Med. 2025 Mar;178(5):586-592. doi: 10.1007/s10517-025-06379-x. Epub 2025 Apr 29.

DOI:10.1007/s10517-025-06379-x
PMID:40299128
Abstract

Pulmonary arterial hypertension (PAH) is accompanied by changes in the pulmonary and systemic circulation. We studied the effect of PAH on the function of the left ventricle (LV). Left ventricular pressure and volume were simultaneously recorded in vivo in rats with monocrotaline-induced PAH (60 mg/kg). LV contractility and mechanical indexes were calculated. In addition, the relationships between LV maximum rate of contraction (dP/dt) or relaxation (dP/dt) and left ventricular end-diastolic volume (EDV) were assessed. PAH leads to a significant decrease in cardiac output at a constant HR as well as to a decrease in stroke volume at unchanged LV ejection fraction. In rats with PAH, the slopes of the dP/dt-EDV and dP/dt-EDV curves were greater than in control animals by 1.93 and 2.5 times, respectively. Thus, PAH leads to a compensatory increase in the dependence of LV contractility and "intensity" of LV relaxation on EDV.

摘要

肺动脉高压(PAH)伴有肺循环和体循环的改变。我们研究了PAH对左心室(LV)功能的影响。在给予60mg/kg野百合碱诱导PAH的大鼠体内同时记录左心室压力和容积。计算左心室收缩性和力学指标。此外,评估左心室最大收缩速率(dP/dt)或舒张速率(dP/dt)与左心室舒张末期容积(EDV)之间的关系。在恒定心率下,PAH导致心输出量显著降低,且在左心室射血分数不变的情况下导致每搏输出量减少。在PAH大鼠中,dP/dt-EDV和dP/dt-EDV曲线的斜率分别比对照动物大1.93倍和2.5倍。因此,PAH导致左心室收缩性和左心室舒张“强度”对EDV的依赖性代偿性增加。

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本文引用的文献

1
Left ventricular underfilling in PAH: A potential indicator for adaptive-to-maladaptive transition.肺动脉高压中的左心室充盈不足:适应性向适应不良转变的潜在指标。
Pulm Circ. 2023 Nov 30;13(4):e12309. doi: 10.1002/pul2.12309. eCollection 2023 Oct.
2
Compensatory Changes of the Diastole under Conditions of Inflow Restriction to the Heart.心脏流入受限情况下舒张期的代偿性变化。
Bull Exp Biol Med. 2021 May;171(1):15-18. doi: 10.1007/s10517-021-05162-y. Epub 2021 May 28.
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Metabolic syndrome, neurohumoral modulation, and pulmonary arterial hypertension.
代谢综合征、神经体液调节与肺动脉高压。
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The overloaded right heart and ventricular interdependence.右心负荷过重与心室相互依存。
Cardiovasc Res. 2017 Oct 1;113(12):1474-1485. doi: 10.1093/cvr/cvx160.
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β-Arrestin mediates the Frank-Starling mechanism of cardiac contractility.β-抑制蛋白介导心脏收缩力的Frank-Starling机制。
Proc Natl Acad Sci U S A. 2016 Dec 13;113(50):14426-14431. doi: 10.1073/pnas.1609308113. Epub 2016 Nov 28.
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Protein changes contributing to right ventricular cardiomyocyte diastolic dysfunction in pulmonary arterial hypertension.导致肺动脉高压时右心室心肌细胞舒张功能障碍的蛋白质变化。
J Am Heart Assoc. 2014 Jun 3;3(3):e000716. doi: 10.1161/JAHA.113.000716.
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Right ventricular diastolic impairment in patients with pulmonary arterial hypertension.肺动脉高压患者的右心室舒张功能障碍。
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10
Dysregulated renin-angiotensin-aldosterone system contributes to pulmonary arterial hypertension.肾素-血管紧张素-醛固酮系统失调导致肺动脉高压。
Am J Respir Crit Care Med. 2012 Oct 15;186(8):780-9. doi: 10.1164/rccm.201203-0411OC. Epub 2012 Aug 2.