LEFT-VENTRICULAR MYOCARDIAL EDEMA - LYMPH-FLOW, INTERSTITIAL FIBROSIS, AND CARDIAC-FUNCTION
LEFT-VENTRICULAR MYOCARDIAL EDEMA - LYMPH-FLOW, INTERSTITIAL FIBROSIS, AND CARDIAC-FUNCTION
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DOI：
10.1161/01.res.68.6.1713
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发表时间：
1991-06-01
影响因子：
20.1
通讯作者：
ALLEN, SJ
中科院分区：
文献类型：
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作者：
LAINE, GA;ALLEN, SJ
我们假设急性和慢性心肌间质水肿（血管外液[EVF]）的积累都会损害心功能。我们还假设心肌间质间隙内的过量液体会加剧间质纤维化，从而进一步损害功能。将狗分为3组：1)对照组，2)慢性肺动脉高压合并右心衰组，3)慢性动脉高血压组。测定EVF的数量（以单位无血量（湿重-干重）/干重比表示）和间质纤维化（胶原含量），并将其与基线和急性冠状静脉压升高、心脏淋巴流量减少后的心功能相关。对照组EVF为2.90 +/- 0.20（平均+/- SD），急性（3小时）冠状窦压升高后EVF为3.45 +/- 0.16。EVF显著损害心功能。慢性高血压犬和慢性右心压升高犬的EVF分别为3.50 +/- 0.30和3.50 +/- 0.08。舒张末期左室间质液压力从控制值14.9 +/- 3.1 （EVF = 2.9）上升至24.8 +/- 3.7 （EVF = 3.5）。当左房压为15 mm Hg时，EVF为3.5会使心脏维持心输出量的能力降低约30%。在这些慢性模型中，冠状静脉压急性升高和心淋巴流量减少会加剧功能受损。在慢性高血压犬和慢性右心压升高犬的非肥厚左心室中，胶原蛋白水平升高至少20%。我们得出结论，急性心肌水肿损害心功能，慢性右心压升高和慢性动脉高血压导致左心室心肌水肿，这也损害了这些常见病理条件下的功能。在这些慢性模型中，心肌水肿的存在也增强了间质纤维化，导致心脏正常功能的能力进一步下降。
We hypothesized that both acute and chronic accumulation of myocardial interstitial edema (extravascular fluid [EVF]) would compromise cardiac function. We also postulated that excess fluid within the myocardial interstitial space would potentiate interstitial fibrosis, thus further compromising function. Dogs were divided into three groups: 1) control, 2) chronic pulmonary hypertensive with right heart failure, and 3) chronic arterial hypertensive. The quantity of EVF, expressed as the unitless blood-free (wet weight-dry weight)/dry weight ratio, and interstitial fibrosis (collagen content) were determined and correlated with cardiac function at baseline and after acute elevation of coronary venous pressure and reduction of cardiac lymph flow. Control EVF was 2.90 +/- 0.20 (mean +/- SD), which increased to 3.45 +/- 0.16 after acute (3-hour) elevation of coronary sinus pressure. This EVF significantly compromised cardiac function. The EVF in chronically hypertensive dogs and in dogs with chronic right heart pressure elevations was 3.50 +/- 0.30 and 3.50 +/- 0.08, respectively. End-diastolic left ventricular interstitial fluid pressure increased from a control value of 14.9 +/- 3.1 (at EVF = 2.9) to 24.8 +/- 3.7 (at EVF = 3.5). An EVF of 3.5 produced approximately 30% reduction of the heart's ability to maintain cardiac output at a left atrial pressure of 15 mm Hg. The compromised function in these chronic models is exacerbated after acute elevation of coronary venous pressure and reduction of cardiac lymph flow. Collagen levels were elevated by at least 20% in the chronic hypertensive dogs and in the nonhypertrophied left ventricles of dogs with chronic right heart pressure elevation. We conclude that acute myocardial edema compromises cardiac function and that chronic right heart pressure elevation and chronic arterial hypertension produce left ventricular myocardial edema, which also compromises function in these common pathological conditions. The presence of myocardial edema in these chronic models also potentiates interstitial fibrosis, leading to a further decrease in the heart's ability to function normally.