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离体兔心脏中的冠状动脉高血压与舒张顺应性

Coronary hypertension and diastolic compliance in isolated rabbit hearts.

作者信息

Wexler L F, Grice W N, Huntington M, Plehn J F, Apstein C S

机构信息

Cardiovascular Institute, Boston University School of Medicine, Massachusetts.

出版信息

Hypertension. 1989 Jun;13(6 Pt 1):598-606. doi: 10.1161/01.hyp.13.6.598.

DOI:10.1161/01.hyp.13.6.598
PMID:2737708
Abstract

Acute pulmonary edema during hypertensive crisis has been attributed to acute left ventricular systolic failure secondary to increased afterload. We tested the hypothesis that the increase in coronary artery perfusion pressure associated with systemic hypertension could also contribute to increased left ventricular filling pressures by acutely increasing coronary intravascular volume and decreasing left ventricular diastolic compliance. Isolated isovolumic (balloon in left ventricle) normal rabbit hearts (n = 13) with pericardium removed and right ventricle vented were blood perfused at an initial coronary artery perfusion pressure of 100 mm Hg; left ventricular balloon volume was adjusted to produce an initial left ventricular end-diastolic pressure of 15 +/- 1 mm Hg; left ventricular systolic pressure was 102 +/- 3 mm Hg. When coronary perfusion pressure was increased to 130 +/- 1 mm Hg to simulate a hypertensive crisis, coronary flow increased from 2.0 +/- 0.2 to 3.0 +/- 0.2 ml/min/g left ventricle (p less than 0.001), left ventricular systolic pressure increased to 116 +/- 4 mm Hg, and isovolumic left ventricular end-diastolic pressure increased to 21 +/- 1 mm Hg (p less than 0.001), which indicated a decrease in left ventricular diastolic compliance. When coronary perfusion pressure was decreased to a physiological level of 70 mm Hg, coronary flow rate decreased to 1.4 +/- 0.1 ml/min/g left ventricle (p less than 0.001), left ventricular systolic pressure fell to 82 +/- 4 mm Hg, and left ventricular end-diastolic pressure fell to 14 +/- 1 mm Hg (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

高血压危象期间的急性肺水肿被认为是后负荷增加继发的急性左心室收缩功能衰竭所致。我们验证了这样一个假说,即与系统性高血压相关的冠状动脉灌注压升高,也可能通过急性增加冠状动脉血管内容量和降低左心室舒张顺应性,导致左心室充盈压升高。去除心包并使右心室排气的离体等容(左心室内有球囊)正常兔心脏(n = 13),在初始冠状动脉灌注压为100 mmHg的情况下进行血液灌注;调整左心室球囊容积,使初始左心室舒张末期压力为15±1 mmHg;左心室收缩压为102±3 mmHg。当冠状动脉灌注压升高至130±1 mmHg以模拟高血压危象时,冠状动脉血流量从2.0±0.2增加至3.0±0.2 ml/min/g左心室(p<0.001),左心室收缩压升高至116±4 mmHg,等容左心室舒张末期压力升高至21±1 mmHg(p<0.001),这表明左心室舒张顺应性降低。当冠状动脉灌注压降至生理水平70 mmHg时,冠状动脉血流速率降至1.4±0.1 ml/min/g左心室(p<0.001),左心室收缩压降至82±4 mmHg,左心室舒张末期压力降至14±1 mmHg(p<0.001)。(摘要截断于250字)

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