Energetics of acute pressure overload of the porcine right ventricle. In vivo 31P nuclear magnetic resonance.
Energetics of acute pressure overload of the porcine right ventricle. In vivo 31P nuclear magnetic resonance.
复制标题
猪右心室急性压力超负荷的能量学。
DOI：
10.1172/jci115671
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Weiner,MW
中科院分区：
文献类型：
--
作者：
Schwartz,GG;Steinman,S;Garcia,J;Greyson,C;Massie,B;Weiner,MW
在体内右心室（RV）游离壁的31 P核磁共振（NMR）波谱被用来确定（a）RV中磷能量代谢物是否随工作负荷而变化，以及（B）急性压力超负荷时限制RV收缩功能的机制。在20头开胸猪中，（与游离ADP浓度呈负相关的能量代谢指数），心肌血流量（微球）和节段缩短（声显微测量法，n = 14）在对照组进行测量（RV收缩压31 +/- 1 mm Hg），并伴有肺动脉收缩以产生中度压力超负荷（RV收缩压45 +/- 1 mm Hg），和明显RV衰竭和全身性低血压（RV收缩压60 +/- 1 mm Hg）前的最大压力超负荷。中度压力超负荷时，PCr/ATP下降至对照组的89%（P = 0.01），而收缩功能增加。腺苷（n = 10，平均剂量0.16 mg/kg-min）使RV血流量增加41%，而不增加PCr/ATP，表明冠状动脉储备未耗尽，PCr/ATP相对于对照组的降低不是由于缺血。在最大压力超负荷和早期RV衰竭的情况下，PCr/ATP进一步下降至对照组的81%，即使使用腺苷，RV血流量也没有进一步增加。由此可见：（a）在没有明显缺血或收缩功能障碍的情况下，伴随中度RV压力超负荷的PCr/ATP下降，支持ATP水解产物对氧化磷酸化的正调节。(b)在最大压力超负荷时，右心室冠状动脉血流储备的消耗伴随着右心室衰竭的发生。
In vivo 31P nuclear magnetic resonance (NMR) spectroscopy of the right ventricular (RV) free wall was employed to determine (a) whether phosphorus energy metabolites vary reciprocally with workload in the RV and (b) the mechanisms that limit RV contractile function in acute pressure overload. In 20 open-chest pigs, phosphocreatine (PCr)/ATP ratio (an index of energy metabolism inversely related to free ADP concentration), myocardial blood flow (microspheres), and segment shortening (sonomicrometry, n = 14) were measured at control (RV systolic pressure 31 +/- 1 mm Hg), and with pulmonary artery constriction to produce moderate pressure overload (RV systolic pressure 45 +/- 1 mm Hg), and maximal pressure overload before overt RV failure and systemic hypotension (RV systolic pressure 60 +/- 1 mm Hg). With moderate pressure overload, PCr/ATP declined to 89% of control (P = 0.01), while contractile function increased. Adenosine (n = 10, mean dose 0.16 mg/kg-min) increased RV blood flow by an additional 41% without increasing PCr/ATP, indicating that coronary reserve was not depleted and that the decrease in PCr/ATP from control was not due to ischemia. With maximal pressure overload and incipient RV failure, PCr/ATP fell further to 81% of control and RV blood flow did not increase further, even with adenosine. Thus: (a) The decline in PCr/ATP with moderate RV pressure overload, without evident ischemia or contractile dysfunction, supports the positive regulation of oxidative phosphorylation by ATP hydrolysis products. (b) Depletion of RV coronary flow reserve accompanies the onset of RV failure at maximal pressure overload.Images