Nitric oxide modulates myocardial oxygen consumption in the failing heart
Nitric oxide modulates myocardial oxygen consumption in the failing heart
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DOI：
10.1161/01.cir.0000021120.90970.b9
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发表时间：
2002-07-09
期刊：
影响因子：
37.8
通讯作者：
Bache, RJ
中科院分区：
文献类型：
--
作者：
Chen, YJ;Traverse, JH;Bache, RJ
背景-内源性一氧化氮（NO）已被报道可抑制正常心脏的耗氧量，因此非选择性抑制NO合酶（NOS）可引起心肌耗氧量增加（M（V）超过dotO（2））。尽管内皮NOS反应在充血性心力衰竭（CHF）中被抑制，但诱导型NOS（iNOS）可在衰竭心肌中表达。方法和结果-本研究测试了在衰竭心脏中NOS抑制将增加M（V）超过dotO（2）的假设。通过使用快速心室起搏模型在狗中产生CHF。与正常值相比，CHF动物静息时冠状动脉血流量减少，M（V）超过dotO（2），对跑步机运动的反应迟钝。用S-甲基异硫脲（1.5 mg/kg IC）选择性抑制iNOS可增加左室收缩压和左室dP/dt，并导致静息和运动时M（V）增加超过dotO（2）（P
Background-Endogenous nitric oxide (NO) has been reported to inhibit oxygen consumption in the normal heart, so that nonselective inhibition of NO synthase (NOS) caused an increase of myocardial oxygen consumption (M(V)over dotO(2)). Although endothelial NOS responses are depressed in congestive heart failure (CHF), inducible NOS (iNOS) may be expressed in failing myocardium.Methods and Results-This study tested the hypothesis that NOS inhibition would increase M(V)over dotO(2) in the failing heart. CHF was produced in dogs by use of the rapid ventricular pacing model. In comparison with normal values, animals with CHF had reduced coronary blood flow and M(V)over dotO(2) at rest, with a blunted response to treadmill exercise. Selective iNOS inhibition with S-methylisothiourea (1.5 mg/kg IC) increased left ventricular systolic pressure and left ventricular dP/dt and caused an increase in M(V)over dotO(2) at rest and during exercise (P