McFalls E O, Duncker D J, Sassen L M, Krams R, Man in't Veld A J, Ruffolo R R, Verdouw P D
Experimental Cardiology, Thoraxcenter, Erasmus University Rotterdam, The Netherlands.
J Hum Hypertens. 1993 Feb;7 Suppl 1:S29-36.
Coronary flow reserve has been shown to be abnormally low in several models of left ventricular hypertrophy induced by long-standing pressure overload. Because the presence of hypertrophy is a risk factor for the development of subendocardial ischaemia and sudden death, efforts to restore alterations in flow reserve may prove beneficial. In the following review, we discuss potential mechanisms which might contribute to this abnormal vasodilator capacity in the hypertrophied heart, with particular emphasis on how chronic therapy may potentially reverse such abnormalities. In addition, we report how the acute administration of various classes of pharmacological agents can alter measurements of coronary flow reserve, as observed in our anaesthetised swine model. Such factors must be considered before interpreting any changes in coronary flow reserve in models of hypertrophy following chronic administration of drugs.
在几种由长期压力超负荷诱导的左心室肥厚模型中,冠状动脉血流储备已被证明异常低。由于肥厚的存在是心内膜下缺血和猝死发生的危险因素,恢复血流储备改变的努力可能被证明是有益的。在以下综述中,我们讨论了可能导致肥厚心脏这种异常血管舒张能力的潜在机制,特别强调了长期治疗如何可能逆转这种异常。此外,我们报告了在我们的麻醉猪模型中观察到的,各类药理药物的急性给药如何改变冠状动脉血流储备的测量。在解释长期给药后肥厚模型中冠状动脉血流储备的任何变化之前,必须考虑这些因素。