Kedem J, Furman E, Acad B, Sonn J, Dvir S
Arch Int Physiol Biochim. 1986 Sep;94(3):197-204. doi: 10.3109/13813458609071419.
In anaesthetized open-chest dogs, regional contractile force, epicardial tissue blood flow, and local NADH redox levels were recorded during graded ventricular pacing in the range 150-285 bpm. These parameters were measured before, and 30 min following LAD coronary artery occlusion. It was found that during pacing, blood supply to the untreated ischaemic region was reduced by 65.4 +/- 11% of control values at a rate of 150 bpm, and fell to -105 +/- 40.2% at a rate of 225 bpm. Hypopneic respiration prevented this pacing induced flow reduction. Pacing in the presence of nitroglycerin resulted in a marked increase in regional flow. Similarly, the vasodilator treatments prevented the marked elevation in NADH levels (77.5 +/- 15.6%) produced by pacing in the untreated ischaemic myocardium. The reduction in regional contractile force in the ischaemic region produced following pacing (-30.5%) was reversed during both vasodilator treatments (+47.2% during nitroglycerin and +23.4% during hypopnea). It was concluded that vasodilation improves regional ischaemic myocardial oxygen balance, thus expanding the functional reserve of the ischaemic muscle. Nitroglycerin is more active.
在麻醉开胸犬中,于150 - 285次/分钟范围内进行分级心室起搏时,记录局部收缩力、心外膜组织血流及局部NADH氧化还原水平。这些参数在左前降支冠状动脉闭塞前及闭塞后30分钟进行测量。结果发现,起搏期间,未处理的缺血区域的血液供应在起搏频率为150次/分钟时较对照值减少65.4±11%,在起搏频率为225次/分钟时降至 - 105±40.2%。低通气呼吸可防止这种起搏诱导的血流减少。在硝酸甘油存在下起搏会导致局部血流显著增加。同样,血管扩张剂治疗可防止未处理的缺血心肌起搏所产生的NADH水平显著升高(77.5±15.6%)。起搏后缺血区域局部收缩力的降低(-30.5%)在两种血管扩张剂治疗期间均得到逆转(硝酸甘油治疗期间为+47.2%,低通气期间为+23.4%)。得出的结论是,血管舒张可改善局部缺血心肌的氧平衡,从而扩大缺血心肌的功能储备。硝酸甘油的作用更强。