Duncker D J, Stubenitsky R, Verdouw P D
Experimental Cardiology, Thoraxcenter, Cardiovascular Research Institute COEUR, Erasmus University Rotterdam, The Netherlands.
Circ Res. 1998 Jun 29;82(12):1312-22. doi: 10.1161/01.res.82.12.1312.
To date, no studies have investigated coronary vasomotor control of myocardial O2 delivery (MDO2) and its modulation by the autonomic nervous system in the porcine heart during treadmill exercise. We studied 8 chronically instrumented swine under resting conditions and during graded treadmill exercise. Exercise up to 85% to 90% of maximum heart rate produced an increase in myocardial O2 consumption (MVO2) from 163+/-16 micromol/min (mean+/-SE) at rest to 423+/-75 micromol/min (P< or =0.05), which was paralleled by an increase in MDO2, so that myocardial O2 extraction (79+/-1% at rest) and coronary venous O2 tension (cvPO2, 23.7+/-1.0 mm Hg at rest) were maintained. Beta-adrenoceptor blockade blunted the exercise-induced increase of MDO2 out of proportion compared with the attenuation of the exercise-induced increase in MVO2, so that O2 extraction rose from 78+/-1% at rest to 83+/-1% during exercise and cvPO2 fell from 23.5+/-0.9 to 19.6+/-1.1 mm Hg (both P< or =0.05). In contrast, alpha-adrenoceptor blockade, either in the absence or presence of beta-adrenoceptor blockade, had no effect on myocardial O2 extraction or cvPO2 at rest or during exercise. Muscarinic receptor blockade resulted in a decreased O2 extraction and an increase in cvPO2 at rest, an effect that waned during exercise. The vasodilation produced by muscarinic receptor blockade was likely due to an increased beta-adrenoceptor activity, since combined muscarinic and beta-adrenoceptor blockade produced similar changes in O2 extraction and cvPO2, as did beta-adrenoceptor blockade alone. In conclusion, in swine myocardium, MVO2 and MDO2 are matched during exercise, which is the result of feed-forward beta-adrenergic vasodilation in conjunction with minimal a-adrenergic vasoconstriction. Beta-adrenergic vasodilation is due to an increase in sympathetic activity but may also be supported by withdrawal of muscarinic receptor-mediated inhibition of beta-adrenergic coronary vasodilation. The observation that cvPO2 levels are maintained even during heavy exercise suggests that a decrease in cvPO2 is not essential for coronary vasodilation during exercise.
迄今为止，尚无研究探讨跑步机运动期间猪心脏中心肌氧输送（MDO2）的冠状动脉血管舒缩控制及其受自主神经系统的调节。我们研究了8只长期植入仪器的猪，分别在静息状态和分级跑步机运动期间进行观察。运动至最大心率的85%至90%时，心肌氧消耗（MVO2）从静息时的163±16微摩尔/分钟（平均值±标准误）增加到423±75微摩尔/分钟（P≤0.05），同时MDO2也增加，从而使心肌氧摄取（静息时为79±1%）和冠状静脉氧张力（cvPO2，静息时为23.7±1.0毫米汞柱）得以维持。β-肾上腺素能受体阻断使运动诱导的MDO2增加减弱，与运动诱导的MVO2增加减弱相比不成比例，结果氧摄取从静息时的78±1%升至运动时的83±1%，cvPO2从23.5±0.9降至19.6±1.1毫米汞柱（均P≤0.05）。相反，无论是否存在β-肾上腺素能受体阻断，α-肾上腺素能受体阻断对静息或运动时的心肌氧摄取或cvPO2均无影响。毒蕈碱受体阻断导致静息时氧摄取减少和cvPO2增加，此效应在运动期间减弱。毒蕈碱受体阻断产生的血管舒张可能是由于β-肾上腺素能受体活性增加，因为毒蕈碱和β-肾上腺素能受体联合阻断产生的氧摄取和cvPO2变化与单独β-肾上腺素能受体阻断相似。总之，在猪心肌中，运动期间MVO2和MDO2相匹配，这是前馈性β-肾上腺素能血管舒张与最小程度的α-肾上腺素能血管收缩共同作用的结果。β-肾上腺素能血管舒张是交感神经活性增加所致，但也可能因毒蕈碱受体介导的对β-肾上腺素能冠状动脉舒张的抑制作用减弱而得到支持。cvPO2水平即使在剧烈运动期间也能维持这一观察结果表明，cvPO2降低并非运动期间冠状动脉血管舒张所必需。
