猪心肌缺血期间冠状动脉血管舒张不完全。
Incomplete coronary vasodilation during myocardial ischemia in swine.
作者信息
Pantely G A, Bristow J D, Swenson L J, Ladley H D, Johnson W B, Anselone C G
出版信息
Am J Physiol. 1985 Sep;249(3 Pt 2):H638-47. doi: 10.1152/ajpheart.1985.249.3.H638.
To determine if endogenous (ENDG) vasodilation was maximum during myocardial ischemia, left anterior descending (LAD) mean pressure (P) was reduced for 20 min in 13 swine. At LAD P of 45 mmHg (LAD P45) flow fell during ENDG = 25 but rose to 44 ml/min during adenosine (AD) infusion (P less than 0.01). Flow increased to subendocardium (ENDG 0.65 vs. AD 1.04 ml X min-1 X g-1) and to subepicardium (ENDG 0.99 vs. AD 1.83 ml X min-1 X g-1; P less than 0.05). No significant change occurred in myocardial O2 consumption (MVO2; ENDG 2.91 vs. AD 3.18 ml X min-1 X g-1), lactate extraction (ENDG = -5 vs. AD-1%), and wall thickening (WTh; ENDG + 16 vs. AD + 17%). At LAD P35, flow during ENDG was 12 but rose to 19 ml/min during AD (P less than 0.01). Flow increased to subendocardium (ENDG 0.24 vs. AD 0.46 ml X min-1 X g-1; P less than 0.02) and subepicardium (ENDG 0.51 vs. AD 0.87 ml X min-1 X g-1; P less than 0.01). No significant change occurred in MVo2 (ENDG 1.38 vs. AD 1.59 ml/min), lactate extraction (ENDG -38 vs. AD -22%), WTh (ENDG -1 vs. AD + 1%). Thus endogenous vasodilation reserve was not used fully during ischemia. AD increased flow but did not improve abnormalities in myocardial function or metabolism.
为确定内源性（ENDG）血管舒张在心肌缺血期间是否达到最大程度，对13头猪的左前降支（LAD）平均压力（P）降低20分钟。在LAD压力为45 mmHg（LAD P45）时，内源性血管舒张期间血流量下降至25，但在腺苷（AD）输注期间升至44 ml/分钟（P<0.01）。血流量增加至心内膜下（内源性血管舒张时为0.65 vs. 腺苷时为1.04 ml·min⁻¹·g⁻¹）和心外膜下（内源性血管舒张时为0.99 vs. 腺苷时为1.83 ml·min⁻¹·g⁻¹；P<0.05）。心肌氧耗（MVO2；内源性血管舒张时为2.91 vs. 腺苷时为3.18 ml·min⁻¹·g⁻¹）、乳酸摄取（内源性血管舒张时为-5 vs. 腺苷时为-1%）和室壁增厚（WTh；内源性血管舒张时为+16 vs. 腺苷时为+17%）均无显著变化。在LAD P35时，内源性血管舒张期间血流量为12，但在腺苷输注期间升至19 ml/分钟（P<0.01）。血流量增加至心内膜下（内源性血管舒张时为0.24 vs. 腺苷时为0.46 ml·min⁻¹·g⁻¹；P<0.02）和心外膜下（内源性血管舒张时为0.51 vs. 腺苷时为0.87 ml·min⁻¹·g⁻¹；P<0.01）。MVo2（内源性血管舒张时为1.38 vs. 腺苷时为1.59 ml/分钟）、乳酸摄取（内源性血管舒张时为-38 vs. 腺苷时为-22%）、WTh（内源性血管舒张时为-1 vs. 腺苷时为+1%）均无显著变化。因此，缺血期间内源性血管舒张储备未被充分利用。腺苷增加了血流量，但未改善心肌功能或代谢异常。
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