Paulus W J, Grossman W, Serizawa T, Bourdillon P D, Pasipoularides A, Mirsky I
Am J Physiol. 1985 May;248(5 Pt 2):H719-28. doi: 10.1152/ajpheart.1985.248.5.H719.
Acute increases in left ventricular (LV) diastolic pressure relative to volume occur during angina in humans and after pacing tachycardia in dogs with coronary stenoses. In this study we assessed myocardial function following pacing tachycardia in dogs with coronary stenoses and compared it with function of the same myocardial segment during coronary occlusion. Also we calculated regional wall stiffness following pacing tachycardia in dogs with coronary stenoses. In anesthetized dogs with two-vessel critical (90%) coronary stenoses, ultrasonic crystals were implanted subendocardially to measure either anterior wall (AW) and lateral wall (LW) segment lengths (SL; n = 14) or LV wall thickness (h; n = 7). LV pressure was measured using a high-fidelity micromanometer catheter. After pacing tachycardia in dogs with two-vessel coronary stenoses, there was a substantial rise in LV end-diastolic pressure (from 6 +/- 1 to 15 +/- 1 mmHg; P less than 0.001), a slight increase in end-diastolic segment length (AWEDSL from 15.6 +/- 1.0 to 16.4 +/- 1.0 mm; p less than 0.01; and LWEDSL from 13.8 +/- 1.4 to 14.3 +/- 1.4 mm; P greater than 0.01) and a reduction of percent systolic shortening of the ischemic segments. An upward shift of the diastolic pressure-SL relation was observed in the postpacing period. During coronary occlusion the diastolic pressure-SL relation of the same segment shifted rightward, or rightward and downward, and systolic shortening became holosystolic bulging. Ischemia due to coronary stenoses plus increased O2 demand had substantially different effects on regional wall motion and segmental diastolic mechanics than did ischemia due to coronary occlusion. Over the same range of residual transmural LV diastolic pressure, the radial stiffness modulus was higher after pacing tachycardia in the presence of coronary stenoses.
在人类心绞痛发作期间以及患有冠状动脉狭窄的犬类进行起搏性心动过速后,左心室(LV)舒张期压力相对于容积会急性升高。在本研究中,我们评估了患有冠状动脉狭窄的犬类在起搏性心动过速后的心肌功能,并将其与同一心肌节段在冠状动脉闭塞期间的功能进行了比较。此外,我们还计算了患有冠状动脉狭窄的犬类在起搏性心动过速后的局部心肌壁硬度。在患有双支冠状动脉严重(90%)狭窄的麻醉犬中,将超声晶体心内膜下植入,以测量前壁(AW)和侧壁(LW)节段长度(SL;n = 14)或左心室壁厚度(h;n = 7)。使用高保真微压计导管测量左心室压力。在患有双支冠状动脉狭窄的犬类进行起搏性心动过速后,左心室舒张末期压力大幅升高(从6±1 mmHg升至15±1 mmHg;P<0.001),舒张末期节段长度略有增加(前壁舒张末期节段长度从15.6±1.0 mm增至16.4±1.0 mm;p<0.01;侧壁舒张末期节段长度从13.8±1.4 mm增至14.3±1.4 mm;P>0.01),缺血节段的收缩期缩短百分比降低。在起搏后阶段观察到舒张期压力 - SL关系向上移位。在冠状动脉闭塞期间,同一节段的舒张期压力 - SL关系向右移位,或向右和向下移位,并且收缩期缩短变为全收缩期膨出。冠状动脉狭窄加上氧气需求增加所导致的缺血对局部心肌壁运动和节段舒张力学的影响与冠状动脉闭塞所导致的缺血有很大不同。在相同范围的左心室跨壁舒张期残余压力下,在存在冠状动脉狭窄的情况下,起搏性心动过速后的径向硬度模量更高。