DIASTOLIC-SYSTOLIC CORONARY FLOW DIFFERENCES ARE CAUSED BY INTRAMYOCARDIAL PUMP ACTION IN THE ANESTHETIZED DOG

DIASTOLIC-SYSTOLIC CORONARY FLOW DIFFERENCES ARE CAUSED BY INTRAMYOCARDIAL PUMP ACTION IN THE ANESTHETIZED DOG
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DOI:
10.1161/01.res.49.3.584
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发表时间:
1981-01-01
影响因子:
20.1
通讯作者:
LAIRD, JD
LAIRD, JD
中科院分区:
医学1区
文献类型:
--
作者:
SPAAN, JAE;BREULS, NPW;LAIRD, JD

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心脏收缩对冠状动脉血流的影响已通过心肌内泵来描述,该泵分别在收缩期和舒张期期间向后和向前移动血液。通常,平均前向流量超过并因此掩盖了该回流。 6 只麻醉的开胸犬的左冠状动脉主动脉通过包含可调节狭窄的灌注线,用恒压源的 Gregg 插管进行灌注。在平均左主动脉压力.hivin.Plc为65、90、125和155mm Hg时,通过不同程度的狭窄对心脏进行灌注,同时维持狭窄远端恒定的平均灌注压(.hivin.Plc)。平均冠状动脉流量与狭窄程度无关。随着狭窄程度的增加,冠状动脉收缩期与舒张期的流量差减小,而冠状动脉舒张期与收缩期的压力差增大。通过在恒定hivin.Plc下改变狭窄等级,获得舒张压-收缩压差和流量差之间的线性关系,并且将其解释为电模拟电位源当量的结果。根据电位源当量,可以确定心肌内泵 pim 的舒张-收缩压变化以及阻碍 pim 引起的血流变化的冠状动脉阻力 Ra。 pim 为 53.1 .+-。 7.02 (SD) mm Hg,并且独立于.hivin.Plc。 Ra与冠状动脉血流阻力Rc相关,Ra=0.63×。 Rc - 12.9 毫米汞柱.cntdot。 s/ml(r = 0.939,n = 25)。 Rc被定义为(.hivin.Plc-14mmHg)/平均冠状动脉流量。瀑布模型扩展为允许自动调节以实现心肌上平均流量的均分,但无法解释这些结果。根据夹紧灌注线后冠状动脉压力的衰减曲线,心肌内冠状动脉容量估计约为每 100 g LV [左心室] 0.07 ml/mm Hg。该值与公布的心肌内血液室的体积压力关系一致。阶段性冠状动脉血流成分需要心肌内动脉容量。冠状动脉血流的收缩期-舒张期变化不是由于阻力变化引起的,而是由活跃的心肌内泵引起的。
The effect of cardiac contraction on coronary arterial flow has been described in terms of an intramyocardial pump, which displaces blood backward and forward during systole and diastole, respectively. Normally, the mean forward flow exceeds, and consequently conceals, this backflow. The main left coronary artery of 6 anesthetized open-chest dogs was perfused with a Gregg cannula from a constant pressure source via a perfusion line containing an adjustable stenosis. At mean left main arterial pressures, .hivin.Plc of 65, 90, 125 and 155 mm Hg, the hearts were perfused via different grades of stenosis, while a constant mean perfusion pressure (.hivin.Plc) distal to the stenosis was maintained. Mean coronary flow was then independent of stenosis grade. With increasing stenosis grade, the systolic-diastolic coronary flow difference decreased, while the diastolic-systolic coronary pressure difference increased. By varying the stenosis grade at constant .hivin.Plc, linear relationships between diastolic-systolic pressure difference and flow difference were obtained and were interpreted as being a result of an electrical analog potential-source equivalent. From the potential-source equivalent, the diastolic-systolic pressure changes of the intramyocardial pump, pim, can be determined as well as the coronary resistance, Ra, impeding the flow variations originated by pim. pim was 53.1 .+-. 7.02 (SD) mm Hg, and was independent of .hivin.Plc. Ra was correlated with the resistance to coronary flow, Rc, via Ra = 0.63 .times. Rc - 12.9 mm Hg .cntdot. s/ml (r = 0.939, n = 25). Rc was defined as (.hivin.Plc - 14 mm Hg)/mean coronary flow. The waterfall model extended to allow for autoregulation to achieve an equal division of mean flow over the myocardium could not explain these results. From a decay curve of coronary arterial pressure following clamping of the perfusion line, intramyocardial coronary capacitance was estimated to be approximately 0.07 ml/mm Hg per 100 g LV [left ventricle]. This value is in agreement with published volume pressure relationships of the intramyocardial blood compartment. The phasic coronary blood flow component requires intramyocardial arterial volume. Systolic-diastolic variations in coronary blood flow are not due to varying resistances but are caused by an active intramyocardial pump.