O'Riordan J B, Flaherty J T, Khuri S F, Brawley R K, Pitt B, Gott V L
Am J Physiol. 1977 Jan;232(1):H49-53. doi: 10.1152/ajpheart.1977.232.1.H49.
Changes in myocardial carbon dioxide (PmCO2) and oxygen tension (PmO2) measured by mass spectrometry have been shown to reflect quantitatively progressive degrees of regional myocardial ischemia associated with stepwise reduction in coronary blood flow. The present study utilized mass spectrometry to assess the severity of regional myocardial ischemia developing during atrial pacing in the presence of a flow-limiting proximal critical coronary artend subendocardial layers was measured by the radioactive microsphere technique. Application of a "critical stenosis" resulted in a 6-mmHg decrease in PmO2 and a 17-mmHg increase in PmCO2 in the region of the myocardium supplied by the stenosed vessel. The addition of atrial pacing resulted in a 3-mmHg further decrease in Pmo2 and a 40-mmHg further increase in PmCO2. In the region of myocardium supplied by the critically stenosed vessel MBF increased in the subepicardial layer, but decreased or remained unchanged in the subendocardial layer. The failure of myocardial blood flow to increase in deeper myocardial layers in response to the increased myocardial oxygen demand of atrial pacing would provide a mechanism for the development of subendocardial ischemia in the presence of a critical coronary stenosis.
通过质谱法测量的心肌二氧化碳（PmCO2）和氧分压（PmO2）的变化已被证明能定量反映与冠状动脉血流逐步减少相关的局部心肌缺血的进展程度。本研究利用质谱法评估在心房起搏期间出现的局部心肌缺血的严重程度，此时存在近端临界冠状动脉狭窄，通过放射性微球技术测量心内膜下各层的心肌血流。施加“临界狭窄”导致狭窄血管供血区域的心肌中PmO2降低6mmHg，PmCO2升高17mmHg。心房起搏的加入导致Pmo2进一步降低3mmHg，PmCO2进一步升高40mmHg。在临界狭窄血管供血的心肌区域，心外膜下层的心肌血流量增加，但心内膜下层的心肌血流量减少或保持不变。在存在临界冠状动脉狭窄的情况下，心肌深层对心房起搏增加的心肌需氧量未能增加心肌血流量，这将为心内膜下缺血的发生提供一种机制。
