Hobbhahn J, Conzen P F, Goetz A, Seidl G, Gonschior P, Brendel W, Peter K
Institute of Anaesthesiology, University of Munich, FRG.
Cardiovasc Res. 1989 Jun;23(6):529-40. doi: 10.1093/cvr/23.6.529.
The validity of myocardial surface tissue PO2 (PtO2) as a reliable indicator of transmural myocardial tissue oxygenation was studied in six anaesthetised, open chest pigs. Epicardial surface PtO2 was correlated with other variables of myocardial tissue oxygenation such as regional blood flow, coronary venous PO2, O2 saturation, PCO2 and regional myocardial lactate extraction. The study design was based on an experimental model in which the effects of a pacing induced tachycardia on tissue oxygenation of ischaemic and normally supplied myocardium were measured. Two platinum multiwire surface electrodes were placed on the epicardium, on the areas supplied by the left anterior descending coronary artery (LAD) and the left circumflex coronary artery (CX). The LAD was constricted to reduce mean surface PtO2 in the LAD area to about 50% of its baseline value. This did not affect surface PtO2 in the CX area. The reduction of surface PtO2 in the LAD area was associated with decreases in coronary venous PO2 and O2 saturation and with increases in coronary venous lactate and PCO2. Subendocardial regional blood flow and the subendocardial to subepicardial flow ratio were significantly lower than in the CX area. Increasing the heart rate by pacing (+45 beats.min-1) led to an increased degree of ischaemia as shown by fall in surface PtO2 in the LAD area to values around zero kPa, by marked increase in coronary venous lactate and PCO2, by reduction in total (-10%) and subendocardial (-40%) LAD flow and by deterioration of the subendocardial to subepicardial flow ratio. The increased degree of ischaemia was not accompanied by an increase in O2 extraction. The marked decrease in surface PtO2 occurred in spite of a slight increase in the subepicardial regional blood flow (+10%); thus the increase in O2 delivery was not sufficient to meet the increase in O2 demand. Total flow was increased by 27% in the CX area without changes in the subendocardial to subepicardial flow ratio and in the surface PtO2 values. When pacing was stopped, surface values of PtO2 in the LAD area returned to prepacing values, as did lactate extraction and coronary venous PCO2. Clear and close relationships with surface PtO2 were found for regional lactate extraction, coronary venous PCO2 and the normalised subendocardial RBF. Poor or no correlations were found for the normalised subepicardial regional blood flow, the coronary venous O2 saturation and the absolute values of subendocardial and subepicardial regional blood flow.(ABSTRACT TRUNCATED AT 400 WORDS)
在六只麻醉开胸猪身上研究了心肌表面组织氧分压(PtO2)作为透壁心肌组织氧合可靠指标的有效性。心外膜表面PtO2与心肌组织氧合的其他变量相关,如局部血流、冠状静脉氧分压、血氧饱和度、二氧化碳分压和局部心肌乳酸摄取。该研究设计基于一个实验模型,在该模型中测量了起搏诱导的心动过速对缺血和正常供血心肌组织氧合的影响。将两个铂多丝表面电极置于心外膜上,位于左前降支冠状动脉(LAD)和左旋支冠状动脉(CX)供血区域。对LAD进行缩窄,使LAD区域的平均表面PtO2降至其基线值的约50%。这并未影响CX区域的表面PtO2。LAD区域表面PtO2的降低与冠状静脉氧分压和血氧饱和度的降低以及冠状静脉乳酸和二氧化碳分压的升高相关。心内膜下局部血流以及心内膜下与心外膜下血流比值显著低于CX区域。通过起搏使心率增加(+45次/分钟)导致缺血程度加重,表现为LAD区域表面PtO2降至约零kPa,冠状静脉乳酸和二氧化碳分压显著升高,LAD总血流(-10%)和心内膜下血流(-40%)减少,以及心内膜下与心外膜下血流比值恶化。缺血程度的增加并未伴随着氧摄取的增加。尽管心外膜下局部血流略有增加(+10%),但表面PtO2仍显著降低;因此,氧输送的增加不足以满足氧需求的增加。CX区域总血流增加27%,心内膜下与心外膜下血流比值及表面PtO2值无变化。当停止起搏时,LAD区域的PtO2表面值、乳酸摄取及冠状静脉二氧化碳分压恢复到起搏前的值。发现局部乳酸摄取、冠状静脉二氧化碳分压和标准化心内膜下RBF与表面PtO2有明确且密切的关系。对于标准化心外膜下局部血流、冠状静脉血氧饱和度以及心内膜下和心外膜下局部血流的绝对值,相关性较差或无相关性。(摘要截取自400字)