Tønnessen T I, Kvarstein G
Department of Anaesthesiology, Rikshospitalet, Oslo, Norway.
Acta Anaesthesiol Scand. 1996 May;40(5):510-9. doi: 10.1111/j.1399-6576.1996.tb04481.x.
Under ischaemic (anaerobic) conditions there will be an accumulation of CO2 in the tissue secondary to a build up of protons that is buffered by HCO3. We reasoned that CO2 could be measured at the surface of the kidney by PCO2 electrodes to detect ischaemic conditions.
Anaesthetized, mechanically ventilated pigs (25-30 kg) were investigated. Two acute porcine models, one of haemorrhagic shock and one of renal artery stenosis were used. Renal blood flow was gradually decreased, either by successive episodes of bleeding through the arterial cannula or by successive snaring of the renal artery.
In both models we found that with decreased blood flow but maintained aerobic metabolism (supply independence) PCO2 both at the surface of the kidney and in the renal vein increased by 2-3 kPa. Thus, the tissue-venous PCO2 difference did not change much. At DO2crit, i.e., at the transition to supply-dependent O2 consumption, the tissue PCO2 started to increase rapidly, as did the tissue-venous PCO2 difference. This is compatible with the notion that a hallmark of ischaemia is decreased ability of the blood to transport away waste products because the contact between large parts of tissue and blood is virtually non-existent. In the renal artery stenosis model kidney surface PCO2 values rose from a baseline of 6.6 +/- 0.6 kPa (mean +/- SEM) to a value near DO2crit of 10.6 +/- 0.8 kPa, reaching a final value of 29.9 +/- 3.5 kPa at no flow. PCO2 in the renal vein, however, reached a maximum of only 8.2 +/- 0.6 kPa. Numbers very similar to these were also found in the haemorrhagic model. The urine production decreased before the onset of ischaemia. When surface PCO2 values increased sharply indicating ischaemia, the urine production was zero. Lactate production by the kidney correlated very well with increasing tissue PCO2 values further corroborating that anaerobic metabolism was detected with the electrodes.
We conclude that PCO2 electrodes placed at the surface of the kidney detect renal cortical ischaemia.
在缺血（无氧）条件下，由于质子积累并由HCO3缓冲，组织中会积聚二氧化碳。我们推测，可以通过PCO2电极在肾脏表面测量二氧化碳来检测缺血情况。
对麻醉状态下、机械通气的猪（25 - 30千克）进行研究。使用了两种急性猪模型，一种是失血性休克模型，另一种是肾动脉狭窄模型。通过动脉插管连续放血或连续结扎肾动脉，使肾血流量逐渐减少。
在两种模型中，我们发现随着血流量减少但有氧代谢维持（供应独立），肾脏表面和肾静脉中的PCO2均升高2 - 3千帕。因此，组织 - 静脉PCO2差值变化不大。在DO2crit时，即向供应依赖型氧消耗转变时，组织PCO2开始迅速升高，组织 - 静脉PCO2差值也如此。这与以下观点相符，即缺血的一个标志是血液运输废物的能力下降，因为大部分组织与血液之间几乎不存在接触。在肾动脉狭窄模型中，肾脏表面PCO2值从基线的6.6±0.6千帕（平均值±标准误）升至接近DO2crit时的10.6±0.8千帕，在无血流时达到最终值29.9±3.5千帕。然而，肾静脉中的PCO2最高仅达到8.
