Thorborg P, Jorfeldt L, Löfström J B, Lund N
Department of Anesthesiology, University Hospital, Linköping, Sweden.
Microcirc Endothelium Lymphatics. 1988 Jun;4(3):205-29.
The relationship between striated muscle tissue oxygenation during hyper- and hypocapnia, and lactate levels and venous pO2 (pvO2) was studied in a rabbit model. Seven rabbits were ventilated with constant volume during ether anesthesia, and arterial pCO2 (paCO2) was varied by addition of CO2. Muscle tissue oxygenation was measured with a multichannel electrode on the striated muscle surface, the results presented as oxygen pressure distributions (OPD:s). The principal result during hypercapnia (paCO2 9.9 kPa) was a tendency toward increased mean oxygen pressure (ptxO2) of the OPD; OPD shape was normal in 5/7 runs. Arterial lactates (aLa) decreased. During duplicate hypocapnia to paCO2 2.9 and 2.8 kPa ptxO2 decreased, but only in 4/14 runs were tissue oxygen pressures (ptO2) below 0.6 kPa found. OPD shape was scattered in 6/14 runs indicating disturbance in regulation of tissue oxygenation (but without signs of hypoxia). An increase in aLa was found, as well as a decrease in arterio-venous lactate difference (avDLa). Lacking direct blood flow measurements, these two results could not be interpreted as increased lactate efflux per se. Muscle lactates (mLa) were high but, on average, not higher than a control group. A decrease in pvO2 was seen during hypocapnia. Subgrouping OPD:s according to shape and presence of low ptO2 values did, however, suggest that lactate was released in cases with low ptO2 values: a covariation was seen in runs with low oxygen pressures between high arterial and muscle lactates, decreased avDLa and pvO2; runs with scattered OPD:s had only intermediately high lactates and low avDLa and pvO2 when compared to normally shaped OPD:s. In this study, hypercapnia influenced striated muscle tissue oxygenation only to a minor degree while hypocapnia influenced it more but not as much as expected. Only when low oxygen pressures were present in the OPD:s were there indications of peripheral lactate release.
在兔模型中研究了高碳酸血症和低碳酸血症期间横纹肌组织氧合与乳酸水平及静脉血氧分压(pvO2)之间的关系。七只兔子在乙醚麻醉下进行定容通气,通过添加二氧化碳来改变动脉血二氧化碳分压(paCO2)。用多通道电极在横纹肌表面测量肌肉组织氧合,结果以氧分压分布(OPD)表示。高碳酸血症(paCO2 9.9 kPa)期间的主要结果是OPD的平均氧分压(ptxO2)有升高趋势;7次实验中有5次OPD形状正常。动脉血乳酸(aLa)降低。在重复的低碳酸血症至paCO2 2.9和2.8 kPa时,ptxO2降低,但14次实验中只有4次组织氧分压(ptO2)低于0.6 kPa。14次实验中有6次OPD形状分散,表明组织氧合调节受到干扰(但无缺氧迹象)。发现aLa增加,动静脉乳酸差值(avDLa)减小。由于缺乏直接的血流测量,这两个结果不能解释为乳酸流出本身增加。肌肉乳酸(mLa)较高,但平均而言不高于对照组。低碳酸血症期间可见pvO2降低。然而,根据形状和低ptO2值的存在对OPD进行亚组分析表明,在低ptO2值的情况下会释放乳酸:在低氧压的实验中,高动脉血和肌肉乳酸、降低的avDLa和pvO2之间存在协变;与正常形状的OPD相比,OPD形状分散的实验中乳酸仅为中等高度,avDLa和pvO2较低。在本研究中,高碳酸血症对横纹肌组织氧合的影响较小,而低碳酸血症对其影响更大,但不如预期。只有当OPD中存在低氧压时,才有外周乳酸释放的迹象。