Striated muscle tissue oxygenation and lactate levels during normo-, hyper- and hypocapnia. A study in the rabbit.

Abstract

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.