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Open in a separate window aMean values of the same parameter were compared. Both paired and unpaired comparisons were made for serum and plasma potassium. The mean serum potassium for the CO2 group was not significantly different from the mean plasma potassium for the same group.
Similarly, a significant difference between mean plasma and serum potassium values was not observed for the KX group. The mean of the differences between serum and plasma potassium levels within individual mice was not significantly different from 0 in the 6 subjects in CO2 group —0.
In addition other variables tested, including site of collection, delivery method, use of serum separators, time allowed for clot formation before serum separation, and time elapsed between collection and analysis of samples collected in serum separator tubes, lacked significant effects on serum potassium concentration.
Discussion Despite the well-known physiologic effects of hyperkalemia, disagreement exists regarding the normal reference interval for serum potassium in mice. Serum potassium levels of 6. The normal reference range for mouse serum potassium 3.
By use of unspecified sampling techniques, other investigators 32 found the reference range of serum potassium in mice to be 5. Mice that underwent CO2 inhalation in our study developed hypercapnia with pCO2 concentrations as high as mmHg, acidemia with pH as low as 6.
In contrast, animals managed with the same experimental controls but given KX anesthesia instead of CO2 revealed physiologically acceptable blood potassium levels that were significantly different from those of the CO2 group.
Compared with those of the CO2 group, the slight elevation in pCO2 and correspondingly modest decrease in blood pH of the KX group indicated milder changes in these mice's acid—base balance and may indicate both respiratory and cardiovascular depression due to the anesthetic cocktail.
Lactate is a common byproduct of cellular anaerobic metabolism. The blood lactate levels for both our CO2 and KX groups exceeded published reference ranges. In a study on CO2-euthanized swine, hypoxia-induced anaerobic metabolism led to increased lactic acid production.
This discrepancy may reflect that circulating lactate concentrations are more dependent on delivery, uptake, and utilization of oxygen in tissues than on the presence of decreased systemic pO2 levels. Similar changes in blood lactate have been reported in veterinary patients stressed during venapuncture.
The presence of this organic acid is unlikely to have contributed to the hyperkalemia, however. Rather, hyperlactatemia serves to indicate underlying tissue hypoxia, a process that may well have contributed to the increase in serum potassium levels.
CO2 is a potent vasodilator in many tissues and, in high concentrations, has been documented to disrupt normal autonomic vascular tone. We hypothesize that compared with the KX mice, the CO2 group sustained more tissue hypoxia because of severe CO2-induced vasodilation, leading to poor tissue perfusion.
We did not measure the mice's blood pressure during CO2 administration, but doing so might help delineate the mechanisms behind the observations we have described.
A second possibility is that the hyperkalemia seen in the CO2-treated mice may be secondary to the severe acute respiratory acidosis observed in this group.
Respiratory acidosis is defined as an increase in pCO2 generally greater than 45 mm Hg and, in the clinical setting, typically is due to alveolar hypoventilation.
In veterinary and human patients, respiratory acidosis has been associated with inhibition or dysfunction of medullary respiratory centers or respiratory muscles, upper airway obstruction, and impaired gas exchange. Although our mice had no predisposing diseases that would have impaired the normal excretion of CO2, the rapid increase in pCO2 hypercapnia was principally due to CO2 administration.PRS provides wide-ranging proofreading & editing services for the authors of academic & scientific papers for publication & examination in all study fields.
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