Journal of applied physiology
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The amount of urea produced in 60 min, [urea]t = 60, from intact guinea pig hepatocytes incubated in NH4Cl, oleate, lactate, NaHCO3, and ornithine at 37 degrees C at pH 7.1 is decreased by ethoxzolamide (EZ): Ki,EZ [urea]t = 60 +/- SD at 37 degrees C, pH 7.1 is 0.14 +/- 0.11 mM (10 Dixon plots). This value is in the same range as Ki,EZ for carbonic anhydrase (CA) activity of disrupted hepatocytes at 37 degrees C: 0.08 +/- 0.06 mM (2). [Urea]t = 60 is pH dependent whether external CO2 is supplied (25 mM HCO-3, 95% O2-5% CO2 and 5 mM HCO-3, 99% O2-1% CO2) or not [20 mM N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES), 100% O2]. Ki,EZ [urea]t = 60 is independent of both external pH and external total CO2. ⋯ This value was approximately 3,000-fold lower than the Ki,EZ [urea]t = 60 for intact hepatocytes or Ki,EZ (CA) for disrupted hepatocytes. These results support the general hypothesis that mitochondrial CA is involved in urea synthesis by intact hepatocytes and that cytosolic components raise the experimentally determined Ki,EZ [urea]t = 60. We also conclude that the value of Ki,EZ [urea]t = 60 is independent of the availability of the substrate HCO-3 from external sources.
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Afterdrop, the continued fall of deep body temperatures during rewarming after hypothermia, is thought to endanger the heart by further cooling from cold blood presumed to be returning from the periphery. However, afterdrop is not always observed, depending on the circumstances. To explore this phenomenon, mild hypothermia was induced quantitatively with a suit calorimeter, using several patterns of cooling and rewarming. ⋯ Central layers continued to give up heat as long as the surrounding layer was cooler. These results, together with recent findings by others that peripheral blood flow is low until afterdrop is complete, make this circulatory explanation of afterdrop improbable. Alternatively, afterdrop can be explained by the way heat moves through a mass of tissue.