The present study was a prospective, nonrandomized, observational examination of the relationship among hypoproteinemia and electrolyte and acid-base status in a critical care population of patients. A total of 219 arterial blood samples reviewed from 91 patients was analyzed for arterial blood gas, electrolytes, lactate, and total protein. Plasma strong-ion difference ([SID]) was calculated from [Na+] + [K+] - [Cl-] - [La-]. Total protein concentration was used to derive the total concentration of weak acid ([A]tot). [A]tot encompassed a range of 18.7 to 9.0 meq/l, whereas [SID] varied from 48.1 to 26.6 meq/l and was directly correlated with [A]tot. The decline in [SID] was primarily attributable to an increase in [Cl-]. A direct correlation was also noted between PCO2 and [SID], but not between PCO2 and [A]tot. The decrease in [SID] and PCO2 was such that neither [H+] nor [HCO-3] changed significantly with [A]tot.

Nuclear and polysomal polyadenylated RNA populations of normal and 16 hour regenerating rat liver have been compared by mRNA-cDNA hybridisations and by unique DNA saturation experiments. It was found that nuclear polyadenylated RNA hybridises to 6.8% of unique DNA in both normal and 16 hour regenerating rat liver. However, cross-hybridisation experiments using cDNA have shown that 10-15% by weight of nuclear polyadenylated RNA sequences are specific to 16 hour regenerating rat-liver. Since both unique DNA and cDNA hybridisation have shown that normal and 16 hour regenerating rat-liver polysomal polyadenylated RNA populations are qualitatively very similar sequences specific to 16 hour regenerating rat-liver nuclear polyadenylated RNA are nucleus confined. Polysomal RNA sequences which were abundant in normal rat-liver have become less abundant in regenerating rat liver.

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Adult rainbow trout, acclimated to external calcium concentrations ranging from 60–5700 μequiv/1, were exposed to pH 4.0-4.1 for 44 h. Initially, this exposure provoked massive net losses of sodium and chloride across the gills which arose through a combination of an inhibition of active transport and, more importantly, a stimulation in diffusional efflux. Subsequently, ion losses declined substantially, largely due to a rapid decline in passive efflux but also to a slower, partial recovery in sodium transport. External calcium concentration was virtually without effect on ion fluxes either prior to or following acid exposure but had a definite effect during acid exposure. This effect was initially upon the ratio of C1− to Na+ loss and later upon the degree of inhibition of sodium and chloride transport. Possible mechanisms to explain the complex interactions of calcium and pH are proposed.

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