Ferrocyanide ingestion may cause false positives in cyanide determination.

CASE REPORT: The authors present a patient who ingested a cyanide containing solution and arrived at the hospital without any clinical evidence of intoxication but an elevated blood cyanide level. The authors explain this discrepancy with the following hypotheses: 1) the patient ingested cyanide as an iron-chelated complex; and 2) the sulfuric acid used in the standard microdiffusion technique released cyanide from its iron-bound state to result in the observed elevated blood cyanide. Through a series of in vitro analyses, the authors demonstrate the following: 1) the ingested solution tested positive for cyanide with the sulfuric acid technique and negative for cyanide with acetic acid; 2) the presence of a ferrous salt in the ingested product by a colorimetric redox titration technique; and 3) release of a small fraction of the total cyanide from ferrocyanide by the sulfuric acid technique. The authors conclude: 1) the patient ingested potassium ferrocyanide; and 2) the strong acid used in the cyanide microdiffusion assay will liberate cyanide that is chelated to iron to yield false positive results.

Influence of high-dose methotrexate on the distribution of body fluid volumes in the dog.

We studied the influence of high-dose methotrexate (HDMTX) on body fluid volumes in the dog, using indicator dilution techniques. In six healthy mongrel dogs total body water volume (TBW), extracellular water volume (ECW), body mass, and plasma osmolality were measured before and after infusion of both saline and HDMTX. TBW and ECW were determined simultaneously, using a double-indicator (D2O/ferrocyanide), single injection technique. In vitro experiments confirmed the reliability of ferrocyanide as an indicator for ECW, also in the presence of methotrexate. Results showed an increase in ECW after HDMTX (P = 0.029, paired Student's t-test), while TBW remained constant. Infusion of the same volume of isotonic saline in the control experiments did not result in any demonstrable change in either TBW or ECW. Therefore, infusion of HDMTX appears to cause a water shift from the intracellular to the extracellular compartment. Such a change in body water volumes may have implications for estimates of body composition and for pharmacokinetic studies in cancer patients receiving HDMTX.

Restoration and maintenance of glomerular filtration by mannitol during hypoperfusion of the kidney.

Glomerular filtration (GF) during progressive reduction of renal perfusion pressure by aortic clamping was studied in hydropenic rats and in rats infused with isotonic saline, hypertonic saline, or mannitol. As judged by visual observation of Lissamine green movements in superficial nephrons. GF was absent in hydropenic or saline-loaded rats at 40 mm Hg aortic pressure, but continued in some nephrons of all rats infused with mannitol and of some rats infused with hypertonic saline. Urine flow persisted only in rats infused with mannitol. By use of the qualitative Hanssen technique, it was found that all glomeruli in superficial and deep portions of the cortex were perfused at 40 mm Hg in all groups of rats. By the same method. GF continued in 1% of nephrons in hydropenic rats, 12% of nephrons in isotonic saline-loaded rats, and 78% of nephrons in rats infused with mannitol. By means of a quantitative Hanssen technique, GF was 5.8 nl/min per nephron in mannitol-infused rats and not measurable (< 0.5 nl) in hydropenic rats. Superficial and deep nephrons were similar in both qualitative and quantitative studies. Although urine flow did not persist in rats infused with hypertonic saline, GF was detected in four of seven studies by the Hanssen method (mean, 9.1 nl/min per nephron). In additional experiments, mannitol infused after perfusion pressure had already been lowered to 40 mm Hg in hydropenic rats reestablished urine flow and GF (mean, 9.8 nl/min). Furosemide, isotonic and hypertonic saline did not restart urine flow; however, GF (Lissamine green) was restarted by hypertonic saline. We conclude that mannitol can maintain or reestablish by an extratubular mechanism GF which otherwise would not occur during renal hypoperfusion. Hypertonic saline has a similar effect on GF in some cases, but urine flow is not maintained, implying complete reabsorption of filtrate.