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R S Abrams

Publications and source records attributed to R S Abrams.

26 records · Page 2Linked to original sources
PubMed1981

Nitrous oxide has multiple deleterious effects on cobalamin metabolism and causes decreases in activities of both mammalian cobalamin-dependent enzymes in rats.

In man, use of the general anesthetic nitrous oxide, N2O, is associated with hematologic and neurologic abnormalities that mimic those seen in cobalamin (Cbl, vitamin B12) deficiency. We have measured a number of aspects of Cbl metabolism in rts exposed to various concentrations of N2O for various periods of time. As little as 2% N2O given for 15 h resulted in 30% inhibition of methionine synthetase (MS) in rat liver. With 50% N2O, inhibition of 70% occurred with 1 h and did not change during the next 48 h. Under these conditions, no inhibition of methylmalonyl-CoA mutase (MMCoAM) was observed. The recovery of MS activity was slow and was only 80% of control values 72 h after N2O was stopped. Studies employing rats previously injected with [57Co]Cbl showed that N2O displaced [57Co]Cbl from MS in a manner that temporally and quantitatively paralleled the loss of MS activity. Recovery of MS activity paralleled the reappearance of [57Co]Cbl on MS. N2O also caused the hepatic content of CH3-[57Co]Cbl to decrease by 20-60%. When [57Co]-Cbl was extracted from liver and analyzed by paper chromatography, [57Co]Cbl analogues were present (10-40% of total [57Co]Cbl) in rats exposed to N2O, but not in control animals. When rats were exposed to 50% N2O for 33 d, the total of endogenous Cbl and Cbl analogues in liver decreased to 35% of control values and endogenous Cbl decreased to 10% of control values. At this time, MS activity was 15% of control values and MMCoAM was only 26% of control values. We conclude that N2O causes multiple defects in Cbl metabolism that include the following: (a) rapid inhibition of MS activity with a slow recovery when N2O is stopped; (b) displacement of Cbl from MS; (c) decreased CH3-Cbl; (d) conversion of Cbl to Cbl analogues; (e) the gradual development of Cbl deficiency and (f) an eventual decrease in MMCoAM activity with a further decrease in MS activity.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMedDate not supplied

Electrolyte changes caused by hydrotherapy in purpura fulminans.

Purpura fulminans is a rare manifestation of meningococcemia that in its full-blown form has a predictive death value of 61%. Those patients who survive usually develop gangrenous lesions that involve skin and underlying structures, mostly of the extremities and sometimes of the cheeks. Experience with early excision and skin grafting of these lesions has generally been unsatisfactory since, due to the unique pathophysiology of the disease and involvement of the most distal branches of the cutaneous circulation, the lesions are not completely demarcated until well after complete recovery from the acute phase of the disease. Recently there was an outburst of purpura fulminans in Southern California and other parts of the country. During the months of January and February 1986 we were consulted on five cases. These ranged from two months to six years in age and consisted of two boys and three girls. One two-month-old died during the acute phase, another six-year-old remained in shock and in need of hemodynamic and respiratory support and succumbed three weeks after the onset of the disease, during which time all four extremities showed progressive necrosis. Of the three patients that survived, one three-year-old girl resolved her purpuric lesions except for small necrotic patches on the buttocks that did not require surgical intervention. The other two children were left with gangrenous lesions of the upper and lower extremities over 30% of total body surface area. One of these two patients demonstrated an electrolyte disturbance.(ABSTRACT TRUNCATED AT 250 WORDS)

Child, Preschool↗