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Intravenous labetolol, a nonselective alpha- and beta-blocking drug, is commonly used to treat severe hypertension. Nonselective beta-blockers can cause hyperkalemia, especially in patients with renal failure. One series reported 3 renal transplant patients who had hyperkalemia after labetolol infusion, but none of these patients developed any serious complication. We report a case of life-threatening hyperkalemia (serum [K+] 9.9 mEq/l) with ventricular tachycardia and hypotension in a patient on maintenance hemodialysis who received labetolol for a hypertensive emergency. Physicians should be aware of this potentially lethal complication, which is easily preventable., (Copyright 2001 S. Karger AG, Basel)

Background: The serum anion gap (serum [Na(+)]-Cl(-)]-[CO(2)]) is still the first-line approach to metabolic acidosis. However, while it is generally acknowledged that hypoalbuminemia mandates a downward adjustment of the expected anion gap, a specific correction factor for the anion gap in the face of low serum albumin has never been demonstrated., Methods: We reviewed initial laboratory data from 432 consecutive patients admitted or transferred to the medical intensive care unit at Nassau County Medical Center over a 6-month period and correlated the serum albumin with the anion gap and the serum [tCO(2)] using multivariate analysis. We looked at the anion gap as a function of delta (albumin), the difference between normal and actual serum albumin, defined as 4.0 - measured serum albumin g/dl. We also assessed [tCO(2)] as an independent variable., Results: For patients with normal or high serum tCO(2), the ratio of change in anion gap (delta anion gap) to delta (albumin) was 1.46 and 1.45, respectively. For patients with serum tCO(2) <22 mEq/l this ratio was 1.89. In the latter group, anion gap was best predicted taking both delta (albumin) and serum tCO(2) into account: anion gap = 36.2 - serum tCO(2) - 2.3 x delta (albumin) (r = 0.71, p < 0.0001)., Conclusion: For intensive care patients with normal or high serum tCO(2) (>21 mEq/l) a simple bedside adjustment of the anion gap by subtracting 1.5 times the difference between measured serum albumin and the 'normal' level of 4.0 g/dl gives a close estimate of the actual anion gap. For intensive care patients with serum tCO(2) <22 mEq/l, correction of the anion gap is well predicted by adding about twice the Delta (albumin) to the calculated gap., (Copyright 2000 S. Karger AG, Basel)

Incubation of the toad bladder epithelia with 100 nM 12-O-tetradecanoylphorbol 13-acetate (TPA) for 1, 3 and 5 min decreased cytosolic protein kinase C (PKC) activity to 85, 80 and 75% of control, while membrane-associated PKC activity increased to 127, 140 and 126% of control, respectively. Long-term treatment of epithelial cells with TPA caused downregulation of PKC with a loss of 80% of the enzymic activity. Incubation with vasopressin (AVP) for 2 min decreased cytosolic PKC activity by 20%, whereas the activity in the membrane fraction increased by 33%. PKC translocation did not occur when epithelia were stimulated with [deamino1-D-arginine8]-vasopressin which binds more specifically to the V2 receptor. Staurosporine inhibited PKC activity as well as the effect of AVP on translocation. Phorbol esters decreased the response to AVP on water transport, whereas staurosporine greatly increased the hormonal response. We conclude that TPA induces an intracellular translocation and downregulation of PKC. The translocation of PKC by AVP and the inhibition of AVP-stimulated water flow by TPA suggest a significant negative feedback loop involving PKC to modulate the action of AVP.