Management of hypertensive emergencies.
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Biomedical subjects
Publications and source records attributed to A Quintanilla.
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The effect of left renal artery infusion of quinidine, 37.5 microgram (base)/kg/min on the renal clearance of ultrafilterable digoxin was studied in eight dogs given 0.06 mg/kg digoxin 24 hr previously. Digoxin was measured by 125I RIA, whose specificity was confirmed by HPLC. Within 15 min of the start of the infusion, the digoxin clearance decreased on the left 7.3 +/- 5.8 ml/min and on the right 6.1 +/- 6.4 ml/min, p < 0.02 and 0.05, respectively, compared to control. Quinidine infusion did not alter Cin. CDIG returned toward prequinidine infusion values after the infusion was stopped. We conclude that quinidine has a prompt and direct effect on the renal clearance of digoxin.
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Complement levels were determined in 12 normal human volunteers while receiving intravenous infusions of inulin for determination of standard inulin clearances. Significant decreases in beta IC globulin and total hemolytic complement activity were observed when inulin was infused, but not following infusion of saline as a control. These effects were noted only when steady-state inulin levels were greater than 26 mg%, suggesting a dose-dependent response. No evidence of increased coagulation was noted as measured by fibrinogen and fibrin degradation products. Since C4 levels remained largely unchanged following inulin infusion, it was concluded that the results most likely occurred through activation of the alternate complement pathway.
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Acute hemolysis in maintenance hemodialysis patients is not a rare occurrence. Significant hemolysis is life-threatening and may be unrecognized because of nonspecific symptomatology. This paper reports observation of a severe hemolytic episode in a hemodialysis patient. The hemolysis was associated with a sudden drop in serum osmolality and profound hyponatremia, resulting from accidental dialysis against deionized water. Recognizing the condition and treating it promptly by dialysis with physiological dialysate are essential for patient survival.
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Sodium salicylate was administered to anesthetized dogs in doses sufficient to produce concentrations in plasma comparable to those common in human salicylate toxicity. Salicylate administration increased the rates of excretion of water, sodium, and chloride in the urine. Salicylate administration also increased the rate of excretion of potassium so that its clearance often exceeded that of creatinine. This enhancement of potassium excretion was dissociated from the alkalosis that accompanies salicyate toxicity. Administration of 5% CO(2) in inspired gas did not attenuate the excretion of potassium; injection of salicylate into one renal artery caused a unilateral kaliuresis. Phosphate excretion increased progressively after administration of salicylate. On several occasions the clearance of phosphate equalled that of creatinine. Salicylate reduced renal tubular glucose reabsorption. When salicylate was injected into a renal artery, a glycosuria occurred ipsilaterally at filtered loads of glucose far below the reabsorptive capacity of the dog kidney. Salicylate administration also was associated with early elevation of glucose, phosphate, and potassium concentration in plasma. Salicylate administration reduced the content of adenosine triphosphate in the renal medulla. Salicylate was concentrated within the medulla between 1.5 and 3 times that of the cortex, a gradient equal to that for chloride.
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A case of recurrent, disseminated sporotrichosis in a renal transplant recipient is reported in which two joints, the skin, and the central nervous system were involved. The disease recurred both eight months and three years after the initial treatment with amphotericin B. The second course of therapy with amphotericin B required systemic and intraarticular administration of the drug. The third course of therapy included systemic and intrathecal administration. The function of the cadaveric transplanted kidney was maintained throughout the first recurrence of disease by careful reduction of immunosuppressive therapy and attention to the level of antifungal therapy. The kidney could not be salvaged after the second recurrence because of continued amphotericin B nephrotoxicity; however, the patient was cured of his infection. Sporothrix (Sporotrichum) schenckii may be a difficult organism to eradicate in chronically immunosuppressed patients, but the disease it causes may be successfully treated with aggressive systemic therapy.