Lactate/acetate buffer base cocktail for hemodialysis.
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Biomedical subjects
Publications and source records attributed to J T Daugirdas.
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In vitro binding of amantadine to plasma protein was assessed by ultrafiltration of plasma samples (from a blood bank) to which amantadine hydrochloride had been added. Approximately two-thirds of the amantadine was found to be protein-bound. The degree of protein binding was constant over a plasma amantadine concentration range of 100-2,000 ng/ml.
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Hemodynamic response to volume depletion by isolated ultrafiltration was compared in uremic (U) and nonuremic (N) conscious dogs. Fluid was removed at a constant rate until mean arterial pressure (MAP) decreased to less than 80 mmHg. Initial MAP was higher in the uremic dogs [132 +/- 8.6 (SD) mmHg] than in nonuremic controls (106 +/- 12, P less than 0.001). Initial cardiac index [U 4.97 +/- 0.831 X min-1 X m-2, N 4.44 +/- 0.62] and total peripheral vascular resistance index [(TPRI) U 2,160 +/- 353 dyn X s X cm-5 X m-2, N 1,976 +/- 420] were slightly, but not significantly, higher in uremic animals. Initial central venous pressure, wedge pressure, and plasma norepinephrine level were greater in the uremic dogs. At the end point of volume depletion, both uremic and nonuremic animals had achieved similar levels of TPRI, despite greatly attenuated or absent increases in plasma renin activity in the uremic group. At end point, blood volumes and plasma norepinephrine levels were comparable. The increase in pulse rate was higher in the uremic animals (59 +/- 37 pulses/min) compared with controls (25 +/- 52, P less than 0.05). In an additional group of uremic dogs, cardiovascular responses to hemorrhage and isolated ultrafiltration were compared and found to be similar, after allowance for blood viscosity changes had been made. The data suggest that in acutely uremic conscious dogs, despite reduced renin-angiotensin responses, hemodynamic adaptation to rapid volume depletion is not impaired.
Peritoneal sclerosis, a disorder similar to that previously identified in nonuremic patients, is being noted in peritoneal dialysis patients with increasing frequency. The etiology in dialysis patients remains unknown. An association with previous or ongoing peritoneal inflammation or irritation suggests that the incidence of peritoneal sclerosis could be reduced by rapidly controlling peritonitis and by eliminating the irritant properties of catheters, dialysate, and other materials used in performing peritoneal dialysis. If peritoneal sclerosis does supervene, weight loss, abdominal pain, and intestinal obstruction may occur and further peritoneal dialysis may become impossible because of abdominal pain or poor fluid and solute transfer.
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The calcium-complexing abilities of acetate, bicarbonate, lactate, succinate, and citrate were quantified, and were found to differ substantially. Acetate was a more potent vasodilator than lactate, and the vasorelaxant potencies of acetate and lactate failed to correlate with their calcium-complexing ability. The vasodilator action of acetate was not abolished after correction for complexing of ionized calcium. Strips constricted with vasopressin were especially sensitive to the vasodilator effects of acetate.
A patient receiving intermittent peritoneal dialysis is reported in whom the peritoneal fluid became milky white without apparent cause 4 months after insertion of his most recent Tenckhoff catheter. Analysis of the fluid revealed elevated triglyceride content and a normal cell count, consistent with chylous ascites. Peritoneal dialysis was continued, and the condition improved spontaneously without treatment.
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Studies in a conscious, nonuremic dog model suggest that use of dialysate hyponatric to plasma tends to cause hypotension during dialytic ultrafiltration by accelerating the rate of contraction of plasma volume. No adverse effect of hyponatric dialysate on total peripheral resistance response could be demonstrated.
Sodium acetate caused dose-dependent relaxation of helical rat tail artery strips constricted by phenylephrine, potassium chloride and arginine vasopressin. Substantial relaxation was evident at acetate concentrations as low as 4 mM. The results suggest that the vasodilatation of acetate is not limited to receptor-dependent or voltage-dependent mechanisms. Acute increases in bath sodium chloride concentration resulted in marked relaxation of vessel strips constricted by phenylephrine and potassium chloride. Arginine vasopressin-constricted strips were quite resistant to the vasorelaxant effect of increased bath sodium chloride.
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