We compared the effect of propofol with that of sevoflurane anesthesia on uric acid (UA) excretion in ASA physical status I and II patients with normal renal function. A propofol group (n = 11) received propofol-nitrous oxide-fentanyl after induction of anesthesia by propofol, while a sevoflurane group (n = 12) received sevoflurane-nitrous oxide-fentanyl after induction of anesthesia by thiamylal. UA, creatinine (Cr), and urea nitrogen concentrations in serum and urine were measured before induction of anesthesia, 1, 2, and 3 h after induction, and on Postoperative Day 1. N-acetyl-beta-D-glucosaminidase, beta2-microglobulin concentrations, and pH in urine were also examined. Plasma clearance of UA (CUA) and Cr (CCr) were calculated. The hourly concentration and excretion of urine UA were significantly higher than those of the sevoflurane group (P < 0.01). Significant correlations were noted between the hourly urine volume and UA concentration (r = 0.58, P < 0.01 for the propofol group; r = 0.51, P < 0.01 for the sevoflurane group). The CUA of the propofol group was significantly higher than that of the sevoflurane group (22.9 +/- 10.6 vs 5.9 +/- 3.4 mL/min, mean +/- SD, P < 0.05). There were no significant differences in other renal variables between the two groups. The present study demonstrated that the UA excretion increased during propofol anesthesia, while it remained stable during sevoflurane anesthesia.
The effects of the administration of Ringer's lactate (L) and Ringer's acetate (A) solution on blood biochemistry in human subjects operated for tympanoplasty under general anesthesia were investigated. And the feasibilities of the clinical use of Ringer's lactate (LD) and Ringer's acetate (AD) solution containing 5% glucose were also assessed. In all cases the rate of infusion was 500 ml for initial 20 min, and then 5 ml.hr(-1).kg(-1) B.W. for 3 hr and 10 min. There were significant increases in blood L- and D-lactate, pyruvate, and L-lactate/pyruvate ratio in L group. A significant increase in blood acetate but not lactate was found in A group. These metabolic changes were minimal and considered as clinically not significant. The urinary excretion of lactate, pyruvate, acetate and glucose were also negligible. In both LD and AD group, the higher blood concentrations of lactate, pyruvate, acetate and glucose were found than in L and A group. Urinary excretions of these metabolites were much higher in LD and AD group than in L and A group. So glucose containing Ringer's lactate or acetate solutions should be administered in appropriate amounts and rate not to induce clinically significant metabolic alterations.
Comparison of the calculation formula, reproducibility, correlation and variation of bicarbonate ion concentration (HCO(3) (-)), and base excess value (BE) among four blood-gas analyzers was performed. No HCO(3) (-) and BE values calculated from the formulas showed any clinically significant difference, and all analyzers showed good correlation on their measurements. On the actual measurement of a specific sample, however, BE values from the same sample ranged between -6.3 and -15.7, which might affect therapeutic strategy. Caution should be taken for the assessment of data if different types of blood-gas analysis devices are used in the same facility.
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