Tehran University Medical Journal

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Background: Propofol and Thiopental are intravenous anesthetics having relatively different hemodynamic influences and adverse effects. In addition, there is significant pain on intravenous injection of propofol. This study was performed to examine the effects of Propofol-Thiopental admixture on hemodynamic variables, pain on injection and hypnotic dose at the time of induction of general anesthesia.
Methods: One hundred and twenty-five ASA I or II patients scheduled for elective surgery were randomized into four groups for induction of anesthesia in a double-blinded manner. With an original concentration of Propofol of 1% and that of Thiopental of 2.5%, we used these drugs in each group as follows: group P100: Propofol alone group P75: ¾ Propofol and ¼ thiopental (volume/volume) group P50: ½ Propofol and ½ thiopental group T100: Thiopental alone (control group). Hemodynamic variables (before and after induction), score of pain on injection and hypnotic doses were recorded and statistically analyzed.
Results: Admixture of Thiopental and Propofol reduces the injection pain of Propofol, as admixtures P75 and P50 were significantly less painful on injection than P100. Induction of hypnosis was significantly more rapid in group T100 than in groups P100 and P75. The interaction of Propofol and Thiopental with regard to their hypnotic effect is additive. Therefore a reduction in the dose of one was compensated by proportional increase in the dose of the other drug for a hypnotic effect. After anesthesia induction, systolic and diastolic blood pressures were significantly lower in group P100 than in groups P75, P50 and T100. The heart rate after laryngoscopy and tracheal intubation was significantly lower in group P100 than in groups P50 and T100.
Conclusion: Propofol-Thiopental admixture causes minimal pain on injection for intravenous induction of anesthesia with modified hemodynamic effects in comparison with each drug when used separately.

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Background: The risk of atherosclerosis and cancer is high in hemodialysis (HD) patients. There is evidence that HD causes oxidative stress. However, the causative factors of oxidative stress are unknown. It has been suggested that HD imposes an additional oxidative stress on patients with chronic renal failure by activation of granulocytes on dialyzer membranes resulting in an imbalance between oxidants and antioxidants. In this regard, a number of reports, either measuring specific analytes or enzymes, or estimating the total antioxidant activity of the plasma have given contradictory and inconclusive results. To investigate the oxidative stress status in Iranian HD patients, in this study, we evaluated GSH and FRAP levels along with Ca and pH in the blood of these patients.

Methods: Along with 20 healthy age and gender matched control subjects, 24 patients underwent dialysis, three times per week, for four hours in each session. Before and after dialysis, blood was taken for biochemical and liver function tests and to evaluate oxidative stress markers and measure Ca and pH levels.

Results: There was a significant decrease in FRAP and GSH levels after dialysis compared to those before treatment. Dialysis caused an increase in pH and Ca levels compared to levels in control subjects after dialysis.

Conclusion: In general, before dialysis, there is a balance between oxidants and antioxidants however, due to higher levels of oxidants as well as the possible binding of antioxidants to the dialyzer membrane during dialysis, an imbalance occurs. The instability in the balance of oxidants and antioxidants may be the major cause of cellular oxidative damage found in HD patients. This study indicates that there is a significant level of oxidative stress in renal chronic patients and this stress is augmented by dialysis. Antioxidant therapy should be considered in these patients.