The effect of propofol on oxidative stress in platelets from surgical patients.

We investigated the changes in oxidative stress in platelets from surgical patients anesthetized with propofol. We studied 60 surgical patients (ASA physical status I and II) and 12 healthy volunteers. The patients were divided into three groups: anesthesia induced with an IV bolus dose of 4 mg/kg thiopental; anesthesia induced with an IV bolus dose of 2 mg/kg propofol; and total IV anesthesia (induction with propofol 2 mg/kg, infusion with propofol 10 mg/kg during the first 10 min, then 8 mg/kg for 10 min, and 6 mg/kg during the rest of the operation). Healthy volunteers were given an IV bolus dose of 10% fat emulsion (Intralipid). We measured the following variables in platelets: thiobarbituric acid reactive substances content, glutathione content, and glutathione peroxidase, reductase, and transferase activities. Thiopental did not modify any of the variables. Propofol decreased thiobarbituric acid reactive substances production by 25.7% and increased total glutathione content by 24.6%. The percentage of glutathione in oxidized form was 29.5% smaller in patients anesthetized with propofol. Glutathione peroxidase activity was 28.3% less, glutathione transferase was 44.5% more, and glutathione reductase was not significantly different. Intralipid had no effect on any of the variables. After infusion of propofol for 1 h, the effects were, in qualitative terms, the same as those seen after an initial bolus dose. In conclusion, our findings show that propofol has an antioxidant effect in humans. This effect may be beneficial in patients who have diseases in which free radicals play an important role. IMPLICATIONS: This study demonstrates that propofol inhibits cellular oxidative damage, measured in platelets from surgical patients. Neither thiopental nor the fat emulsion (Intralipid) showed any effect. Moreover, propofol increased the antioxidant defense of glutathione. This could be applied in the protection of tissues from ischemic damage.     

The effect of hypotensive anesthesia with nitroglycerin and verapamil on platelets

Recently, there have been many cases in which nitroglycerin (TNG) is used for anesthesia for patients with low blood pressure. Since, it has been reported that TNG suppresses the platelet aggregation function in vitro. Verapamil (Vp), known as another platelet aggregation suppressant, and nicardipine (Nc) were used together with TNG and the platelet aggregation function was studied in vitro and in vivo. The results of the in vitro experiment showed that TNG 250 ng.ml-1 + Vp 250 ng.ml-1 suppressed the platelet aggregation function, and when TNG + Vp (was used for low hypotensive anesthesia, a large amount of Vp i.e. over 15 mg of Vp is injected as a bolus into the artery, there is a possibility the platelet aggregation function will be suppressed. No platelet aggregation function suppression was found when TNG+Nc was used in hypotensive anesthesia.     

Etomidate and thiopental inhibit platelet function in patients undergoing infrainguinal vascular surgery

BACKGROUND: Postoperative platelet hyperaggregability following general anesthesia has been reported in patients undergoing major vascular surgery. In contrast, since anesthetic agents inhibited platelet function both in vitro and in vivo, an increased risk for postoperative bleedings due to prolonged platelet dysfunction has been discussed. Nevertheless, data describing platelet-affecting properties of induction agents such as etomidate and thiopental in patients undergoing major vascular surgery are lacking. METHODS: Platelet function was determined at 0, 2, 20, and 200 microg/ml thiopental and at 0, 0.2, 2, 20 microg/ml etomidate in vitro in blood samples drawn from 16 patients suffering from severe occlusive arterial disease. In addition, 30 patients undergoing vascular surgery were investigated before (PRE) and after anesthesia induction (T0) either with etomidate (ETO group, n=16) or thiopental (THIO group, n=14), and 2 h after the beginning of surgery (T2). Platelet function was determined according to platelet aggregation, in vitro bleeding time, and flow cytometric measurements. RESULTS: In vitro, P-selectin expression was inhibited by etomidate at 2 and 20 microg/ml (-28% and -38%, respectively) and also by thiopental at 200 microg/ml (-27%). In patients undergoing vascular surgery, anesthesia induction in the ETO group resulted in a 31% prolongation of the in vitro bleeding time and an inhibition of ADP- and collagen-induced platelet aggregation (-30% and -17%, respectively) and of P-selectin expression (-25%) at T0. In the THIO group, only ADP-induced platelet aggregation was affected (-16%). At T2, all parameters had reached PRE level again in both groups. Furthermore, in comparison with the THIO group, operation time was significantly prolonged and transfusion volume was significantly increased in the ETO group. In addition, platelet count and hematocrit significantly decreased at T2, whereas levels of tPA, PAI-1, fibrinogen and antithrombin III and partial thromboplastin time remained unchanged in both groups during the study period. CONCLUSIONS: In the present study, etomidate and, to a minor extent, thiopental offered significant platelet inhibitory properties. Anesthetic-induced platelet inhibition may lead to higher transfusion rates and prolonged operation times. Therefore, anesthetic-related platelet inhibitory properties should be considered when searching for the anesthetic agent of choice, especially in patients with compromised hemostasis and co-existing bleeding disorders.     

In Vitro Effect of Clinical Propofol Concentrations on Platelet Aggregation

The inhibitory effect of propofol on platelet aggregation remains unclear, and studies on the subject disagree. Furthermore, although propofol infusions are widely used for general anesthesia and as sedatives for patients in intensive care units, little information is available on its concentration‐ and time‐related effects on platelet aggregation. Here, the authors investigated the in vitro effect of propofol, at concentrations required for sedation and general anesthesia, on platelet aggregation after 1, 2, or 3 h. Blood from healthy volunteers (n = 9) was incubated at propofol plasma concentrations of 0, 2, 4, and 10 μg/mL in a water bath at 37°C. Platelet aggregation was measured using a platelet function analyzer (PFA‐100) after 1, 2, or 3 h of incubation. Times to occlude collagen/epinephrine (CEPI) or collagen/adenosine 5'‐diphosphate (CADP)‐coated membranes (closure times, CTs) were measured. The CEPI and CADP CTs of non‐incubated blood were 125.6 ± 19.5 s and 93.0 ± 12.2 s, respectively, and no significant difference in CEPI CTs was observed at propofol plasma concentrations of 0, 2, 4, and 10 μg/mL after incubation for 1, 2, or 3 h. CADP CTs were comparable at propofol concentrations of 0, 2, 4, and 10 μg/mL at each incubation time. These findings suggest that propofol at concentrations required for sedation and general anesthesia has no inhibitory effect on platelet aggregation after 3 h of incubation.     

Rocuronium pharmacokinetic-pharmacodynamic relationship under stable propofol or isoflurane anesthesia

PURPOSE: To compare the pharmacokinetics, pharmacodynamics and the concentration-effect relationship of rocuronium in patients under stable propofol or isoflurane anesthesia. METHODS: Ten patients were randomized to receive fentanyl, propofol and nitrous oxide (60%) or fentanyl, thiopental, isoflurane (1.2% end-tidal concentration) and nitrous oxide (60%). To obtain good intubation conditions and maintain adequate muscle relaxation during surgery, patients received two bolus doses of rocuronium: 0.5 mg x kg(-1) (1.7 x ED95) at induction followed one hour later by 0.3 mg x kg(-1) (1 x ED95). Arterial blood samples were obtained over six hours after the second bolus dose. Plasma concentrations of rocuronium were measured using high pressure liquid chromatography. Muscle twitch tension was monitored by mechanomyography for the two doses. Pharmacokinetic and pharmacodynamic parameters were determined. RESULTS: No differences in rocuronium pharmacokinetic parameters were observed between both groups. After the second bolus, clinical duration was 20 +/- 6 min in the propofol group vs 39 +/- 8 min in the isoflurane group (P <0.05). The effect compartment concentration corresponding to 50% block, EC50, was higher under propofol anesthesia: 1008 vs 592 microg x L(-1) (P <0.05). CONCLUSION: Rocuronium body disposition is similar under stable propofol or isoflurane anesthesia. In contrast to isoflurane, propofol does not prolong the neuromuscular block. Therefore, the potentiating effect of isoflurane is of pharmacodynamic origin only, as explained by an increased sensitivity at the neuromuscular junction. In contrast with isoflurane anesthesia where the dose of rocuronium has to be decreased under stable conditions, no dose adjustment is required under propofol anesthesia.     

Anesthesia for craniotomy: total intravenous anesthesia with propofol and alfentanil compared to anesthesia with thiopental sodium, isoflurane, fentanyl, and nitrous oxide

STUDY OBJECTIVE: To compare a total intravenous (IV) anesthetic technique based on propofol and alfentanil with a commonly used anesthetic technique for craniotomy. DESIGN: Open-label, randomized, clinical study. SETTING: Neurosurgical clinic at a university hospital. PATIENTS: Forty patients, aged 18 to 55 years, scheduled for brain tumor surgery. INTERVENTIONS: In 20 patients, anesthesia was induced with fentanyl and thiopental sodium and maintained with fentanyl, dehydrobenzperidol, isoflurane, nitrous oxide (N2O), and a thiopental sodium infusion. Twenty patients were anesthetized with a propofol loading infusion followed by a maintenance infusion at a fixed rate. In addition, alfentanil was administered as a loading bolus, followed by a variable-rate infusion, with additional doses as necessary to maintain hemodynamic stability. MEASUREMENTS AND MAIN RESULTS: A decrease in blood pressure (BP) after induction with thiopental sodium was followed by a significant increase in BP and heart rate (HR) during intubation. BP and HR did not change during the propofol loading infusion. However, the administration of alfentanil was followed by a similar decrease in BP with a return to baseline values during the intubation period. Return of normal orientation (7 +/- 5 minutes vs 27 +/- 23 minutes) and concentration (12 +/- 12 minutes vs 35 +/- 37 minutes) was shorter and more predictable for the propofol-alfentanil-treated patients than for the thiopental sodium patients. Maintenance propofol concentration (nine patients) was between 3 +/- 0.69 micrograms/ml and 3.36 +/- 1.17 micrograms/ml, while the concentration at awakening was 1.09 microgram/ml. Alfentanil concentration at extubation (nine patients) was 79 +/- 34 ng/ml. CONCLUSION: A total IV anesthetic technique with propofol and alfentanil is a valuable alternative to a more commonly used technique based on thiopental sodium, N2O, fentanyl, and isoflurane.     

Reinfusion of autologous platelet-rich plasma improves hemostasis after cardiopulmonary bypass]

Although it is reported that postoperative bleeding is reduced by reinfusing autologous platelet-rich plasma (PRP) after cardiopulmonary bypass (CPB), the effect of PRP on hemostasis is not reported in detail. We prepared PRP and fresh whole blood (WB) from the blood of seven patients each prior to their undergoing CPB, and reinfused them autologously to the patients intravenously after the CPB was terminated. In this article, the effect on hemostasis of autologous PRP and WB was described. Platelet aggregation rates and blood coagulation factors were examined before, during and after bypass. Platelet counts, ADP-induced platelet aggregation and the activities of coagulation factors II, V and VII-X were significantly greater in prepared PRP than in WB (p less than 0.01 or p less than 0.05). A mean volume of 724 +/- 109 ml of PRP or 401 +/- 63 ml of WB was reinfused within about 30 minutes after heparin was neutralized by protamine sulfate. The platelet counts increased from 4.3 +/- 1.4 x 10(4)/mm3 to 14.1 +/- 1.6 x 10(4)/mm3 after PRP reinfusion and the platelet aggregation rates increased significantly (p less than 0.01) after PRP reinfusion compared to WB transfusion. The activities of coagulation factors VII-X also increased significantly (p less than 0.05) after reinfusion of PRP when compared to transfusion of WB. The activated partial thromboplastin time decreased to 1.2 times the baseline in the PRP group but remained 1.5 times the baseline in the WB group (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Venodilation contributes to propofol-mediated hypotension in humans.

The present investigation explored the possibility that the commonly observed hypotension that occurs during induction of anesthesia with propofol might be related to its ability to produce venodilation. Thirty-six ASA I and II patients who received no premedication were studied. The first 20 patients were divided into two equal groups. Hemodynamic measurements consisted of heart rate, arterial blood pressure, and forearm venous compliance by occlusive plethysmography. Baseline measurements were made in awake patients while resting in a supine position. Repeat measurements were made during steady-state infusions of propofol (2.5 mg/kg bolus injection, followed by a continuous infusion at 200 micrograms.kg-1.min-1) or thiopental (4 mg/kg bolus injection, followed by continuous infusion at 200 micrograms.kg-1.min-1), 10 min after tracheal intubation while patients were artificially ventilated. Both anesthetics resulted in a significant (P less than 0.05) and similar tachycardia; however, propofol produced significant decreases in systolic (-30 +/- 9 mm Hg) and diastolic (-11 +/- 4 mm Hg) arterial blood pressure. Forearm venous compliance was significantly increased during propofol administration but unchanged in patients receiving thiopental. In four additional patients receiving smaller consecutive infusions of propofol (50 and 100 micrograms.kg-1.min-1), significant subtle increases in forearm compliance were also recorded. These increases were not observed in four patients who received placebo infusions. Thus, one mechanism promoting hypotension during propofol anesthesia in humans seems to be related to its direct effects on venous smooth muscle tone and presumably venous return.     

Platelet aggregation during and after general anesthesia and surgery

Because of evidence suggesting that volatile anesthetics interfere with platelet aggregation in vitro, platelet function was investigated in patients exposed to combinations of nitrous oxide, halothane, and enflurane during brief surgical procedures. In 12 patients undergoing elective operations, blood was sampled before anesthesia, after induction but prior to surgery, during surgery, and postoperatively. Platelet aggregation by ADP, epinephrine, and collagen was similar during each sampling period in all but two subjects in whom only minor changes were noted. During brief exposure to these general anesthetics, there appears to be no clinically important inhibition of platelet function.     

Effects of long-term treatment with simvastatin on some hemostatic parameters in continuous ambulatory peritoneal dialysis patients.

BACKGROUND/AIM: Disturbances in serum lipids, hemostasis and platelet functions are frequent features in uremia and may contribute to the progression of atherosclerosis and its thrombotic complications. Recently, attention has been paid to beneficial effects of statins on serum lipids and hemostasis in uremic patients. Peritoneally dialyzed (continuous ambulatory peritoneal dialysis; CAPD) subjects are particularly prone to dyslipidemia and have a high risk of cardiovascular death. The purpose of this work was to assess platelet functions, some hemostatic parameters and serum lipids in 8 hyperlipidemic CAPD patients treated with simvastatin (Zocor, MSD) for 6 months. METHODS: Platelet aggregation in whole blood and in platelet-rich plasma (PRP) induced by collagen (2 microg/ml for whole blood and PRP), arachidonic acid (0.75 mM for whole blood and PRP), ADP (10 microM for whole blood and 5 microM for PRP) and ristocetin (0.75 mg/ml for whole blood and 1.5 mg/ml for PRP) was studied before and after 1, 3 and 6 months of simvastatin (dose: 10 mg at bedtime) treatment. RESULTS: Whole-blood platelet aggregation induced by collagen decreased significantly after 3 and 6 months of the therapy, whereas in PRP, platelet aggregation induced by collagen and ADP decreased significantly after 6 months. Ristocetin-induced platelet aggregation in PRP decreased significantly after 3 and 6 months of simvastatin therapy. P-selectin remained unaltered by 6 months of simvastatin therapy. The fibrinolytic activity index was significantly higher after 3 months of the therapy when compared to the baseline values. Thrombomodulin, a marker of endothelial cell injury, was significantly lower after 3 and 6 months of the therapy. Prothrombin fragments 1 + 2 did not change significantly during 6 months of simvastatin administration. Cholesterol and LDL fell significantly as early as after 1 month and remained lowered during further months of the therapy. CONCLUSION: Simvastatin is an effective hypolipemic agent and favorably affects platelet aggregation, endothelial function and fibrinolysis in CAPD patients.     

The comparative effects of propofol versus thiopental on middle cerebral artery blood flow velocity during electroconvulsive therapy

Electroconvulsive therapy provokes abrupt changes in both systemic and cerebral hemodynamics. An anesthetic that has a minor effect on cerebral hemodynamics might be more suitable for patients with intracranial complications, such as cerebral aneurysm. The purpose of our present study was to compare the effects of thiopental and propofol on cerebral blood flow velocity. We continuously compared cerebral blood flow velocity at the middle cerebral artery (MCA) during electroconvulsive therapy, using propofol (1 mg/kg, n = 20) versus thiopental (2 mg/kg, n = 20) anesthesia. Systemic hemodynamic variables and flow velocity at the MCA were measured until 10 min after the electrical shock. Heart rate and arterial blood pressure increased in the thiopental group until 5 min after the electrical shock. In the propofol group, an increase in mean blood pressure was observed to 1 min after the electrical shock. Mean flow velocity at the MCA decreased after anesthesia in both groups, and increased at 0.5-3 min after the electrical shock in the thiopental group and at 0.5 and 1 min after the shock in the propofol group. The flow velocities at 0.5-5 min after the electrical shock were significantly more rapid in the thiopental group compared with the propofol group. ?abs? Implications: Cerebral blood flow velocity change, measured by transcranial Doppler sonography during electroconvulsive therapy, was minor using propofol anesthesia compared with barbiturate anesthesia. Propofol anesthesia may be suitable for patients who cannot tolerate abrupt cerebral hemodynamic change.     

Platelet aggregation during hypotensive anesthesia using prostaglandin E1]

We studied platelet aggregation during hypotensive anesthesia using prostaglandin E1 (PGE1) on 22 patients (6 males, 16 female). All the patients underwent operations on head, neck, abdomen, breast, or lower extremities under general anesthesia. They had no history of hematological disease or taking drugs which affected platelet aggregation. The blood was sampled three times under a constant condition of anesthesia with intravenous drip: firstly, before using PGE1, secondly, under hypotensive state during PGE1 infusion at the speed of 0.05-0.3 micrograms.kg-1.min-1, and thirdly, after cessation of PGE1, after the blood pressure had recovered to the level before PGE1 infusion. ADP, collagen and epinephrine were added to the platelet rich plasma as clumping agents; their final concentrations were 0.3 microM, 2 micrograms.ml-1, and 2 micrograms.ml-1 respectively. The aggregating curves were recorded for 7 min. There were no significant differences in platelet aggregation among the three blood samples; neither in platelet count nor in bleeding time. Bleeding did not seem to have increased due to PGE1 infusion. These results suggest that PGE1 at hypotensive dose could be used safely under general anesthesia regarding hemostasis.     

Recovery following outpatient anesthesia: Use of enflurane versus propofol

Study Objective: To compare the intraoperative conditions and postoperative recovery of patients following the use of either propofol-nitrous oxide (N₂O) or enfurane-N₂O for maintenance of outpatient anesthesia.

Design: Randomized, single-blind study.

Setting: University hospital outpatient surgery center.

Patients: 61 ASA physical status I and II, healthy female outpatients undergoing laparoscopic surgery.

Interventions: Patients were randomly assigned to one of three anesthetic regimes. Group 1 (control) received thiopental sodium 4 mg/kg intravenously (IV), followed by 0.5% to 1.5% enfurane and 67% N₂0 in oxygen (O₂). Group 2 received propofol 2 mg/kg IV, followed by 0.5% to 1.5% enfurane and 67% N₂O in O₂. Group 3 received propofol 2 mg/kg IV, followed by propofol 50 to 160 μg/kg/min IV and 67% N₂O in O₂. All patients received succinylcholine 1 mglkg IV to facilitate tracheal intubation and atracurium 10 to 20 mg IV to provide adequate relaxation during the maintenance period.

Measurements and Main Results: Recovery from anesthesia was assessed by a research nurse who was unaware of the anesthetic technique used. The mean ± SD time to eye opening was significantly longer in the thiopental-enflurane-N₂O group (Group 1) than in the propofol-propofol-N₂0 group (Group 3) (6.1 ± 2.5 minutes vs. 3.5 ± 2.8 minutes, respectively). In addition, the mean time to respond to verbal commands was significantly shorter in the propofol induction groups compared with the thiopental induction group. However, the use of enfurane versus propofol for maintenance of anesthesia did not significantly prolong the time from arrival in the recovery room to sitting, tolerating oral fluids, walking, or being judged “fit for discharge.” There were no differences among the three groups with respect to postoperative pain or analgesic requirements. Finally, patients who received enfurane for maintenance of anesthesia had a significantly higher frequency of nausea and vomiting than the propofol maintenance group.

Conclusion: Induction of anesthesia with propofol is associated with a more rapid emergence from anesthesia than induction with thiopental. Maintenance of anesthesia with enfurane did not prolong recovery compared with maintenance with propofol, but enfurane was associated with increased frequency of postoperative nausea and vomiting.     

In Vivo and In Vitro Studies of the Inhibitory Effect of Propofol on Human Platelet Aggregation

Background: The inhibitory effects of propofol on platelet aggregation are controversial because the fat emulsion used as the solvent for propofol may affect platelet function. The effects of propofol on platelet intracellular calcium ion concentration and on aggregation were investigated.

Methods: Platelet aggregation was measured in 10 patients who received an intravenous infusion of propofol. Intralipos, the propofol solvent, was infused in 10 healthy volunteers and platelet aggregation were measured. The in vitro effects of propofol and Intralipos on platelets were also investigated. The inhibitory effects of various concentrations of propofol were studied. The effects of propofol on the changes in intracellular calcium level using a fluorescent dye, fura-2, were also observed. Template bleeding time was measured to determine the effect of propofol in clinical use.

Results: Platelet aggregation was significantly inhibited by infusion of propofol, although bleeding time was not prolonged. Intralipos did not inhibit platelets either in vivo or in vitro. Propofol significantly inhibited platelet aggregation in vitro and at 5.81 +/- 2.73 micro gram/ml but not at 2.08 +/- 1.14 micro gram/ml. The increase of intracellular calcium concentration was inhibited both in influx and discharge of calcium.     

Effects of Propofol or Isoflurane Anesthesia on Cardiac Conduction in Children Undergoing Radiofrequency Catheter Ablation for Tachydysrhythmias

Background: To determine suitability for ablation procedures in children, two commonly used anesthetic agents were studied: propofol and isoflurane.

Methods: Twenty patients presenting for a radiofrequency catheter ablation procedure were included and randomly assigned to two groups. A baseline electrophysiology study was performed during anesthesia with thiopental, alfentanil, nitrous oxide, and pancuronium in all patients. At the completion of the baseline electrophysiology study (EPS), 0.8-1.2% isoflurane was administered to patients in group 1 and 2 mg/kg propofol bolus plus an infusion of 150 micro gram *symbol* kg sup -1 *symbol* min sup -1 was administered to patients in group 2. Nitrous oxide and pancuronium were used throughout the procedure. After 30 min of equilibration, both groups underwent a repeat EPS. The following parameters were measured during the EPS: cycle length, atrial-His interval, His-ventricle interval, corrected sinus node recovery time, AV node effective refractory period, and atrial effective refractory period. Using paired t tests, the electrophysiologic parameters described above measured during propofol or isoflurane anesthesia were compared to those measured during baseline anesthesia. Statistical significance was accepted as P < 0.05.

Results: There was no statistically significant difference in the results obtained during baseline anesthesia when compared with those measured during propofol or isoflurane anesthesia.     

Effects of calcium channel-blocking agents on platelet-osteogenic sarcoma interaction: platelet aggregation and electron microscopic findings

A variety of tumors stimulate platelet activation. Because platelet activation may, in part, require calcium channel mobilization, we evaluated whether calcium channel blocking agents inhibit osteogenic sarcoma induced platelet aggregation. Platelet rich plasma (PRP) from normal subjects was incubated with one of four calcium channel-blocking agents: nifedipine, diltiazem, verapamil, or amlodopine, all 0-25 micrograms/ml, or diluent. Osteogenic sarcoma cells (2 or 4 x 10(6)/ml) were then added. Platelet aggregation was monitored by light transmission through PRP, and residual PRP was processed for electron microscopy. MG63 cells caused aggregation of PRP in most subjects (mean, 36 +/- 3%). Calcium channel-blocking agents (nifedipine greater than diltiazem greater than amlodopine greater than verapamil) caused partial inhibition of osteogenic sarcoma-induced platelet aggregation, at high concentrations only. Electron microscopy showed platelets aggregating to each other and to tumor cell membranes within 1-5 minutes. Changes in pattern of platelet clumping around tumor cells occurred when PRP was incubated with high concentration of diltiazem (50 micrograms). This study shows that calcium channel-blocking agents inhibit osteogenic sarcoma-induced platelet aggregation when used in high doses.     

Plasma vitamin E, total lipids and myeloperoxidase levels during spinal surgery. A comparison between two anesthetic agents: propofol and isoflurane

Plasma levels of vitamin E (Vit. E), total lipids (TL), Vit. E to TL ratio and myeloperoxidase (MPO) were studied in 20 patients undergoing lumbar spinal surgery and randomly allocated to two anesthetic groups: propofol (bolus dose + continuous infusion and thiopental/isoflurane. Peripheral blood samples were withdrawn prior to induction, each hour during anesthesia and 1 h after the end of surgery. Mean Vit. E and TL levels as well as mean Vit. E to TL ratios remained in the normal range over the entire period of study whatever the anesthetic regimen. MPO levels rose significantly in the post-operative period only, but without statistical difference between the two groups. Therefore, anesthesia with propofol or thiopental/isoflurane modifies neither total lipid concentrations nor plasma Vit. E, which is a potent endogenous inhibitor of lipid peroxidation bound to lipoproteins. The rise of plasma MPO suggests a moderate post-operative neutrophil activation which is not influenced by anesthetic techniques.     

The effect of nitric oxide on platelets when delivered to the cardiopulmonary bypass circuit

Nitric oxide (NO) decreases platelet adhesion to foreign surfaces in the in vitro models of cardiopulmonary bypass (CPB). We hypothesized that NO, delivered into the membrane oxygenator (MO), would exert a platelet-sparing effect after CPB. Forty-seven patients scheduled for coronary artery surgery were randomized to either a NO group, in which NO (100 ppm) was delivered into the MO, or a control group, in which CPB was conducted without NO. Platelet numbers, platelet aggregation response to 2.5-20 microM adenosine diphosphate, and beta-thromboglobulin levels were measured after induction of anesthesia, after 1 h on CPB and 2 h after the end of CPB. Met-hemoglobin levels were measured during CPB. The amount of blood products administered and chest tube drainage were measured in the first postoperative 18 h. NO delivered into the MO for up to 180 min did not increase met-hemoglobin levels above 4%. NO inhibited the platelet aggregation response to 2.5 microM ADP during CPB, otherwise NO had no other detectable effect on the aggregation responses or the levels of beta-thromboglobulin. Platelet numbers were not significantly altered by NO. NO did not alter the use of blood products or chest tube drainage. In conclusion, this study suggests that NO delivered into the MO of the CPB circuit does not significantly alter platelet aggregation and numbers, and does not affect bleeding. IMPLICATIONS: Nitric oxide affects platelet function. We demonstrated that nitric oxide delivered into the gas inflow of the cardiopulmonary bypass circuit membrane oxygenator does not significantly alter platelet numbers or function.     

Recovery of Consciousness after Thiopental or Propofol: Bispectral Index and the Isolated Forearm Technique

Background: Currently, there exists no effective monitor that can predict the probability of a patient being conscious during general anesthesia. The electroencephalogram-derived bispectral index (BIS) is a promising new method to assess anesthetic adequacy. This study used the BIS to predict the probability of recovery of consciousness after a single bolus induction dose of propofol or thiopental.

Methods: Twenty unpremedicated surgical patients were anesthetized with 4 mg/kg thiopental and 20 patients with 2 mg/kg propofol. The BIS was monitored throughout the study. After induction, before administration of neuromuscular blocking agent, a tourniquet was applied to one arm and inflated above the systolic blood pressure. This allowed preservation of the ability to move the hand after neuromuscular blocking agent onset. Patients were then prompted to squeeze the investigator's hand every 30 s, until they responded to the request. At the time of response, anesthesia was reinduced and the study terminated.

Results: The BIS at loss of consciousness and recovery of a response was not statistically different between propofol and thiopental. No patient with a BIS less than 58 was conscious. In both groups, a BIS of less than 65 signified a less than 5% probability of return of consciousness within 50 s.     

A comparison of induced hypotensive anesthesia using trimetaphan, prostaglandin E1 and nicardipine for neurosurgery

We performed hypotensive anesthesia using trimetaphan, prostaglandin E1, or nicardipine for eighteen patients undergoing cerebral aneurysm clipping. We measured the hemodynamic parameters (systolic arterial pressure, diastolic arterial pressure, and heart rates), concentration of catecholamines in blood (epinephrine, norepinephrine), blood platelet counts, and aggregation of blood platelets, before induction of anesthesia, before induced hypotension, during hypotension, after hypotension, and at the end of operation. Hypotension was produced rapidly, and hemodynamics was stable with any of the three drugs. In trimetaphan group, however, recovery time of arterial pressure was longer than in other two groups. There was no significant change of catecholamine during induced hypotension in prostaglandin E1 and nicardipine groups. However, in trimetaphan group, concentration of norepinephrine in blood decreased significantly during hypotension. No significant change was observed in either platelet count or platelet aggregation. These results suggest that trimetaphan has an effect to suppress excretion of stress hormones, and prostaglandin E1 and nicardipine have no influence on blood catecholamine levels and aggregation of platelet. We consider that nicardipine is useful as a hypotensive drug for neurosurgery.