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PubMed2003

Plasma propofol concentration and EEG burst suppression ratio during normothermic cardiopulmonary bypass.

BACKGROUND: During cardiopulmonary bypass (CPB), several factors affect drug disposition and action. This topic has not been studied extensively during normothermic CPB. In this study, we related propofol dose to plasma propofol concentration and burst suppression of the EEG during normothermic bypass. METHODS: After institutional approval and informed consent, 45 patients having cardiac surgery were assigned randomly to receive propofol infusions at 4 (Group A), 5 (Group B) and 6 (Group C) mg kg(-1) h(-1) during normothermic CPB. In all patients, small to moderate doses of fentanyl were also administered. Plasma propofol concentration and burst suppression ratio (BSR) were measured at the following times: (1) 10 min before CPB, (2) 10 min after the start of CPB, (3) 30 min after the start of the CPB, (4) just after aortic declamping, and (5) 60 min after CPB. RESULTS: At baseline, plasma propofol concentrations were similar among the three groups. After the start of CPB, the concentrations of propofol decreased significantly by 41, 35, and 30% of control values in Groups A, B, and C, respectively. In Group A, the concentration of propofol during CPB remained unchanged at less than the concentration before bypass. In Groups B and C, plasma propofol concentrations gradually increased during CPB to the pre-bypass concentrations. In Group A, BSR values did not change significantly during CPB. In Groups B and C, BSR values gradually increased and became significantly greater than baseline values. No patient reported intraoperative awareness. CONCLUSION: The pharmacokinetics and pharmacodynamics of propofol change during normothermic CPB. During normothermic CPB, the efficacy of propofol may be enhanced compared with before CPB.

Adult↗
PubMed2005

Baroreflex control of heart rate during and after propofol infusion in humans.

BACKGROUND: This study was designed to determine cardiovagal baroreflex gain during propofol infusion and to characterize its recovery profile using the pharmacological and spontaneous sequence methods in 13 healthy volunteers without cardiovascular or autonomic disorders. METHODS: After an 8- to 10-h fast and no premedication, measurements of RR intervals obtained from the electrocardiogram and non-invasive beat-to-beat systolic blood pressure (SP) were made at conscious baseline, at 60 and 120 min after induction of general anaesthesia using propofol, and at 20, 60, 120 and 180 min after emergence from anaesthesia. During propofol anaesthesia, ventilation was mechanically controlled to maintain normocapnia and calculated propofol concentration was adjusted by a TCI system at 5 microg ml(-1). Baroreflex responses were triggered by bolus i.v. injections of phenylephrine and nitroprusside to alter SP by 15-30 mm Hg. The linear portions of the baroreflex curves relating RR intervals and SP by least-square regression analysis were determined to obtain pharmacological gains. In addition, spontaneous sequence baroreflex gains were calculated from spontaneously fluctuating SP and RR intervals. RESULTS: Baseline pressor and depressor test gains before propofol anaesthesia were 29.1 (SD 14.9) and 12.5 (7.8) ms mm Hg(-1), respectively. They were significantly depressed by 65-73% during propofol infusions. Similarly, baseline up- and down-sequence baroreflex gains were 33.8 (28.9) and 27.3 (19.8) ms mm Hg(-1), respectively, and were significantly depressed by 71-87% during propofol anaesthesia. Pressor test and up-sequence baroreflex gains returned to the baseline values 20 min after emergence from propofol anaesthesia, but depressor test and down-sequence baroreflex gains did not recover until 60 min after emergence. CONCLUSIONS: We conclude that heart rate responses to both lowering and elevating blood pressure were depressed by propofol anaesthesia, and 60 min was required for their full recovery after discontinuation of propofol infusion.

Adult↗
PubMed2005

Changes in apparent systemic clearance of propofol during transplantation of living related donor liver.

BACKGROUND: Propofol is used during living-related donor liver transplantation because its metabolism is not greatly affected by liver failure. However, the pharmacokinetics of propofol during liver transplantation have not been fully defined. The purpose of this study was to evaluate the apparent systemic clearance of propofol during the dissection, anhepatic and reperfusion phases of living-related donor liver transplantation, and to estimate the role of the small intestine and lung as extrahepatic sites for propofol disposition. METHODS: Ten patients scheduled for living-related donor liver transplantation were enrolled in the study. Anaesthesia was induced with vecuronium 0.1 mg kg(-1) and propofol 2 mg kg(-1), and then maintained by 60% air, 0.5-1.5% isoflurane in oxygen and a constant infusion of propofol at 2 mg kg(-1) h(-1). Apparent systemic clearance during the dissection, anhepatic and reperfusion phases was calculated from the pseudo-steady-state concentration for each phase. Disposition in the small intestine was determined by measuring arteriovenous blood concentration in 10 liver transplantation donors. Pulmonary disposition was determined by measuring the arteriovenous blood concentration in 10 recipients during the anhepatic phase. The data are expressed as mean (sd). RESULTS: Apparent systemic clearances in the dissection, anhepatic and reperfusion phases were 1.89 (sd 0.48) litre min(-1), 1.08 (0.25) litre min(-1) and 1.53 (0.51) litre min(-1), respectively. The concentration of propofol in the portal vein was lower than in the radial artery. The intestinal extraction ratio calculated from the concentration in the radial artery and portal vein was 0.24 (0.12). There were no significant differences in propofol concentrations between the radial and pulmonary arteries. CONCLUSION: Apparent systemic clearance was decreased by approximately 42 (10)% during the anhepatic phase compared with the dissection phase. After reperfusion, liver allografts rapidly began to metabolize propofol. The small intestine also participates in the metabolism of propofol.

Adult↗
PubMed2000

Effects of propofol on functional activities of hepatic and extrahepatic conjugation enzyme systems.

The effect of propofol on the hepatic and extrahepatic conjugation enzyme systems was assessed in vitro using microsomal and cytosolic preparations of human liver, hamster kidney, lung and gut. The functional activities of phase-II enzymes, including uridine diphosphate-glucuronosyltransferase (UDPGT), glutathione S-transferase (GST) and N-acetyltransferase (NAT) were evaluated in the presence of various concentrations of propofol (0.05-1.0 mmol litre-1), using 1-naphthol, 1-chloro-2,4-dinitrobenzene and p-aminobenzoic acid as substrates respectively. Propofol produced concentration-dependent inhibition of UDPGT activity in human liver microsomes. Propofol did not produce significant inhibition of human hepatic GST activity at concentrations below 1.0 mmol litre-1. In contrast, NAT activity was unaffected by propofol 0.05-1.0 mmol litre-1 in human liver cytosolic preparations. In extrahepatic tissues, hamster renal and intestinal UDPGT activities were significantly inhibited by propofol at 0.25-1.0 mmol litre-1. In these tissues, GST and NAT were unaffected by propofol at 1.0 mmol litre-1. Propofol produced differential inhibition of human liver and hamster extrahepatic conjugation enzymes as a result of different substrate and tissue specificities. The potential interference of the metabolic profile of phase-II enzymes as a result of inhibition by propofol (especially of UDPGT and GST) should be considered when using propofol with other drugs for anaesthesia.

Acetyltransferases↗
PubMed1996

Reducing pain during propofol injection: the role of the solvent.

We hypothesized that the concentration of propofol in the aqueous phase may be the most important variable responsible for the pain experienced during injection of the drug. The concentration of propofol in the aqueous phase (18.57 micrograms/mL) can be decreased by increasing the fat content of the solvent. To test this hypothesis, 36 patients were randomly allocated to one of three groups, each receiving a different formulation of propofol. Group A received 20 mL of propofol alone in a commercial preparation (Diprivan(R) with 10 mL of saline); Group B, 20 mL of propofol to which 5 mL of long-chain triglyceride (LCT) fat emulsion and 5 mL of saline and been added; and Group C, 20 mL of propofol and 10 mL of LCT fat emulsion. The propofol emulsion was injected over 30-60 s into a dorsal vein of the hand. Patients reported pain during injection as none, mild, moderate, or severe (almost intolerable). In Group A, 8 of 12 patients reported moderate or severe pain upon injection whereas in Group C only mild pain was reported by 6 of 12 patients. Our results suggest that a smaller concentration of propofol in the aqueous phase of the emulsion reduces pain on injection. With the addition of more lipid (10 mL), a higher percentage of propofol is absorbed by fat particles. If solvents that permit a smaller concentration of the drug in the aqueous phase of oil-in-water emulsions were used for propofol and other drugs that cause pain on injection, pain would be reduced and patient satisfaction may be increased.

Adsorption↗
PubMed1997

Effects of topical nitroglycerin and intravenous lidocaine on propofol-induced pain on injection.

We performed a randomized, placebo-controlled, double-blind study to compare the efficacy of intravenous (I.V.) lidocaine and topical nitroglycerin ointment in preventing pain during propofol injection. Nitroglycerin or placebo ointments were applied to the back of the hand over the skin area overlying the I.V. catheter tip; lidocaine was or was not added to the propofol solution. One hundred twenty-four patients were randomly assigned to receive one of four treatments: placebo and plain propofol, propofol mixed with lidocaine, nitroglycerin ointment and plain propofol, and nitroglycerin ointment and propofol mixed with lidocaine. Hence, there were 31 patients in each treatment group. Patients receiving nitroglycerin ointment and plain propofol had the highest incidence of pain on propofol injection (23 of 31 patients, 74%), and the highest median pain score. Only when lidocaine was added to propofol did it effectively reduce the incidence and severity of pain. Patients aged 50 yr and older had a significantly lower incidence and less severe pain. We conclude that lidocaine and age, but not topical nitroglycerin ointment, are factors associated with a decreased incidence of propofol-induced pain.

Administration, Topical↗
PubMed1998

The influence of the bolus injection rate of propofol on its cardiovascular effects and peak blood concentrations in sheep.

UNLABELLED: The influence of the bolus injection rate of propofol on its cardiovascular effects has not been extensively studied. We therefore examined the influence of the injection rate of i.v. bolus doses of propofol on its acute cardiovascular effects and peak blood concentrations in seven chronically instrumented sheep. Each received i.v. propofol (200 mg) over 2 min (slow injection) and 0.5 min (rapid injection) on separate occasions in random order. The rapid injection was associated with more profound decreases in mean arterial blood pressure than slow injection (35.7% vs 23.7% maximal reductions from baseline, respectively; P = 0.02). There were no significant differences between the injection rates for peak reductions in myocardial contractility, increases in heart rate, or degree of respiratory depression. Concurrently, the rapid injections were associated with significantly higher arterial (26.9 vs 11.9 mg/L) propofol concentrations in a manner consistent with indicator dilution principles. There were no differences in the peak coronary sinus concentrations between the injection rates. We conclude that the rapid injection of propofol in the context of the induction of anesthesia produced significantly higher peak arterial propofol concentrations and suggest that it is these higher concentrations that produced relatively greater reductions in arterial blood pressure from rapid injections. IMPLICATIONS: Propofol is injected into a vein to initiate anesthesia. It can cause a rapid decrease in blood pressure, which may be dangerous to the patient. We examined the effect of rapid and slow injection rates of propofol in sheep and found that rapid injection caused a greater decrease in blood pressure. This was because rapid injection caused higher concentrations of propofol in the blood immediately after the injection. We believe that if the same processes occur in humans, there may be little advantage in injecting propofol rapidly.

Anesthetics, Intravenous↗
PubMed1999

A comparison of the effects of propofol and sevoflurane on the systemic toxicity of intravenous bupivacaine in rats.

UNLABELLED: We compared the effects of propofol and sevoflurane on bupivacaine-induced central nervous system and cardiovascular toxicity in rats. Thirty-four male Sprague-Dawley rats were anesthetized with 70% N2O/30% O2 plus the 50% effective dose (ED50) of propofol (propofol group, n = 12); 70% N2O/30% O2 plus ED50 of sevoflurane (sevoflurane group, n = 11); or 70% N2O/30% O2 (control group, n = 11). Bupivacaine was infused at a constant rate of 2 mg x kg(-1) x min(-1) while electrocardiogram, electroencephalogram, and invasive arterial pressure were continuously monitored. The cumulative doses of bupivacaine that induced dysrhythmias, seizures, and 50% reduction of heart rate were larger in the propofol and sevoflurane groups than in the control group. The cumulative dose of bupivacaine that induced a 50% reduction in the mean arterial blood pressure was larger in the propofol group than in the sevoflurane and control groups. The margin of safety, assessed by the time between the onset of dysrhythmias and 50% reduction of mean arterial blood pressure, was wider in the propofol group than in the sevoflurane group. We conclude that propofol and sevoflurane attenuate bupivacaine-induced dysrhythmias and seizures and that propofol has a wider margin of safety than sevoflurane. IMPLICATIONS: In anesthetized patients, dysrhythmias may be the only warning sign of intravascular injection of bupivacaine. Because propofol has a wider margin of safety than sevoflurane, life-threatening cardiovascular depression may be prevented by stopping the injection of bupivacaine at the onset of dysrhythmias during propofol anesthesia.

Anesthetics, Inhalation↗
PubMed1999

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

UNLABELLED: 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.

Adult↗
PubMed2000

Propofol without muscle relaxants for conventional or fiberoptic nasotracheal intubation: a dose-finding study.

UNLABELLED: Endotracheal intubation has been performed during the administration of propofol anesthesia without neuromuscular blockade. In this study, we determined the propofol dose required for conventional nasotracheal or for fiberoptic nasotracheal intubation of all patients. Thirty-two patients undergoing maxillofacial surgery were randomly assigned to the conventional (n = 16) or to the fiberoptic (n = 16) intubation group. In both groups, anesthesia was induced by using IV fentanyl and IV titrated propofol according to clinical need (spontaneous respiration rate, verbal response). An endotracheal tube was placed nasally in the pharynx and the vocal cords visualized by using a fiberscope inserted via the tube. In the conventional group, the larynx was visualized additionally with a laryngoscope blade (Miller). In both groups propofol was titrated until the vocal cords opened. Patients were tracheally intubated, and the propofol dose was recorded. In all patients, the trachea could be intubated without the use of muscle relaxants. Considerable interindividual differences of dose requirements were observed. The amount of propofol required in the conventional group was significantly (P < 0.0001) larger (median +/- SD: 2.74 +/- 1.59 mg/kg; range 1.95-7.07 mg/kg) than in the fiberoptic group (1.37 +/- 0.59 mg/kg; 0.72-2.86 mg/kg). Hemodynamics remained stable in all patients. Postintubational hoarseness occurred in three patients of each group. Fiberoptic nasal intubation without a muscle relaxant can be facilitated with significantly smaller and more predictable dosages of propofol than conventional nasal endotracheal intubation. The possibility of titrating the propofol dose under assisted ventilation until the vocal cords open during fiberoptic nasotracheal intubation and the better predictability of the required dose favors the fiberoptic approach. IMPLICATIONS: In this study, contrary to all preceding studies using predefined doses of propofol and opioids, we determined the minimal required propofol dose in combination with fentanyl for conventional or fiberoptic nasotracheal intubation without muscle relaxants.

Adult↗
PubMed2001

A lack of evidence of superiority of propofol versus midazolam for sedation in mechanically ventilated critically ill patients: a qualitative and quantitative systematic review.

UNLABELLED: Propofol and midazolam are often used for sedation in the intensive care unit. The aim of this systematic review was to estimate the efficacy and harm of propofol versus midazolam in mechanically ventilated patients. A systematic search (Medline, Cochrane Library, Embase, bibliographies), any language, up to June 1999 was performed for reports of randomized comparisons of propofol with midazolam. Data from 27 trials (1624 adults) were analyzed. The average duration of sedation varied between 4 and 339 h. In 10 trials, the duration of adequate sedation was longer with propofol (weighted mean difference 2.9 h; 95% confidence interval [CI], 0.2-5.6 h). In 13 trials (mostly postoperative), sedation lasted 4 to 35 h; in 9 of those, average weaning time from mechanical ventilation with propofol was 0.8-4.3 h; with midazolam it was 1.5-7.2 h (weighted mean difference 2.2 h [95% CI, 0.8 to 3.7 h]). In 8 trials, sedation lasted 54 to 339 h; there was a lack of evidence for difference in weaning times. Arterial hypotension (relative risk 2.5 [95% CI, 1.3 to 4.5]; number-needed-to-treat, 12), and hypertriglyceridemia (relative risk 12.1 [95%CI, 2.9 to 49.7]; number-needed-to-treat, 6) occurred more often with propofol. The duration of adequate sedation time is longer with propofol compared with midazolam. In postoperative patients with sedation <36 h, weaning is faster with propofol. IMPLICATIONS: The duration of adequate sedation time is longer with propofol compared with midazolam. In postoperative patients with sedation < 36 h, weaning is faster with propofol.

Critical Care↗
PubMed2001

The clinical and biochemical effects of propofol infusion with and without EDTA for maintenance anesthesia in healthy children undergoing ambulatory surgery.

UNLABELLED: We conducted this randomized, double-blinded, comparative, parallel-group study to determine whether adding EDTA to propofol would affect the clinical profile, calcium and magnesium homeostasis, or renal function in healthy children. After the induction of anesthesia with halothane, 69 ambulatory surgical patients (1 mo to <17 yr old), received propofol without EDTA (n = 33) or propofol with EDTA (n = 36). Blood samples were obtained for the measurement of ionized calcium, ionized magnesium, and laboratory indicators of renal function. Hemodynamic measurements, recovery, and adverse events were recorded. Propofol with EDTA produced no significant effects on clinical efficacy or renal function. Propofol and propofol EDTA produced a statistically significant decrease from baseline in serum concentrations of ionized calcium and magnesium during infusion (P<0.05), but with no apparent clinical effect. Hemodynamic measurements generally remained stable and were similar for both groups. Statistically significant changes in systolic blood pressure, mean arterial pressure, and heart rate were not considered clinically significant. Adverse events were mild or moderate. The addition of EDTA does not alter the clinical profile of propofol in pediatric ambulatory surgical patients. With or without EDTA, propofol is associated with a decrease in ionized calcium with no apparent clinical effect. IMPLICATIONS: The addition of EDTA does not alter the clinical profile of propofol in pediatric ambulatory surgical patients. With or without EDTA, propofol is associated with a decrease in ionized calcium with no apparent clinical effect.

Adolescent↗
PubMed2002

Tissue antioxidant capacity during anesthesia: propofol enhances in vivo red cell and tissue antioxidant capacity in a rat model.

UNLABELLED: The effects of anesthesia on ischemia-reperfusion injury are of considerable scientific and clinical interest. We examined the effects of propofol (known to possess antioxidant activity) and halothane (devoid of antioxidant activity in vitro) on tissue and red blood cell (RBC) antioxidant capacity. Adult male Wistar rats were anesthetized with halothane 0.5%-1.0% (n = 7), propofol 500 microg x kg(-1) x min(-1) with halothane 0.25%-0.5% (small-dose propofol; n = 9), or propofol 2000 microg x kg(-1) x min(-1) (large-dose propofol; n = 8) for 45 min. Blood and tissue samples of liver, kidney, heart, and lung were then harvested for in vitro exposure to a peroxidizing agent. Red cell malondialdehyde and tissue thiobarbituric acid reactive substances were determined spectrophotometrically. Antioxidant capacities of blood and tissues in the Large-Dose Propofol group, and of blood and all tissues except lung in the Small-Dose Propofol group, were increased significantly compared with halothane (P < 0.003). The increases in tissue antioxidant capacities varied in their magnitude: RBC > liver > kidney > heart > lung. There was a high correlation between changes in RBC susceptibility to oxidative damage and corresponding changes in tissues. These findings demonstrate that large-dose propofol significantly enhances tissue antioxidant capacity, and RBC antioxidant capacity can serve as a functional measure of tissue activity, in vivo. IMPLICATIONS: We designed this study to investigate the antioxidant effects of propofol in various tissues in a rat model. Pretreatment of animals with propofol led to a reduction in the susceptibility to an in vitro oxidative stress of five different tissues investigated, demonstrating the drug's ability to limit oxidative injury. This may have future application in limiting organ dysfunction after periods of tissue ischemia (which results in oxidative damage).

Analysis of Variance↗
PubMed2002

Esmolol and anesthetic requirement for loss of responsiveness during propofol anesthesia.

UNLABELLED: The administration of esmolol decreases the propofol blood concentration, preventing movement after skin incision during propofol/morphine/nitrous oxide anesthesia. However, interaction with esmolol has not been tested when propofol is infused alone. Accordingly, we tested the hypothesis that esmolol decreases the propofol blood concentration, preventing response to command (CP50-awake) when propofol is infused alone in healthy patients presenting for minor surgery. With approval and consent, we studied 30 healthy patients, who were randomized to esmolol bolus (1 mg/kg) and then infusion (250 microg x kg(-1) x min(-1)) or placebo. Five minutes later, a target-controlled infusion of propofol was commenced. Ten minutes later, responsiveness was assessed by a blinded observer. Oxygen saturation, heart rate, and noninvasive arterial blood pressure were recorded every 2 min. Arterial blood samples were taken at 5 and 10 min of propofol infusion for propofol assay. Results were analyzed with a generalized linear regression model: P <0.05 was considered statistically significant. The probability of response to command decreased with increasing propofol blood concentration (CP50-awake = 3.42 microg/mL). Esmolol did not alter the relative risk of response to command. We conclude that the previously observed effect of esmolol on propofol CP50 was not caused by an interaction between these two drugs. IMPLICATIONS: There is no evidence to suggest that esmolol, an ultra-short-acting cardioselective beta-blocker, affects anesthetic requirement for loss of responsiveness during propofol anesthesia.

Adult↗
PubMed2002

Heart rate response to intravenous atropine during propofol anesthesia.

UNLABELLED: We studied the dose-response relationships for atropine-induced heart rate (HR) changes in 61 patients during propofol anesthesia. The control group (n = 15) received no propofol. Group P-5 (n = 22) received IV propofol 1.25 mg/kg over 1 min followed by propofol at 5 mg. kg(-1). h(-1). After tracheal intubation, anesthesia was maintained with propofol 5 mg. kg(-1). h(-1) and 67% nitrous oxide in oxygen. Group P-10 (n = 24) received IV propofol 2.5 mg/kg over 1 min followed by propofol at 10 mg. kg(-1). h(-1). The P-10 protocol was otherwise identical. All patients received incremental doses of IV atropine 5 microg/kg over 5 s at 2-min intervals until HR increased >20 bpm from baseline values. Heart rate response to atropine 10 microg/kg was attenuated in Groups P-5 (12 +/- 7 bpm) and P-10 (9 +/- 6 bpm) compared with the control group (28 +/- 13 bpm, P<0.05). When atropine 20 microg/kg was administered, HR increased >20 bpm in all patients of the control group, but in only 43% and 13% of patients in Groups P-5 and P-10, respectively (P<0.05). These results indicate the decreased HR responsiveness to IV atropine in patients receiving propofol, which cannot be effectively overcome by a large dose of atropine, is possibly attributable to propofol-induced suppression of the sympathetic nervous system. IMPLICATIONS: Heart rate response to IV atropine is attenuated during propofol anesthesia, and the decreased responsiveness to atropine cannot be effectively overcome by a large dose of atropine.

Adjuvants, Anesthesia↗
PubMed1992

The effects of propofol on brain electrical activity, neurologic outcome, and neuronal damage following incomplete ischemia in rats.

This study compares the effects of propofol and fentanyl/N2O on spontaneous brain electrical activity, neurologic outcome, and neuronal damage due to incomplete cerebral ischemia in rats. Thirty Sprague-Dawley rats were assigned to one of three groups: group 1 (n = 10) received 70% N2O in O2 plus fentanyl (bolus 10 micrograms.kg-1, infusion 25 micrograms.kg-1.h-1); group 2 (n = 10) received 70% N2 in O2 and propofol (infusion 0.8-1.2 mg.kg-1.min-1) adjusted to maintain EEG burst suppression during ischemia; group 3 (n = 10) was anesthetized with propofol and received 6 ml.kg-1 10% glucose intraperitoneally 15 min before the start of ischemia. Incomplete cerebral ischemia was produced by right common carotid artery occlusion combined with hemorrhagic hypotension (35 mmHg) for 30 min. Arterial blood gases, pH, and rectal temperature were kept constant in all groups. Plasma glucose was lower during ischemia in propofol-anesthetized rats compared to that in fentanyl/N2O- (P = 0.009) and glucose-loaded propofol-treated rats (P = 0.008). Neurologic outcome and brain tissue injury were significantly better in propofol-anesthetized compared to fentanyl/N2O-anesthetized rats (P less than 0.05). Elevated plasma glucose in propofol-treated rats resulted in similar neurologic outcome and histopathologic injury as seen in propofol-anesthetized rats given no glucose. Recovery of EEG theta-alpha activity after ischemia was inversely correlated to neurologic deficit (fentanyl/N2O: r = -0.71; propofol: r = -0.83; P less than 0.01). These results show that propofol improves neurologic outcome and decreases neuronal damage from incomplete cerebral ischemia when compared to fentanyl/N2O. This effect is not dependent on plasma glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

In vitro effects of propofol on rat myocardium.

Propofol is a short-acting intravenous induction agent that induces cardiovascular depression. However, the effects of propofol on intrinsic myocardial contractility remain debatable. Thus, we studied the effects of three concentrations of propofol (1, 3, and 10 micrograms.ml-1, respectively) and its solvent on the mechanics and energetics of isolated rat left ventricular papillary muscles. Propofol and its solvent did not induce any significant inotropic effect as shown by the lack of significant changes in maximum unloaded shortening velocity and in active isometric force. Nevertheless, propofol induced a slight decrease in isometric force (92 +/- 6%, 95 +/- 5%, and 95 +/- 4%, respectively, all P less than 0.01) under certain experimental conditions (i.e., after isometric stabilization). Using various afterloaded twitches, the peak power output and the curvature of the force-velocity curve were calculated. Propofol and its solvent did not significantly modify these two energetic parameters, indicating that it did not change myothermal economy and cross-bridge kinetics. Propofol impaired isotonic relaxation, suggesting that it decreased calcium uptake by the sarcoplasmic reticulum, whereas its solvent alone did not. However, alteration of sarcoplasmic reticulum function was moderate, since postrest potentiation and postrest recovery were unmodified after propofol. It was concluded that propofol induces moderate changes on intrinsic myocardial contractility. These results suggest that cardiovascular depression observed with propofol in vivo is not related to intrinsic myocardial depression.

Animals↗
PubMed1992

Pharmacodynamics of propofol in female patients.

Although the clinical properties of propofol have been studied extensively, the pharmacodynamics have not yet been described fully. We studied the propofol concentration-effect relationships for loss of eyelash reflex, loss of consciousness, and hemodynamic changes in 18 female patients, ASA physical status 1, aged 20-49 yr. Propofol was given by computer-controlled infusion. The initial target concentration of 0.5-1 microgram/ml was increased every 12 min by 0.5-1 microgram/ml until the patients lost consciousness. Every 3 min, loss of eyelash reflex and loss of consciousness were tested and an arterial blood sample was taken for analysis of the blood propofol concentration. The concentration-response relationships for loss of eyelash reflex and loss of consciousness were defined by fitting a sigmoid Emax function (where Emax = the maximum effect that can be reached; i.e., 100% of the patients showing loss of eyelash reflex or loss of consciousness) to the response/no response data versus the propofol concentration, using nonlinear regression. The effect of propofol on hemodynamic parameters was analyzed by linear regression. The propofol concentrations at which 50% and 90% of the patients showed loss of eyelash reflex were 2.07 and 2.78 micrograms/ml, respectively. The corresponding values for loss of consciousness were 3.40 and 4.34 micrograms/ml. The systolic and diastolic blood pressure decreased with increasing blood propofol concentration. The correlation coefficients for the decrease in systolic and diastolic blood pressure versus the blood propofol concentration were r2 = -0.663 and r2 = -0.243, but heart rate did not change. In conclusion, propofol concentrations inducing loss of eyelash reflex are less than those inducing loss of consciousness.

Adult↗