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PubMed2005

Anti-inflammatory and antioxidative effects of propofol on lipopolysaccharide-activated macrophages.

Sepsis is a serious and life-threatening syndrome that often occurs in intensive care unit (ICU) patients. During sepsis, inflammatory cytokines and nitric oxide (NO) can be overproduced, causing tissue and cell injury. Propofol is an intravenous agent used for sedation of ICU patients. Our previous study showed that propofol has immunosuppressive effects on macrophage functions. This study was designed to evaluate the anti-inflammatory and antioxidative effects of propofol on the biosyntheses of tumor necrosis factor alpha (TNF-alpha), interleukin 1beta (IL-1beta), IL-6, and NO in lipopolysaccharide (LPS)- activated macrophages. Exposure to a therapeutic concentration of propofol (50 microM), LPS (1 ng/mL), or a combination of these two drugs for 1, 6, and 24 h was not cytotoxic to the macrophages. ELISA revealed that LPS increased macrophage TNF-alpha, IL-1beta, and IL-6 protein levels in a time-dependent manner, whereas propofol significantly reduced the levels of LPS-enhanced TNF-alpha, IL-1beta, and IL-6 proteins. Data from RT-PCR showed that LPS induced TNF-alpha, IL-1beta, and IL-6 mRNA, but propofol inhibited these effects. LPS also increased NO production and inducible nitric oxide synthase (iNOS) expression in macrophages. Exposure of macrophages to propofol significantly inhibited the LPS-induced NO biosynthesis. The present study shows that propofol, at a therapeutic concentration, has anti-inflammatory and antioxidative effects on the biosyntheses of TNF-alpha, IL-1beta, IL-6, and NO in LPS-activated macro-phages and that the suppressive effects are exerted at the pretranslational level.

Animals↗
PubMed2005

Propofol for emergency department procedural sedation and analgesia: a tale of three centers.

OBJECTIVES: To characterize propofol procedural sedation and analgesia (PSA) encounters for a large patient population at multiple emergency department (ED) sites. The authors sought to assess the frequency of respiratory and cardiovascular events during propofol PSA within these settings. METHODS: This study was a prospective, descriptive series of a consecutive sample of ED patients receiving propofol for PSA at three study sites. Patients were monitored for PSA-related events, including predefined clinically relevant cardiovascular and respiratory events. Data collection was performed during PSA with a standardized data collection sheet unique to each site. RESULTS: Propofol was administered during PSA to 792 patients during the respective reporting period at each center. Indications for sedation included dislocation reduction (38%), cardioversion (10%), fracture reduction (35%), abscess incision and drainage (8%), computed tomography imaging (2%), and tube thoracostomy (1%). The cumulative rate of oxygen desaturation events for all study sites was 7.7% with a brief period of assisted ventilation with bag-valve mask in 3.9%. The cumulative rate of PSA-related hypotensive events was 3.5%. Increasing patient age and specific clinical procedure were clinical variables most associated with any propofol-related respiratory event. All PSA-related events resolved with supportive interventions during the PSA encounter. No patients required endotracheal intubation, prolonged observation, or admission for PSA-related complications. CONCLUSIONS: Propofol typically confers a deep sedation experience for ED PSA. The most common PSA events associated with propofol are respiratory related and appear consistent across these three practice settings. All propofol-related PSA events resolved with brief supportive interventions in the ED with no adverse sequelae.

Adolescent↗
PubMed2004

Intracarotid propofol test for speech and memory dominance in man.

OBJECTIVE: To evaluate the usefulness of propofol as an alternative drug to amobarbital for the Wada test. METHODS: The authors analyzed 67 right-handed patients out of 123 patients who were candidates for neurosurgical therapy and thus underwent the Wada test as a preoperative evaluation. Twelve were tested with propofol and 55 were tested with amobarbital. Test conditions of the Wada test, recovery time of muscle power to manual muscle testing (MMT) Grade 3 (T3/5) and Grade 5 (T5/5), onset time of the first verbal response (Tverb) after injection and that of the first nonverbal response (Tnon-verb), were compared between the two groups. Power spectrum analysis of EEG background activity during the Wada test was performed and the time and spatial distribution of polymorphic slow activities were also compared in three cases. RESULTS: With propofol injection, lateralities of language and memory function were identified in 12 and 9 of 12 patients in comparison to amobarbital (52 and 41 of 55 patients detection in language and memory function). No complications with direct intracarotid injection of propofol were observed. T3/5 and T5/5 with propofol injection were shorter while Tverb and Tnon-verb were longer compared to amobarbital. Absolute power of polymorphic slow EEG waves gradually increased and then rapidly decreased with propofol, which was in contrast to amobarbital injection. CONCLUSIONS: With direct intracarotid propofol injection, the Wada test was satisfactorily performed in all 12 patients and 2 more patients with left-handedness or with different injection dose for each side without any complications. Clinical usefulness of propofol as an alternative drug to amobarbital for the Wada test was indicated.

Adolescent↗
PubMed1992

Subhypnotic doses of propofol possess direct antiemetic properties.

Propofol is associated with a low incidence of postoperative nausea and vomiting. In a prospective, randomized, double-blind, placebo-controlled study, we investigated the possible direct antiemetic properties of a subhypnotic dose of propofol. Fifty-two ASA physical status I or II patients, aged 15-60 yr with nausea and vomiting after minor gynecologic, orthopedic, or digestive tract surgery, were included in the study and received either propofol (10 mg = 1 mL) or placebo (1 mL Intralipid) intravenously in the postanesthesia care unit. Patients treated with propofol experienced a larger reduction in nausea and vomiting than patients treated with placebo (81% vs 35% success rate; P less than 0.05). Patients successfully treated had a similar incidence of relapse (propofol 28%; placebo 22%) within the first 30 min after therapy. Thirty-three percent of the propofol-treated patients and 44% of the placebo-treated patients showed a minor increase in sedation. The level of postoperative pain did not change in either group. Hemodynamic values remained unchanged in both groups. Pain on injection (7.6%) or dizziness (3.6%) only occurred in the propofol group. We conclude that propofol has significant direct antiemetic properties.

Adolescent↗
PubMed1993

Inhibitory effects of propofol on cytochrome P450 activities in rat hepatic microsomes.

The effects of propofol on cytochrome P450 activity in rat hepatic microsomes were evaluated to determine the potential influence of this anesthetic on the metabolism of coadministered agents. In microsomes from untreated and isoniazid-treated rats, propofol was a weak inhibitor of enflurane metabolism, inhibiting activity only at 0.35 mM propofol. In contrast, toluene, a related compound, effectively impaired enflurane defluorination in microsomes from untreated, and isoniazid- and phenobarbital-treated rats at concentrations as low as 0.025 mM. Propofol, in contrast to toluene, was an effective inhibitor of benzphetamine demethylation where it inhibited this activity at propofol concentrations as low as 0.025 mM in microsomes from phenobarbital-treated rats. In microsomes from phenobarbital-treated rats, propofol potently inhibited the metabolism of aniline. Sixty-four percent inhibition was achieved at 0.03 mM propofol, whereas toluene had no effect at 1 mM. These data demonstrate that propofol does not effectively inhibit enflurane metabolism performed by the isoniazid-inducible cytochrome P450IIE1 but effectively impairs activities of the phenobarbital-inducible cytochrome P450 isozymes.

Aniline Compounds↗
PubMed1993

The effects of propofol on cerebral and spinal cord blood flow in rats.

The effects of low and high doses of propofol on global cerebral blood flow (CBF) and spinal cord blood flow (SCBF) as a function of mean arterial blood pressure were investigated. CBF and SCBF during propofol infusion were compared to the levels in rats anesthetized with nitrous oxide (N2O) and fentanyl. Rats in the fentanyl/N2O group (control, n = 13) received 70% N2O in O2 plus fentanyl (bolus: 10 micrograms/kg; infusion: 25 micrograms.kg-1 x h-1). Rats in the low-dose propofol group (n = 10) received 30% O2 in air and propofol infusion (0.5 mg.kg-1 x min-1). Rats in the high-dose propofol group (n = 8) received 30% O2 in air and propofol infusion (2.0 mg.kg-1 x min-1). Blood flow autoregulation was tested by manipulating the mean arterial blood pressure with phenylephrine infusion or trimethaphan infusion and blood withdrawal by measuring CBF and SCBF using radioactive microspheres. Arterial blood gases, pHa, and skull temperature were controlled. Cerebral and spinal cord vasculature showed autoregulation in all treatment groups with a pressure range of 50-140 mm Hg. Within this pressure range, when compared to fentanyl/N2O, propofol decreased cortical CBF 60% (P < 0.001), subcortical CBF 40% (P < 0.001), midbrain blood flow 30% (P < 0.001), and SCBF 20% (P < 0.05). These results indicate that propofol maintains CBF and SCBF autoregulation.

Animals↗
PubMed1993

Inotropic and electrophysiologic effects of propofol and thiamylal in isolated papillary muscles of the guinea pig and the rat.

We compared the inotropic and electrophysiologic effects of propofol and thiamylal in isolated papillary muscles of the guinea pig and rat. Propofol applied in clinical 10% intralipid emulsion showed concentration-dependent negative inotropic effects, accompanied by decreased action potential duration, in the guinea pig. Intralipid alone had no effect. Although thiamylal showed a concentration-dependent depression similar to propofol in the guinea pig, depolarization of resting membrane potential was seen at 0.1 and 0.3 mM, and a slight prolongation of action potential duration at 90% repolarization at 0.1 mM, and then a decrease of action potential duration at 0.3 mM. In rat papillary muscles, propofol did not produce any depression of contractile force, whereas thiamylal produced a concentration-dependent negative inotropic effect. The important findings observed in the action potential in rat papillary muscles were the modest shortening of action potential duration after propofol application, and the significant decrease of resting membrane potential and the significant prolongation of action potential duration caused by thiamylal. Both propofol and thiamylal depressed slow action potentials and contractile force in guinea pig papillary muscles depolarized by 25 mM K+ solution. In conclusion, the negative inotropic effects of propofol and thiamylal might be caused by inhibition of trans-sarcolemmal Ca2+ influx accompanied by shortening of action potential duration in guinea pig papillary muscles. The action potential of thiamylal might be affected by the suppression of K+ current in guinea pig and rat papillary muscles that was never observed in the propofol-treated tissue.

Action Potentials↗
PubMed1994

Propofol and autonomic reflex function in humans.

The effects of continuous infusions of propofol on baroreceptor reflex regulation of cardiac rate and peripheral sympathetic nerve activity were evaluated in seven healthy, normotensive, young (19-26 yr), male volunteers. Heart rate, radial artery pressure, and continuous recordings of efferent sympathetic vasoconstrictor outflow (from the peroneal nerve) were monitored. Baroreceptor perturbations were produced by bolus intravenous injections of nitroprusside (100 micrograms) followed 60 s later by phenylephrine (150 micrograms). These stimuli were delivered to subjects while conscious and during propofol anesthesia (200 micrograms.kg-1 x min-1) at least 25 min after subjects were paralyzed (vecuronium), had tracheas intubated, and were ventilated (30% O2:70% N2) to maintain normocarbia. Additional data were collected during hypercarbic conditions and during a lower infusion rate of propofol (100 micrograms.kg-1 x min-1) combined with 70% nitrous oxide. Propofol infusions significantly lowered sympathetic nerve activity (SNA) and blood pressure (BP) and increased heart rate (HR). Cardiac baroreceptor sensitivity determined during nitroprusside was reduced 60% during propofol infusions and was only subtly improved during simultaneous N2O administration. In contrast, reflex sensitivity during phenylephrine was not changed from awake values during each of the three experimental conditions. Reflex regulation of SNA was nearly abolished during normocarbic conditions under propofol anesthesia but restored to conscious levels during hypercarbia and during N2O administration. These data indicate that propofol markedly attenuates reflex responses to hypotension, but that reflex sympathetic responses are better maintained in hypercarbic conditions and when lower doses of propofol are used in conjunction with N2O.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

The effect of propofol on the interaction of platelets with leukocytes and erythrocytes in surgical patients.

UNLABELLED: We tested the antiplatelet effect described for propofol in vitro in surgical patients. Platelet aggregation induced by adenosine diphosphate, collagen, and arachidonic acid was tested in samples of whole blood, platelet-rich plasma (PRP), PRP with red blood cells, and PRP with leukocytes. Also measured were platelet production of thromboxane (Tx)B(2) and leukocyte production of 6-keto-prostaglandin F(1 alpha) (a stable metabolite of prostacyclin) and plasma levels of nitrites + nitrates (indicator of nitric oxide production). Anesthesia was induced with a bolus IV injection of sodium thiopental 4 mg/kg (n = 10), with a bolus dose of 2.5 mg/kg of propofol (n = 20), or with propofol total IV anesthesia (n = 20). Sodium thiopental did not modify any of the analytical values. In patients who received a bolus injection of propofol, platelet aggregation was significantly reduced in whole blood and in PRP + leukocytes. Platelet production of TxB(2) was reduced by 35%; the inhibition of 6-keto-prostaglandin F(1 alpha) was not statistically significant. Plasma levels of nitrites + nitrates increased by 37%; this change correlated significantly with the decrease in systolic and diastolic blood pressure (both P < 0.05). Similar changes, albeit of larger magnitude, were seen in patients who were given total IV anesthesia with propofol. In conclusion, propofol inhibited platelet aggregation in surgical patients mainly as a result of the inhibition of Tx synthesis and the increase in nitric oxide production. These effects are thought to be related to the hypotensive effect of this anesthetic. IMPLICATIONS: In vitro experiments have shown that propofol inhibits platelet aggregation and increases nitric oxide production. This study shows that doses habitually used to induce or maintain anesthesia also have these effects. These findings have potential applications for patients at increased risk for bleeding and may partly explain the hypotensive effect of propofol.

6-Ketoprostaglandin F1 alpha↗
PubMed2003

Hemodynamic interactions of propofol and dantrolene in chronically instrumented dogs.

UNLABELLED: The hemodynamic interaction of dantrolene, a specific drug for malignant hyperthermia, and propofol which appears to be safe in malignant hyperthermia-susceptible patients, has not been investigated. We performed this study to examine the hemodynamic actions of dantrolene at a therapeutic dose during propofol anesthesia. Ten dogs were chronically instrumented for the measurements of systemic and coronary hemodynamics. The dogs were assigned to receive propofol with vehicle or dantrolene in a random manner on separate experimental days. Propofol significantly decreased mean arterial blood pressure, left ventricular systolic and end-diastolic pressure, the maximal rate of increase in left ventricular pressure, and left ventricular regional segment shortening. Coronary blood flow (CBF) was unchanged but coronary vascular resistance (CVR) decreased. Dantrolene reversed the decrease in mean arterial blood pressure and left ventricular systolic pressure caused by propofol, and significantly increased heart rate. However, left ventricular end-diastolic pressure, cardiac output, maximal rate of increase in left ventricular pressure, and segment shortening were unchanged. CBF was significantly increased with a decrease in CVR. These results suggest that dantrolene reverses the hypotensive action produced by propofol and causes an increase in CBF with a decrease in CVR, but does not significantly change the negative inotropic effects. Thus, dantrolene exerts favorable hemodynamic effects during propofol anesthesia. IMPLICATIONS: Our study suggests that dantrolene reverses the hypotensive action produced by propofol and causes an increase in coronary blood flow with a decrease in coronary vascular resistance, but does not significantly change the negative inotropic effects.

Anesthetics, Intravenous↗
PubMed2003

Propofol displays no protective effect against hypoxia/reoxygenation injury in rat liver slices.

UNLABELLED: Using precision-cut liver slices (20-25 mg wet weight) from male Wistar rats, we examined whether clinically relevant propofol concentrations have hepatoprotective or -toxic effects during hypoxia/reoxygenation. Slices were preincubated for 2 h in sealed roller vials (three slices per vial) containing Waymouth's medium (37 degrees C; 95% oxygen/5% CO(2)). Then, propofol or Intralipid was added to create four different groups (control, Intralipid, small-concentration propofol [0.5-1.5 micro g/mL], and large-concentration propofol [2.0-6.0 micro g/mL]). Thereafter, each group was incubated for 4 h under 95% oxygen/5% CO(2) (no hypoxia) or for 2 h under 100% nitrogen plus 2 h under 95% oxygen/5% CO(2) (hypoxia/reoxygenation). Slice viability and hypoxia/reoxygenation injury were assessed at 2, 3, and 4 h after incubation began by using the slice intracellular K(+) concentration, energy status (adenosine triphosphate content, total adenine nucleotides content, and energy charge), and liver enzyme leakage (aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase). Propofol and Intralipid caused a significant delay in energy charge recovery in comparison with the control. There were no significant differences between the propofol groups and the other two groups in intracellular K(+) content or liver enzyme leakage. Propofol had no hepatotoxic effect under no-hypoxia conditions in rat liver slices, nor did it have a protective effect against hypoxia/reoxygenation-induced hepatic injury. IMPLICATIONS: Propofol had no hepatotoxic effect under no-hypoxia conditions in rat liver slices, nor did it have a protective effect against hypoxia/reoxygenation-induced hepatic injury.

Adenine Nucleotides↗
PubMed2003

The effect of sevoflurane and propofol on cerebral neurotransmitter concentrations during cerebral ischemia in rats.

UNLABELLED: Sevoflurane and propofol are neuroprotective possibly by attenuating central or peripheral catecholamines. We evaluated the effect of these anesthetics on circulating catecholamines and brain neurotransmitters during ischemia in rats. Forty male Sprague-Dawley rats were randomly assigned to one of the following treatment groups: fentanyl and N(2)O/O(2) (control), 2.0% sevoflurane, 0.8-1.2 mg x kg(-1) x min(-1) of propofol, and sham-operated rats with fentanyl and N(2)O/O(2). Ischemia (30 min) was produced by unilateral common carotid artery occlusion plus hemorrhagic hypotension to a mean arterial blood pressure of 32 +/- 2 mm Hg. Pericranial temperature, arterial blood gases, and pH value were maintained constant. Cerebral catecholamine and glutamate concentrations, sampled by microdialysis, and plasma catecholamine concentrations were analyzed using high-pressure liquid chromatography. During ischemia, circulating catecholamines were almost completely suppressed by propofol but only modestly decreased with sevoflurane. Sevoflurane and propofol suppressed brain norepinephrine concentration increases by 75% and 58%, respectively, compared with controls. Intra-ischemia cerebral glutamate concentration was decreased by 60% with both sevoflurane and propofol. These results question a role of circulating catecholamines as a common mechanism for cerebral protection during sevoflurane and propofol. A role of brain tissue catecholamines in mediating ischemic injury is consistent with our results. IMPLICATIONS: During incomplete cerebral ischemia, the neuroprotective anesthetics sevoflurane and propofol suppressed cerebral increases in norepinephrine and glutamate concentrations. In contrast, propofol, but not sevoflurane, suppressed the ischemia-induced increase in circulating catecholamines to baseline levels. The results question a role for plasma catecholamines in cerebral ischemic injury.

Anesthetics, Inhalation↗
PubMed2003

Physicochemical compatibility of propofol-lidocaine mixture.

UNLABELLED: To examine the physicochemical stability of combinations of propofol-lidocaine mixtures frequently used in clinical practice, we added lidocaine 5, 10, 20, or 40 mg to commercially available 1% propofol 20 mL. To assess chemical stability, propofol concentrations were determined by gas chromatography assay for 24 h after preparation of the mixture. In addition, scanning electron microscopy was used to determine the maximum detectable droplet size in randomly selected fields. Macroscopically, separate, colorless layers were first seen at 3 and 24 h after the addition of 40 and 20 mg of lidocaine to propofol, respectively, whereas the mixture with 5 or 10 mg of lidocaine was macroscopically stable. Propofol concentrations in the mixture with 40 mg of lidocaine decreased linearly and significantly from 4 to 24 h after preparation, whereas those combined with other lidocaine doses were unchanged compared with baseline concentrations. Scanning electron microscopy showed that droplets with diameters >or=5 microm first appeared 30 min after the addition of 40 mg of lidocaine to propofol, and the emulsion droplets were enlarged in a time- and dose-dependent fashion. Our results indicate that the addition of lidocaine to propofol results in a coalescence of oil droplets, which finally proceeds to a visible separate layer. Depending on the dose of lidocaine and the duration between its preparation and administration, this combination may pose the risk of pulmonary embolism. IMPLICATIONS: The addition of lidocaine to propofol results in time- and dose-dependent increases in oil droplet diameters in emulsion. This mixture is physicochemically unstable over time and may cause pulmonary embolism, depending on the dose of lidocaine.

Anesthetics, Intravenous↗
PubMed2004

Assessing propofol induction of anesthesia dose using bispectral index analysis.

UNLABELLED: In this study we sought to determine the propofol requirement and hemodynamic effects as guided by bispectral index (BIS) analysis during induction of anesthesia. Sixty patients were enrolled in this study. Propofol, 2 mg/kg, was given to Group I for induction. Propofol was administered for induction until loss of response to verbal commands and until BIS values were around 50 to Groups II and III. After induction, the smallest BIS value was different in Group I. Decreases in total propofol dose were 36% and 43% in Groups II and III respectively as compared with Group I. The dose of propofol assessed by BIS analysis results in an important reduction of propofol requirement without side effects. IMPLICATIONS: Hypotension during induction of anesthesia with propofol is common. This study has shown that propofol requirement assessed by bispectral index analysis during anesthesia induction may decrease the dose and side effects and provide for satisfactory depth of anesthesia.

Adult↗
PubMed2004

Comparison of recovery profile after ambulatory anesthesia with propofol, isoflurane, sevoflurane and desflurane: a systematic review.

UNLABELLED: In this systematic review we focused on postoperative recovery and complications using four different anesthetic techniques. The database MEDLINE was searched via PubMed (1966 to June 2002) using the search words "anesthesia" and with ambulatory surgical procedures limited to randomized controlled trials in adults (>19 yr), in the English language, and in humans. A second search strategy was used combining two of the words "propofol," "isoflurane," "sevoflurane," or "desflurane". Screening and data extraction produced 58 articles that were included in the final meta-analysis. No differences were found between propofol and isoflurane in early recovery. However, early recovery was faster with desflurane compared with propofol and isoflurane and with sevoflurane compared with isoflurane. A minor difference was found in home readiness between sevoflurane and isoflurane (5 min) but not among the other anesthetics. Nausea, vomiting, headache, and postdischarge nausea and vomiting incidence were in favor of propofol compared with isoflurane (P < 0.05). A larger number of patients in the inhaled anesthesia groups required antiemetics compared with the propofol group. We conclude that the differences in early recovery times among the different anesthetics were small and in favor of the inhaled anesthetics. The incidence of side effects, specifically postoperative nausea and vomiting, was less frequent with propofol. IMPLICATIONS: A systematic analysis of the literature comparing postoperative recovery after propofol, isoflurane, desflurane, and sevoflurane-based anesthesia in adults demonstrated that early recovery was faster in the desflurane and sevoflurane groups. The incidence of nausea and vomiting were less frequent with propofol.

Ambulatory Surgical Procedures↗
PubMed2004

Pain during injection of propofol: the effect of prior administration of butorphanol.

Propofol causes pain or discomfort on injection in 28%-90% of patients. A number of techniques have been tried for minimizing propofol-induced pain with variable results. We compared the efficacy of butorphanol and lidocaine for prevention of propofol-induced pain. One-hundred-fifty ASA I-II adults, undergoing elective surgery were randomly assigned into 3 groups of 50 each. Group I (NS) received normal saline, Group II (L) received lidocaine 2% (40 mg), and Group III (B) received butorphanol 2 mg. All patients received pretreatment solutions made in 2 mL with normal saline administered over 5 s. One min after pretreatment patients received one-fourth of the total calculated dose of propofol (2.5 mg/kg) over 5 s. Assessment of pain with IV propofol was done by using a four-point scale: 0 = no pain, 1 = mild pain, 2 = moderate pain and 3 = severe pain at the time of propofol injection. In the control Group 39 (78%) patients had pain during propofol injection as compared to 21 (42%) and 10 (20%) in the lidocaine and butorphanol groups, respectively (P < 0.05). Butorphanol was the most effective. We therefore suggest the IV pretreatment with butorphanol 2 mg for attenuation of pain associated with propofol injection.

Adult↗
PubMed2004

A neuronal mechanism of propofol-induced central respiratory depression in newborn rats.

The neural mechanisms of propofol-induced central respiratory depression remain poorly understood. In the present study, we studied these mechanisms and the involvement of gamma-aminobutyric acid (GABA)A receptors in propofol-induced central respiratory depression. The brainstem and the cervical spinal cord of 1- to 4-day-old rats were isolated, and preparations were maintained in vitro with oxygenated artificial cerebrospinal fluid. Rhythmic inspiratory burst activity was recorded from the C4 spinal ventral root. The activity of respiratory neurons in the ventrolateral medulla was recorded using a perforated patch-clamp technique. We found that bath-applied propofol decreased C4 inspiratory burst rate, which could be reversed by the administration of a GABAA antagonist, bicuculline. Propofol caused resting membrane potentials to hyperpolarize and suppressed the firing of action potentials in preinspiratory and expiratory neurons. In contrast, propofol had little effect on resting membrane potentials and action potential firing in inspiratory neurons. Our findings suggest that the depressive effects of propofol are, at least in part, mediated by the agonistic action of propofol on GABAA receptors. It is likely that the GABAA receptor-mediated hyperpolarization of preinspiratory neurons serves as the neuronal basis of propofol-induced respiratory depression in the newborn rat.

Anesthetics, Intravenous↗
PubMed2005

The effects of intravenous lidocaine on pain during injection of medium- and long-chain triglyceride propofol emulsions.

Propofol formulated in medium- and long-chain triglycerides (MCT/LCT) is thought to cause less pain on injection. In this study we sought to determine if adding lidocaine to propofol-MCT/LCT is more effective in decreasing pain compared with propofol-MCT/LCT alone or conventional propofol-lidocaine mixtures. Seventy-five patients were randomized into three groups. Group A received conventional propofol-lidocaine mixtures with 20 mg lidocaine, group B received propofol-MCT/LCT with saline, and group C received propofol-MCT/LCT with 20 mg lidocaine. The incidence of pain was 24% in groups A and B and 4% in group C. The number needed to treat to prevent pain was 5. We conclude that propofol-MCT/LCT-lidocaine mixtures significantly reduce pain.

Adolescent↗