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PubMedDate not supplied

Antimicrobial properties of topical anesthetic liquids containing lidocaine or benzocaine.

Six species of microorganisms commonly found within the oral cavity were exposed for either one minute or two hours to 5% lidocaine liquid topical anesthetic and benzocaine liquid topical anesthetic. Mixtures of microorganisms and anesthetics were diluted and plated onto a brain heart infusion medium. Reduction in cell viability was 73-100% after exposure to the anesthetic agents when compared with the saline/buffer controls. A significant reduction (p < .005) in cell growth by Streptococcus mutans, S. sanguis, S. mitis, S. salivarius, Actinomyces viscosus, and Candida albicans was associated with a one-minute and two-hour exposure to lidocaine, benzocaine, 5% lidocaine, and the benzocaine vehicle control. Five percent lidocaine reduced growth of the test orgainisms more than benzocaine in one-minute exposures to S. mutans, A. viscosus and S. salivarius and with a two-hour exposure to S. salivarius.Five percent lidocaine was bacteriocidal or fungicidal to all microorganisms for both time periods whereas, benzocaine liquid topical anesthetic was predominately bacteriostatic or fungistatic after one-minute exposures and bacteriocidal or fungicidal after two hours.The results indicated that two dental liquid topical anesthetics containing lidocaine or benzocaine possessed considerable antimicrobial activity to selected oral microorganisms. The exclusive use of a topical liquid anesthetic may be an adequate means to render the oral mucosa aseptic before injection of a local anesthetic.

Actinomyces↗

PubMedDate not supplied

Cardiovascular and respiratory effects of beta-endorphin in anesthetized and conscious rats.

This study deals with the effects of beta-endorphin on blood pressure, heart rate, and respiratory frequency in anesthetized and conscious rats after both peripheral and central administration. Intravenous injection of beta-endorphin (40 and 160 micrograms/kg) in urethane-anesthetized rats resulted in a prolonged decrease in blood pressure, which, after the higher dose, was accompanied by bradycardia. In the pentobarbitone-anesthetized animals the same doses of beta-endorphin caused a small rise in blood pressure without affecting heart rate. No effect on respiratory frequency was observed. In urethane-anesthetized rats with hemorrhagic shock intravenous naloxone elicited a small pressor effect. Intracerebroventricular injection (i.c.v.) of beta-endorphin (40 micrograms/rat) in urethane-anesthetized rats resulted in severe respiratory depression and death. With lower doses there was a decrease in all parameters studied without ensuing death. Respiratory depression was even more pronounced in pentobarbitone-anesthetized rats, occurring with much lower doses of the peptide than in the urethane-anesthetized animals. beta-endorphin in the dose of 0.6 micrograms/rat still reduced respiratory frequency as well as heart rate without affecting blood pressure. Naloxone pretreatment antagonized the respiratory depression and death, while the decrease in heart rate was diminished. In conscious rats 10 microgram/rat, i.c.v., of beta-endorphin resulted in a decrease in heart rate and blood pressure without affecting respiratory frequency. It is concluded that beta-endorphin, or related opioid peptides, may be involved in cardiovascular and respiratory regulation. The effects of beta-endorphin, however, are markedly modified by the anesthetic agent used.

Animals↗

PubMed2000

Effects of intravenous and local anesthetic agents on omega-conotoxin MVII(A) binding to rat cerebrocortex.

PURPOSE: The cellular target site(s) for anesthetic action remain controversial. In this study we have examined any interaction of i.v. anesthetics (thiopental, pentobarbital, ketamine, etomidate, propofol, alphaxalone), local anesthetics (lidocaine, prilocaine, procaine and tetracaine), and the non anesthetic barbiturate, barbituric acid with the omega-conotoxin MVII(A) binding site on N-type voltage sensitive Ca2+ channels in rat cerebrocortical membranes. METHODS: [125I] omega-conotoxin MVII(A) binding assays were performed in 0.5 ml volumes of Tris.HCl buffer containing BSA 0.1% for 30 min at 20 degrees C using fresh cerebrocortical membranes (5 microg of protein). Non-specific binding was defined in the presence of excess (10(-8) M) omega-conotoxin MVII(A). The interaction of i.v. (alphaxolone, etomidate, propofol, pentobarbitone, ketamine and thiopentone), local (lidocaine, prilocaine, procaine and tetracaine) anesthetics and barbituric acid was determined by displacement of [125I] omega-conotoxin MVII(A) (approximately 1 pM). RESULTS: The binding of [125I] omega-conotoxin was concentration-dependent and saturable with Bmax and Kd of 223 +/- 15 fmol/mg protein and 2.13 +/- 0.14 pM, respectively. Unlabelled omega-conotoxin MVII(A) displaced [125I] omega-conotoxin MVII(A) yielding a pKd of 11.04 +/- 0.04 (9.2 pM). All i.v. and local anesthetics at clinically relevant concentrations did not show any interaction with the omega-conotoxin MVII(A) binding site. CONCLUSION: The present study suggests that omega-conotoxin MVII(A) binding site on N-type voltage sensitive Ca2+ channels may not be a target for i.v. and local anesthetic agents.

Anesthetics, Intravenous↗

PubMed2003

Effects of local and intravenous anesthetics on the activity of glutamate transporter type 2.

Glutamate transporters may be important targets for anesthetic action in the central nervous system. The authors investigated the effects of the intravenous anesthetics, thiopental and ketamine, and the local anesthetics, lidocaine and bupivacaine, on the activity of glutamate transporter type 2, EAAT2. EAAT2 was expressed in Xenopus oocytes by injection of its mRNA. By using two-electrode voltage clamping, membrane currents were recorded after the application of L-glutamate (30 microM) in the presence or absence of various concentrations of anesthetics. Lidocaine and bupivacaine did not change glutamate-induced inward currents at the tested concentrations (1-1000 microM). Thiopental and ketamine also did not affect the activity of EAAT2 at the tested concentrations (0.3-300 microM). Our results suggest that the two commonly used local anesthetics (lidocaine and bupivacaine) and intravenous anesthetics (thiopental and ketamine) do not affect the activity of EAAT2 expressed in oocytes. EAAT2 may not be a target for these anesthetics.

Anesthetics, Intravenous↗

PubMed2002

Electrophysiologic cardiac effects of the new local anesthetic IQB-9302 and of bupivacaine in the anesthetised dog.

BACKGROUND: Local anesthetics are not free from potentially fatal complications. Therefore every new local anesthetic should be tested to demonstrate a lower, or at least similar, degree of toxicity over clinically used analogs. Most toxic effects from local anesthetics affect the cardiac electrophysiologic function, so the aim of this study was to characterize the electrophysiologic effects of a new long-acting local anesthetic (IQB-9302, Ciprocaine), and compare them with those of bupivacaine in the anesthetized dog. METHODS: Eight Beagle dogs received three increasing infusion doses of either IQB-9302 or bupivacaine. Under isoflurane anesthesia, dogs were instrumented to monitor cardiovascular (cardiac output, arterial and venous blood pressures) and cardiac electrophysiologic data (sinus and atrioventricular (AV) node function, atrial, nodal and ventricular conduction times, and refractoriness). RESULTS: Only the highest dose of both drugs induced hemodynamic or electrophysiologic alterations: cardiac output and heart rate were reduced while blood pressures remained unchanged. Atrial and intranodal conduction times and atrial refractoriness increased similarly with both anesthetics, but to a slightly lesser extent with IQB-9302. Significant increases in His-Purkinje and intraventricular conduction times were the most severe noxious effects and occurred only with large doses of either drug. IQB-9302 was slightly less toxic than bupivacaine and, unlike this latter drug, potentially fatal arrhythmias were not induced. CONCLUSION: IQB-9302 has hemodynamic and cardiac electrophysiologic effects similar to those caused by bupivacaine. Nevertheless, slightly less toxic effects were derived from IQB-9302 administration than with bupivacaine, and, unlike the latter, the former might be less proarrhytmogenic. The new long-acting local anesthetic IQB-9302 may offer clinical advantages compared with bupivacaine.

Anesthetics, Inhalation↗

PubMed1995

Regional anesthesia and local anesthetic-induced systemic toxicity: seizure frequency and accompanying cardiovascular changes.

We sought to determine the contemporary frequency of seizures, and the associated cardiovascular changes, resulting from local anesthetic-induced seizures in all patients undergoing brachial plexus, epidural, and caudal regional anesthetics. We investigated the following variables: development and treatment of seizure or cardiac arrest during the regional anesthetic, type of anesthetic (including local anesthetic used), gender, age, ASA physical status class and type of operation (elective or emergent). In addition, each patient who experienced a seizure underwent retrospective review of the acute event to determine the arterial blood pressure and heart rate changes accompanying the seizure, as well as details of the regional block technique. There was a significant difference between the rate of seizure development between epidural, brachia, and caudal anesthetics, with caudal > brachial > epidural. A significant difference was also noted in the rate of seizure development within types of brachial block, with supraclavicular and interscalene > axillary. No adverse cardiovascular, pulmonary or nervous system events were associated with any of the seizures, including the 16 patients who received bupivacaine blocks. The frequency of local anesthetic-induced seizures stratified by block type has a wide range, and cardiovascular collapse after bupivacaine-associated seizure has a low incidence.

Adult↗

PubMed1997

Effects of inhaled nonimmobilizer, proconvulsant compounds on desflurane minimum alveolar anesthetic concentration in rats.

UNLABELLED: Anesthetics depress the central nervous system, whereas nonimmobilizers (previously called nonanesthetics) and transitional compounds having the same physical properties (e.g., solubility in lipid) do not produce anesthesia (nonimmobilizers) or are less potent anesthetics than might be predicted from their lipophilicity (transitional compounds). Potential explanations for the absent or decreased anesthetic effect of nonimmobilizer and transitional compounds include the theories that the nonimmobilizers are devoid of anesthetic effect and that transitional compounds have a decreased capacity to produce anesthesia; that the effects of these compounds are not apparent because the concentrations examined are too low; or that anesthesia, or lack thereof, results from a balance between depression and excitation (all nonimmobilizer and transitional compounds produce convulsions). To examine these issues further, we tested the effect of various multiples of the convulsive 50% effective dose (ED50) of three nonimmobilizers and one transitional compound on the minimum alveolar anesthetic concentration (MAC) of desflurane in rats. The nonimmobilizer 2,3-dichlorooctafluorobutane (NI-1), from 0.7 to 1.1 times its convulsive ED50, increased the MAC of desflurane by 14%-27%, but at 1.6 times its convulsive ED50 caused no change in MAC; the nonimmobilizer 1,2-dichlorohexafluorocyclobutane (NI-2) did not change MAC at concentrations up to its convulsant ED50, but it increased MAC by 25% and 36% at 1.3 and 1.7 times its convulsant ED50, respectively. The nonimmobilizer flurothyl (NI-3) decreased the MAC of desflurane by 20% +/- 6% (mean +/- SD) at 0.5 times its convulsant ED50, but it caused no change at higher partial pressures (up to 7.8 times its convulsant ED50), and the transitional compound CF3CCl2-O-CF2Cl (T-1) significantly decreased MAC by 16% +/- 7% at 0.8 times its convulsant ED50, but the 6%-8% decreases in MAC at 0.4 and 1.6 times its convulsant ED50 were not significant. Thus, neither nonimmobilizer nor transitional compounds produced a consistent dose-related effect on the MAC of desflurane, and any changes were small. These results suggest that the excitation produced by transitional compounds or nonimmobilizers does not explain their limited ability or inability to produce anesthesia. The data are consistent with a decreased anesthetic efficacy of transitional compounds and the lack of efficacy of nonimmobilizers. IMPLICATIONS: Inhaled compounds that do not cause anesthesia (nonimmobilizers) are used to test theories of anesthetic action. Their use presumes that a trivial explanation, such as cancelling stimulatory and depressant effects, does not explain the absence of anesthesia. The present results argue against such an explanation.

Anesthetics↗

PubMed1997

Volatile anesthetics protect the ischemic rabbit myocardium from infarction.

BACKGROUND: The influence of anesthetic agents on the infarction process in the ischemic myocardium is unclear. This study evaluated the effects of three intravenous and three inhalational anesthetic agents on myocardial infarction within a quantified ischemic risk zone in rabbit hearts subjected to a standardized regional ischemia-reperfusion insult. METHODS: Both in vitro and in situ rabbit models were used to investigate the effects of anesthetic agents on infarct size. In all rabbits the heart was exposed and a coronary artery surrounded with a suture to form a snare for subsequent occlusion. In in situ preparations, both intravenous and inhalational agents were tested, whereas only the latter were used in isolated hearts. Infarct size was determined by triphenyltetrazolium chloride staining. To determine whether an adenosine-mediated protective mechanism was involved, 8-(p-sulfophenyl)theophylline, an adenosine receptor blocker, was added to halothane-treated isolated hearts. Adenosine concentration in the coronary effluent was also measured in isolated hearts exposed to halothane. In other protocols, chelerythrine, a highly selective protein kinase C inhibitor, was administered to both halothane-treated and untreated isolated hearts. RESULTS: Infarcts in the three in situ groups anesthetized with halothane, enflurane, and isoflurane were about one half as large as infarcts in rabbits that underwent anesthesia with pentobarbital, ketamine-xylazine, or propofol. Volatile anesthetics also protected isolated hearts by a similar amount. Both adenosine receptor blockade and chelerythrine abolished cardioprotection from halothane in isolated hearts. Halothane treatment did not increase adenosine release. CONCLUSIONS: The volatile anesthetics tested protected the ischemic rabbit heart from infarction, in contrast to the three intravenous agents tested. Protection was independent of the hypotensive effect of the inhalational agents because halothane also protected isolated hearts, in which changing vascular tone is not an issue and coronary perfusion pressure is constant. Cardioprotection by volatile anesthetics depended on both adenosine receptors and protein kinase C, and thus is similar to the mechanism of protection seen with ischemic preconditioning.

Adenosine↗

PubMed2004

Effects of anesthetic agents on focal adhesion kinase (pp125FAK) tyrosine phosphorylation in rat hippocampal slices.

BACKGROUND: Tyrosine protein kinase proteins exert a prominent control on signaling pathways and may couple rapid events, such as action potential and neurotransmitter release, to long-lasting changes in synaptic strength and survival. Whether anesthetics modulate tyrosine kinase activity remains unknown. The aim of the current study was therefore to examine the effects of intravenous and volatile anesthetics on the phosphorylation of focal adhesion kinase (ppFAK), a functionally important nonreceptor tyrosine kinase, in the rat hippocampus. METHODS: Phosphorylation of ppFAK was examined in hippocampal slices by immunoblotting with both antiphosphotyrosine and specific anti-ppFAK antibodies. Experiments were performed in the absence (control) or presence of various concentrations of pharmacologic or anesthetic agents or both. RESULTS: Clinically relevant concentrations of thiopental, propofol, etomidate, isoflurane, sevoflurane, and desflurane induced a concentration-related increase in tyrosine phosphorylation. In contrast, ketamine (up to 100 microm) and the nonimmobilizer F6 (1,2-dichlorohexafluorocyclobutane, 25 microm) did not significantly affect ppFAK phosphorylation. The anesthetic-induced increase in ppFAK phosphorylation was blocked by GF 109203X, RO 318220, and chelerythrin (100 microm), three structurally distinct inhibitors of protein kinase C and U 73122 (50 microm), an inhibitor of phospholipase C. The propofol- and isoflurane-induced increase in ppFAK phosphorylation was reversible and showed nonadditivity of effects with phorbol 12-myristate 13-acetate (an activator of protein kinase C, 0.1 microm). In contrast, ketamine (up to 100 microm), MK801 (10 microm, an N-methyl-d-aspartate receptor antagonist), bicuculline (10 microm, a gamma-aminobutyric acid type A receptor antagonist), and dantrolene (30 microm, an inhibitor of the ryanodine receptor) were ineffective in blocking anesthetic-induced activation of tyrosine phosphorylation. CONCLUSION: Except for ketamine, anesthetic agents markedly increase tyrosine phosphorylation of ppFAK in the rat hippocampus, most likely via the phospholipase C-protein kinase C pathway, whereas the nonimmobilizer F6 does not. These results suggest that ppFAK represents a target for anesthetic action in the brain.

Anesthetics↗

PubMed1991

Molecular details of anesthetic-lipid interaction.

By means of isotopic labeling with deuterium (2H) and observation by nuclear magnetic resonance (NMR), it has been possible to measure the conformational ordering and dynamics of lipids and anesthetics in membranes. The local anesthetic tetracaine causes disordering in the acyl chains of the lipids, very little effect near the glyceryl residue, and minor ordering effects in the charged head group. The anesthetic itself is well ordered within the lipid matrix. The magnitudes of these effects depend upon the nature of the lipid, and upon whether or not the anesthetic is charged. A model can be constructed for the location of the anesthetic within the lipid bilayers. Confirmation of the model comes from Fourier transform infrared spectroscopy (FTIR), which also shows directly the pressure-driven exclusion of local anesthetic from lipid, and the augmentation of this effect by the presence of cholesterol. Future studies by solid-state NMR of protein, and neutron diffraction of specifically deuterated components of anesthetic-nerve systems, should reveal even more precise details of the molecular events involved in anesthesia.

Anesthesia↗

PubMed1975

Absence of sensitization to epinephrine-induced cardiac arrhythmia and fibrillation in dogs and cats anesthetized with CI 744.

Ci 744 (20 mg/kg, given intramuscularly (IM) produced a reliable level of surgical anesthesia in both dogs and cats. Animals anesthetized in this way did not have an increased sensitivity to cardiac fibrillation after they were given epinephrine. Epinephrine-induced ventricular arrhythmia observed in C1 744-anesthetized animals was eliminated in cats and was markedly reduced in dogs by bilateral vagotomy. Myocardial fibrillation was not produced by epinephrine (0.1 to 100 mug/kg, intravenously (IV) in dogs and cats anesthetized with C1 744 alone. Pentobarbital anesthesia, like C1 744 anesthesia, did not sensitize the heart, whereas a significant number of thiamylal-halothane-anesthetized animals died from cardiac fibrillation after they had been given epinephrine. Additional dogs were anesthetized with C1 744 or pentobarbital and given a series of pressor and depressor agents (isoproterenol, epinephrine, tyramine, 1, 1-dimethyl-4-phenylpiperazium iodide (DMPP) plus bilateral carotid occlusion) before and after vagotomy. The responses with either anesthetic were similar with the exception that the reflex bradycardia to pressor agents was more evident in C1 744- than in pentobarbital-anesthetized dogs.

Anesthesia, General↗

PubMed2005

Effects of local anesthetics on human bladder contractility.

AIMS: We investigated the invitro effects of local anesthetics on the contractility of the human bladder. METHODS: By measuring the invitro isometric contractions of human bladder strips, we determined the effects of tetracaine, bupivacaine, lidocaine, and ropivacaine on the basal spontaneous contractions and contractions induced by various stimuli, namely, KCl (60 mM), carbachol (CCh), and electrical field stimulation (EFS). The effect of local anesthetic agents on Ca(2+)-independent sustained tonic contraction (SuTC) of the detrusor was also investigated. RESULTS: Local anesthetics increased phasic and tonic spontaneous contractile activity dose dependently in the concentration range 1-500 muM, but abolished phasic activity at higher concentrations. Local anesthetic agents inhibited nerve-mediated contraction (EFS, 0.8 msec) in a concentration-dependent manner (ropivacaine > tetracaine = bupivacaine > lidocaine), and inhibited non-nerve mediated contractions induced by KCl, long pulse EFS (direct muscle stimulation, 100 msec), and CCh. Inhibitory potency on non-nerve mediated contraction was for long pulse EFS: ropivacaine = tetracaine > bupivacaine = lidocaine and for KCl- and CCh-induced contractions: ropivacaine > tetracaine > bupivacaine = lidocaine. Higher concentrations of local anesthetics were needed to inhibit non-nerve-mediated bladder contraction than nerve-mediated contraction. SuTC was suppressed by all local anesthetics concentration dependently. CONCLUSIONS: Our study demonstrates that local anesthetics have inhibitory effects on the contraction of human bladder as induced by different stimulants and concentrations. Their effects and differences suggest that they may be considered potentially useful as diagnostic and therapeutic agents for bladder dysfunction.

Amides↗

PubMed1986

Anesthesiology in the 21st century: analgesic, sedative and anesthetic focusing.

The specialty of anesthesiology is on the verge of a major technological evolution (revolution) which will utilize the computative and logic powers of the computer as well as the recent and rapid advances in magnetic imaging and laser and drug receptor technology to introduce the concept of anesthetic drug focusing by the beginning of the next century. This will result in the need for only a few molecules of future anesthetic compounds because they will only be necessary at a limited number of receptors in a few neurons or nuclei in the brain and/or spinal cord. Analgesic, sedative and anesthetic action may not be dependent on any drug but rather be produced solely by a wave form or energy source focused via a computer on the appropriate receptors in the brain, spinal cord or peripheral nerves. Anesthetic drug focusing will enable anesthetic depth to be ideal, anesthetic action to be localized to only those cells, tissues or organs where it is desired and anesthetic onset and termination to be measured in micro-seconds.

Analgesics↗

PubMed2002

Myocardial protection by anesthetic agents against ischemia-reperfusion injury: an update for anesthesiologists.

PURPOSE: The aim of this review of the literature was to evaluate the effectiveness of anesthetics in protecting the heart against myocardial ischemia-reperfusion injury. SOURCE: Articles were obtained from the Medline database (1980-, search terms included heart, myocardium, coronary, ischemia, reperfusion injury, infarction, stunning, halothane, enflurane, desflurane, isoflurane, sevoflurane, opioid, morphine, fentanyl, alfentanil sufentanil, pentazocine, buprenorphine, barbiturate, thiopental, ketamine, propofol, preconditioning, neutrophil adhesion, free radical, antioxidant and calcium). PRINCIPAL FINDINGS: Protection by volatile anesthetics, morphine and propofol is relatively well investigated. It is generally agreed that these agents reduce the myocardial damage caused by ischemia and reperfusion. Other anesthetics which are often used in clinical practice, such as fentanyl, ketamine, barbiturates and benzodiazepines have been much less studied, and their potential as cardioprotectors is currently unknown. There are some proposed mechanisms for protection by anesthetic agents: ischemic preconditioning-like effect, interference in the neutrophil/platelet-endothelium interaction, blockade of Ca2+ overload to the cytosolic space and antioxidant-like effect. Different anesthetics appear to have different mechanisms by which protection is exerted. Clinical applicability of anesthetic agent-induced protection has yet to be explored. CONCLUSION: There is increasing evidence of anesthetic agent-induced protection. At present, isoflurane, sevoflurane and morphine appear to be most promising as preconditioning-inducing agents. After the onset of ischemia, propofol could be selected to reduce ischemia-reperfusion injury. Future clinical application depends on the full elucidation of the underlying mechanisms and on clinical outcome trials.

Analgesics, Opioid↗

PubMed2003

[High resolution fluorescence microscopy in combination with mathematical modelling. First evidence of sub-cellular anesthetic effects on Ca2+ sparks in situ].

Volatile anesthetics used in daily clinical routine, are associated with a rare but life-threatening disease, malignant hyperthermia. To date it is well known that, with the exception of xenon and nitrous oxide, all volatile anesthetics have the potential to trigger calcium (Ca(2+)) release from the sarcoplasmic reticulum, thereby influencing the Ca(2+) homeostasis in muscle fibers. The effects of volatile anesthetics have been previously studied by recording Ca(2+)-activated force transients in muscle fibers and by quantifying the effects on isolated intracellular Ca(2+)-release channels (ryanodin receptors). The use of high resolution fluorescence microscopy methods in combination with spatio-temporal mathematical models allows the effects of volatile anesthetics on functional clusters of ryanodin receptors in mammalian skeletal muscle fibers to be studied in situ for the first time.Thus, the analysis of cellular Ca(2+)-activated force production and single channel properties in conjunction with mathematical models allows the quantification of the effects of volatile anesthetics on Ca(2+)-release in the natural physiological environment on the basis of the underlying molecular architecture. In addition to the basic understanding of alterations in the Ca(2+) homeostasis induced by volatile anesthetics in muscle and nerve cells, the results are also of direct clinical importance for the understanding of the pathogenesis of malignant hyperthermia,where ryanodin receptor mutations are currently thought to result in an increased Ca(2+) release under the influence of volatile anesthetics.

Anesthetics, Inhalation↗

PubMed2005

Effect of volatile anesthetics on oxidative stress due to occupational exposure.

Possible health hazards from long-term exposure to inhalation anesthetics cannot yet be definitively excluded. One of the adverse effects of general anesthetics is the exogen sources of reactive oxygen radicals that are responsible for several diseases. We designed the present study to determine the effect of volatile anesthetics on oxidative stress due to occupational exposure. We enrolled 30 anesthesia and surgery personnel who had been exposed to inhalation anesthetics for 3 years and 30 healthy volunteer personnel who had not been exposed to inhalation anesthetics at any period of their life as the control group. Blood samples were taken from both groups for determination of superoxide dismutase, glutathione peroxidase, and their cofactors, which are selenium, copper, and zinc levels. Our results revealed that plasma and erythrocyte antioxidant activity and trace element levels were significantly lower in operating room personnel compared to that in the control groups. We concluded that the antioxidant defense system was affected by free radical injury in anesthesia and surgery personnel who had been exposed to inhalation anesthetics chronically. Therefore, minimizing occupational exposure to volatile anesthetics is important for protecting operation room personnel from hazards. Operating room personnel should also take antioxidant supplements.

Adult↗

PubMed2005

Volatile anesthetics constrict pulmonary artery in rabbit lung perfusion model.

Volatile anesthetics are generally considered to possess a vasodilator action. Some of their actions on pulmonary vessels, however, are not clearly understood. We examined the effects of various volatile anesthetics on pulmonary vessels using an in situ rabbit isolated-lung perfusion model. We prepared a rabbit constant-flow lung-perfusion model by sending blood to the pulmonary artery and removing blood from the left atrium, and observed the changes in pulmonary arterial perfusion pressure caused by inhalation of 0.5, 1, 2, and 3 minimum alveolar concentration (MAC) volatile anesthetics: halothane, enflurane, isoflurane, and sevoflurane, in random order. These volatile anesthetics increased pulmonary arterial perfusion pressure in a dose-dependent manner and caused the pulmonary arteries to constrict. In particular, halothane at all concentrations induced significantly greater pulmonary vasoconstriction than the other volatile anesthetics. Therefore, it is suggested that volatile inhalation anesthetics induce the pulmonary arteries to constrict, and halothane exhibits the most potent pulmonary vasoconstrictor effect among the volatile anesthetics tested.

Anesthetics, Inhalation↗

PubMed1975

Effects of local anesthetics on membrane properties. II. Enhancement of the susceptibility of mammalian cells to agglutination by plant lectins.

Treatment of untransformed mouse and hamster cells with the tertiary amine local anesthetics dibucaine, tetracaine and procaine increases their susceptibility to agglutination by low doses of the plant lectin concanavalin A. Agglutination of anesthetic-treated untransformed cells by low doses of concanavalin A is accompanied by redistribution of concanavalin A receptors on the cell surface to form patches, similar to that occurring in spontaneous agglutination of virus-transformed cells by concanavalin A. Immunofluorescence and freeze-fracture electronmicroscopic observations indicate that local anesthetics per se do not induce this redistribution of concanavalin A receptors but modify the plasma membrane so that receptor redistribution is facilitated on binding of concanavalin A to the cell surface. Fluorescence polarization measurements on the rotational freedom of the membrane-associated probe, diphenylhexatriene, indicate that local anesthetics produce a small increase in the fluidity of membrane lipids. Spontaneous agglutination of transformed cells by low doses of concanavalin A is inhibited by colchicine and vinblastine but these alkaloids have no effect on concanavalin A agglutination of anesthetic-treated cells. Evidence is presented which suggests that local anesthetics may impair membrane peripheral proteins sensitive to colchicine (microtubules) and cytochalasin-B (microfilaments). Combined treatment of untransformed 3T3 cells with colchicine and cytochalasin B mimics the effect of local anesthetics in enhancing susceptibility to agglutination by low doses of concanavalin A. A hypothesis is presented on the respective roles of colchicine-sensitive and cytochalasin B-sensitive peripheral membrane proteins in controlling the topographical distribution of lectin receptors on the cell surface.

Agglutination↗