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Results for “Calcium Compounds”

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PubMed1991

Pre- and postjunctional effects of phorbol 12-myristate-13-acetate in the mouse vas deferens.

The protein kinase C stimulator phorbol 12-myristate-13-acetate (PMA) increased the release of noradrenaline from field-stimulated mouse vasa deferentia and antagonized the inhibitory effect of xylazine and FK 33-824. The mechanical response to field stimulation was not modified by PMA in unpretreated vasa, but the contractility was partly restored when the stimulation-response curve had been depressed by xylazine or FK 33-824. In contrast, PMA decreased the contractile response to exogenous noradrenaline and bethanechol. A similar but smaller reduction was obtained with 1,2-dioctanoyl-sn-glycerol. In vasa depolarized by KCl, PMA and verapamil reduced the amplitude of contractions elicited by CaCl2. Only the effect of verapamil could be reversed by the calcium ionophore A 23187, while the effect of PMA was greatly attenuated in muscles pretreated with ouabain. Phorbol 12-myristate-13-acetate-4-O-methylether was ineffective in all experiments. These results suggest that PMA increases noradrenaline release (prejunctional effect) and decreases vasal contractility (postjunctional effect) by activation of protein kinase C.

Animals↗

PubMed2003

IgE alone stimulates mast cell adhesion to fibronectin via pathways similar to those used by IgE + antigen but distinct from those used by Steel factor.

We recently demonstrated that immunoglobulin E (IgE), in the absence of cross-linking agents, activates signaling pathways in healthy murine bone marrow-derived mast cells (BMMCs) and that this activation enhances BMMC survival, at least in part, via secretion of autocrine-acting cytokines. We report herein that IgE alone also triggers the adhesion of both BMMCs and connective tissue mast cells (CTMCs) to the connective tissue component, fibronectin (FN). This adhesion occurs to the same extent as that triggered by optimal levels of Steel factor (SF) or IgE + antigen (IgE + Ag) and is mediated by an increased avidity of the integrin very late antigen 5 (VLA-5). Moreover, this IgE-induced adhesion, which is prolonged compared with that elicited by SF or IgE + Ag, requires phosphatidylinositol 3-kinase (PI3K), phospholipase C gamma (PLCgamma), and extracellular calcium but not extracellular-regulated kinase (Erk) or p38. Interestingly, we found, using the calcium channel blocker, 2-APB (2-aminoethoxydiphenyl borate) and Lyn-/- BMMCs that both IgE- and IgE + Ag-induced adhesion to FN require extracellular calcium entry, whereas SF does not. Furthermore, our data suggest that FN acts synergistically with IgE to prolong intracellular phosphorylation events and to enhance IgE-induced inflammatory cytokine production and BMMC survival.

3T3 Cells↗

PubMed1987

Agonist- and voltage-gated calcium entry in cultured mouse spinal cord neurons under voltage clamp measured using arsenazo III.

Spinal cord neurons is dissociated cell culture were loaded with the calcium indicator arsenazo III using the whole-cell patch-clamp recording technique. Under voltage-clamp, depolarizing voltage steps evoked transient increases in absorbance at 660 nm, with no change at 570 nm, the isosbestic wavelength for calcium-arsenazo III complexes. The optical response occurred with a threshold depolarization to -30 mV, peaked at +10 mV, and decreased with further depolarization, consistent with an elevation of cytoplasmic free calcium resulting from Ca2+ flux through voltage-dependent calcium channels. Inward current responses to the excitatory amino acids N-methyl-D-aspartic acid (NMDA) and L-glutamate were also accompanied by calcium transients; these were dose-dependent, varied with the driving force for inward current, and were blocked by extracellular Mg2+ in a voltage-dependent manner, suggesting Ca2+ flux through NMDA-receptor channels. Responses to kainate, quisqualate, and GABA were not accompanied by comparable calcium transients. [Ca2+]i transients evoked by depolarizing voltage steps were of maximal amplitude at the start of recording and declined with time, reflecting rundown of voltage-dependent calcium channels. In contrast, [Ca2+]i transients evoked by NMDA gradually increased in amplitude during periods of whole-cell recording lasting 1-2 hr. Procedures resulting in loading of the neuron with Ca2+ accelerated the increase in amplitude of [Ca2+]i transients evoked by NMDA, but slowed the decay of [Ca2+]i transients evoked by voltage steps. Our results provide evidence for 2 independent sources of transmembrane Ca2+ flux in vertebrate neurons, through voltage-gated calcium channels and through NMDA-receptor channels. The Ca2+ flux gated by NMDA-receptor-specific agonists may play a role in synaptic plasticity, in regulating excitability, and in the excitotoxic response to excitatory amino acids.

Amino Acids↗

PubMed1993

Angiotensin II receptor subtypes and biological responses in the rat heart.

The distribution and function of AII receptor subtypes was evaluated in different preparations of rat hearts. Autoradiographic experiments and binding experiments on isolated membranes showed a large expression of [125I]Sar1,Ile8-AII binding sites in the atria of neonatal Wistar Kyoto rats which were predominantly of the AT2 subtype. Atrial and ventricular cells, isolated from neonatal rat hearts and maintained for 3 days in culture demonstrated primarily AT1 binding sites. Stimulation of cultured atrial cells with AII resulted in an increase in inositol phosphate turnover and in intracellular calcium. The latter action was completely abolished by Losartan. Finally, in atria isolated from 2-month-old rats, AII produced a 17-19% increase in contractile force that was completely abolished by Losartan but not by PD 123319, thus indicating the presence of functional AT1 receptors.

Angiotensin Receptor Antagonists↗

PubMed2005

Brief application of AF2 produces long lasting potentiation of nAChR responses in Ascaris suum.

Resistance of parasitic nematodes to the cholinergic anthelmintic levamisole is associated with a reduction in the proportion of time that acetylcholine receptor ion-channels are in the open state decreasing the response of nematode parasites to the drug. Here we examine electrophysiological and contractile responses to acetylcholine and the cholinergic agonist, levamisole, in Ascaris suum muscle looking for a pharmacological approach that may be developed to increase the response to cholinergic agonists. We found that short application of the FMRFamide, AF2, produced modulation (long lasting potentiation) of the peak membrane potential response to acetylcholine but not to levamisole. Since levamisole preferentially activates L-type acetylcholine receptors, we also tested the effect of nicotine (selective activator of N-type acetylcholine receptors) and bephenium (selective activator of B-type acetylcholine receptors) and found again no effect of AF2 on peak membrane potential responses. We then tested atropine on the AF2 potentiation of acetylcholine and found it to inhibit the peak potentiation suggesting that AF2 receptors interact with muscarinic receptors to produce the potentiation of acetylcholine. We saw similar atropine sensitive potentiation of acetylcholine responses in our muscle contraction experiments. The potentiation of the acetylcholine responses shows that nematode acetylcholine receptors are capable of a level of plasticity. A model involving calcium release from the sarcoplasmic reticulum, CaM Kinase, calcineurin, muscarinic receptors and AF2 receptors is proposed to explain our observations. These observations are important because they point to a pharmacological approach that may be developed to counter resistance to cholinergic anthelmintics.

Acetylcholine↗

PubMed1996

Intracellular calcium response to hydraulic pressure in human trabecular cells.

AIMS: To understand the mechanism for regulation of intraocular pressure, human trabecular cells were examined to determine whether they could respond to the change in hydraulic pressure. METHODS: Human trabecular cells were cultured from trabeculum tissue fragments excised during trabeculectomy in four eyes of three patients with primary open angle glaucoma and exposed to the change of hydraulic pressure in a tissue culture flask connected to a glass syringe. The pressure was exerted by automatic infusion of the piston of the syringe and monitored by a pressure gauge. The intracellular calcium concentration was measured in real time with a calcium binding fluorescent dye, fluo-3. RESULTS: A small number (about 10%) of cells appearing morphologically to be trabecular cells showed transient elevations or oscillations of the intracellular calcium concentration in response to the elevation of hydraulic pressure to 20-30 mm Hg, indicating that a part of the human trabecular cells could sense the change in hydraulic pressure. CONCLUSION: Some cells in the human trabecular tissue seem to sense the change in intraocular pressure and might play a role in its regulation.

Aged↗

PubMed2004

Irbesartan but not amlodipine suppresses diabetes-associated atherosclerosis.

BACKGROUND: It remains controversial whether specific blockade of the renin-angiotensin system confers superior antiatherosclerotic effects over other antihypertensive agents in diabetes. Therefore, the aim of this study was to compare equihypotensive doses of the angiotensin II subtype 1 (AT1) receptor blocker irbesartan with the calcium antagonist amlodipine on diabetes-induced plaque formation in the apolipoprotein E (apoE)-null mouse and to explore molecular and cellular mechanisms linked to vascular protection. METHODS AND RESULTS: Diabetes was induced by injection of streptozotocin in 6-week-old apoE-null mice. Diabetic animals were randomized to no treatment, irbesartan, or amlodipine for 20 weeks. Diabetes was associated with an increase in plaque area and complexity in the aorta in association with a significant increase in aortic AT1 receptor expression, cellular proliferation, collagen content, macrophage- and alpha-smooth muscle actin-positive cell infiltration, as well as an increased expression of platelet-derived growth factor-B (PDGF-B), monocyte chemoattractant protein-1 (MCP-1), and vascular cell adhesion molecule-1 (VCAM-1). Irbesartan but not amlodipine treatment attenuated the development of atherosclerosis, collagen content, cellular proliferation, and macrophage infiltration as well as diabetes-induced AT1 receptor, PDGF-B, MCP-1, and VCAM-1 overexpression in the aorta despite similar blood pressure reductions by both treatments. CONCLUSIONS: Diabetes-associated atherosclerosis is ameliorated by AT1 receptor blockade but not by calcium channel antagonism, providing further evidence for the vascular renin-angiotensin system playing a pivotal role in the development and acceleration of atherosclerosis in diabetes.

Amlodipine↗

PubMed2006

Inhibitory effects of magnolol on distal colon of guinea pig in vitro.

The influence of plant product magnolol (0-100 microM) on the contractile activity of isolated colonic muscle strips in guinea pig and related mechanism were investigated. Magnolol did not affect the base tone of colon muscle strips, but it dose-dependently inhibited 40 mM KCl-, 1 microM carbachol (CCh)- and 10 microM serotonin (5-HT)-induced contractions at concentrations higher than 10 microM. And also, magnolol inhibited the 5-HT- or CCh-induced muscle contraction in calcium-free buffer. Furthermore, magnolol inhibited the KCl-induced contraction under the condition of procaine. In addition, inhibition rate of nifedipine plus magnolol on muscle strips was lower than that of nifedipine alone. Moreover, magnolol dose-dependently decreased the velocity of pellet propulsion in the concentration range of 0.1-10 microM, and totally inhibited pellet propulsion at the concentration higher than 30 microM. Thus, it can be concluded that magnolol may 1) block receptor-operated cation channels and the voltage dependent Ca2+ channel, and 2) inhibit calcium release from the sarcolemmal membrane (SR) through blocking InsP3-sensitive and ryanodine-sensitive pathways. This explains, at least partially, that Cortex magnoliae officinalis exerts therapeutic effects on gastrointestinal disease through relaxation of GI tract smooth muscles.

Anesthetics, Local↗

PubMed2000

Pivotal role for acidic sphingomyelinase in cerebral ischemia-induced ceramide and cytokine production, and neuronal apoptosis.

Stroke is a major cause of long-term disability, the severity of which is directly related to the numbers of neurons that succumb to the ischemic insult. The signaling cascades activated by cerebral ischemia that may either promote or protect against neuronal death are not well understood. One injury-responsive signaling pathway that has recently been characterized in studies of non-neural cells involves cleavage of membrane sphingomyelin by acidic and/or neutral sphingomyelinase (ASMase) resulting in generation of the second messenger ceramide. We now report that transient focal cerebral ischemia induces large increases in ASMase activity, ceramide levels, and production of inflammatory cytokines in wild-type mice, but not in mice lacking ASMase. The extent of brain tissue damage is decreased and behavioral outcome improved in mice lacking ASMase. Neurons lacking ASMase exhibit decreased vulnerability to excitotoxicity and hypoxia, which is associated with decreased levels of intracellular calcium and oxyradicals. Treatment of mice with a drug that inhibits ASMase activity and ceramide production reduces ischemic neuronal injury and improves behavioral outcome, suggesting that drugs that inhibit this signaling pathway may prove beneficial in stroke patients.

Animals↗

PubMedDate not supplied

[Comparative characteristics of the activity of lithium preparations and anti-arrhythmia agents in strophanthin, calcium chloride and barium chloride arrhythmias in an experiment].

During disorders of cardiac rhythm induced by strophanthine K in anesthesized cats, by calcium chloride in mice and anesthesized rats, and by barium chloride in rabbits, lithium hydroxybutyrate (0.55-3.2 mg/kg according to cation) compares very favourably with lithium chloride, novocainamide, lidocaine, trimecaine, etmozine, quinidine and verapamil as regards antiarrhythmic activity and the range of therapeutic action.

Animals↗

PubMed1998

Phosphate-binding capacities of calcium and aluminum formulations.

Calcium and aluminum phosphate binders are used to treat hyperphosphatemia which is responsible for the development of osteodystrophy commonly seen in patients with end-stage renal disease. The purpose of this study was to determine the phosphate binding capacities of several frequently used calcium and aluminum formulations. The effect of formulation types on phosphate binding was evaluated. Calcium and aluminum phosphate binders were administered to six healthy volunteers after phosphate load on separate study days. Total urine outflow was collected afterwards to determine the amount of phosphate recovered, which indicates the ability of the phosphate binder to reduce gastrointestinal phosphate absorption. The amounts of urinary phosphate recovered were different after administration of the phosphate binders. Calcium acetate resulted in the least amount of phosphate excreted. Calcium carbonate suspension, when compared with the tablet formulation, caused a smaller amount of phosphate excreted in the urine. Different phosphate binders formulations were found to have different phosphate binding capacities. Patients should therefore be closely monitored for efficacy after switching from one phosphate binder to another.

Acetates↗

PubMed2000

Dentin bonding and sealing ability of a new root canal resin sealer.

The aims of this study were to find a dentin bonding system suitable for root canal treatment using a newly developed root canal resin sealer, and to examine its sealing ability. The sealer was composed of vinylidene fluoride/hexafluoropropylene copolymer, methyl methacrylate, zirconia, and tributylborane catalyst. The effects of dentin conditioners and primers on dentin bonding were studied by tensile bond strength testing and scanning electron microscopy. Apical and coronal leakage were evaluated at 1-, 4-, and 12-wk intervals by a dye penetration test using a methylene blue solution. Pulp Canal Sealer EWT and Sealapex were used as controls. Significantly high bond strength was obtained by treating dentin with EDTA, followed by application of a glutaraldehyde/2-hydroxyethyl methacrylate primer. The experimental resin sealer produced a significantly superior coronal seal at 12 wk when compared with the two control sealers (p < 0.05). Scanning electron microscopic examination revealed few gaps at the resin sealer-dentin interface.

Alkenes↗

PubMed1999

Calcium-dependent PAF-stimulated generation of reactive oxygen species in a human keratinocyte cell line.

During inflammation and other pathological states, the lipid mediator platelet-activating factor (PAF) and reactive oxygen species (ROS) are both generated. We have been investigating the effect of exogenous PAF on ROS formation in the human keratinocyte cell line (HaCaT). ROS production, measured using luminol-enhanced chemiluminescence (CL), proved to be rapid, transient, PAF receptor-mediated, and totally dependent on an increase in intracellular Ca2+ ([Ca2+]i) and on the presence of extracellular Ca2+. Repeated administration of PAF resulted in refractoriness to the agonist in terms of both capacities to increase [Ca2+]i and generate ROS. The cells, however, continued to respond fully to other stimulants (bradykinin, epidermal growth factor, thapsigargin). The PAF-induced increases in [Ca2+]i (monitored using the fluorescent probe Fluo-3) were also rapid and transient and paralleled those of ROS generation. Relatively specific inhibitors of potential ROS-producing systems were administered in an attempt to characterize the ROS producing system(s). Inhibitors of xanthine oxidase, phospholipase A2, lipoxygenase, cyclooxygenase and NO synthase did not interfere with PAF evoked ROS. The flavoprotein inhibitor diphenyleneiodonium and the mitochondrial cytochrome oxidase inhibitor KCN, prevented generation of ROS, making NAD(P)H a candidate for the electron source of the ROS and the mitochondria a potential major site of formation.

Aniline Compounds↗

PubMed2005

Regulation of skeletal muscle fiber type and slow myosin heavy chain 2 gene expression by inositol trisphosphate receptor 1.

Innervation-dependent signaling cascades that control activation of downstream transcription factors regulate expression of skeletal muscle fiber type-specific genes. Many of the innervation-regulated signaling cascades in skeletal muscle are dependent on intracellular calcium and the mechanisms by which calcium is released from the sarcoplasmic reticulum (SR). We report that the inositol trisphosphate receptor 1 (IP3R1), responsible for calcium release from the SR as a slow wave, was more abundant in fast contracting compared to slow contracting avian muscle fibers. Furthermore, inhibition of IP3R1 activity by 2-aminoethoxydiphenylborate (2-APB) and xestospongin D induced a fiber type transition and expression of the slow myosin heavy chain 2 (slow MyHC2) gene in innervated fast muscle fibers. Activation of the slow MyHC2 promoter by IP3R1 inhibition was accompanied by a reduction in protein kinase C activity. In addition, inhibition of IP3R1 activity resulted in a reduction of nuclear factor of activated T cells (NFAT)-dependent transcription and nuclear localization, indicating that IP3R1 activity regulated NFAT transcription factor activity in skeletal muscle fibers. Myocyte enhancer factor 2 (MEF2)-dependent transcriptional activity was increased by innervation, but unaffected by IP3R1 activity. The results indicate that IP3R1 activity regulates muscle fiber type-specific gene expression in innervated muscle fibers.

Animals↗

PubMed1999

Hyperpolarization-activated inward potassium and calcium-sensitive chloride currents in beating pacemaker insect neurosecretory cells (dorsal unpaired median neurons).

Hyperpolarization-activated inward currents were studied in single adult cockroach Periplaneta americana pacemaker neurosecretory cells, identified as dorsal unpaired median neurons using the whole-cell patch-clamp technique. Under current clamp, injection of negative current produced a hyperpolarization of the cell membrane with a sag in the membrane potential toward the resting value. Under voltage clamp, the whole-cell current-voltage relationship exhibited an unexpected biphasic aspect. The global hyperpolarization-activated inward current could be dissociated by means of 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid and tetraethylammonium chloride sensitivity, ionic selectivity, voltage dependence and activation threshold as inward potassium and calcium-sensitive chloride currents. The inward potassium current was activated around -80 mV. The reversal potential followed the potassium equilibrium potential when the extracellular potassium concentration was raised. This current was not dependent on the external sodium concentration and was sensitive to 10 mM tetraethylammonium chloride or 5 mM barium chloride. The hyperpolarization-activated inward calcium-sensitive chloride current was activated in a range of potential 20 mV more positive than the potassium current. The estimated reversal potential (-71 mV) was very close to the equilibrium potential for chloride ions ( 73 mV). Intracellularly applied 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid and external application of 1 mM zinc chloride, calcium-free saline or high concentrations of intracellular 1,2-bis-(2-aminophenoxy)ethane-N,N,N',N'-tetra-acetate blocked the inward chloride current. Current-clamp experiments indicated that the inward potassium current accounted for inward rectification of dorsal unpaired median neurons. Our findings report, for the first time in pacemaker neurosecretory cells, the co-existence of two distinct hyperpolarization-activated inward currents which have specialized function in pacemaker activity.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1992

Activation of a single alpha-1-adrenoceptor subtype in rat aorta mobilizes intracellular and extracellular pools of calcium.

The calcium channel antagonist, nifedipine (0.1 microM), only slightly inhibited the response to the full alpha 1-adrenoceptor agonist, (-)-norepinephrine, in rat aorta, but nearly completely inhibited the response to the partial alpha 1-adrenoceptor agonist, (-)-dobutamine, indicating that (-)-norepinephrine primarily utilizes intracellular stores of calcium to produce vasoconstriction, whereas (-)-dobutamine relies primarily upon the translocation of extracellular calcium. It has been proposed that the different pools of calcium mobilized by (-)-norepinephrine and (-)-dobutamine in rat aorta result from the activation of two different alpha 1-adrenoceptor subtypes by these agonists. Because the irreversible alpha 1-adrenoceptor antagonist, phenoxybenzamine, has been proposed to inactivate an alpha 1-adrenoceptor subtype coupled specifically to the mobilization of intracellular stores of calcium, this compound should selectively inhibit the response of (-)-norepinephrine, and not the response of (-)-dobutamine, if two distinct alpha 1-adrenoceptor subtypes exist in rat aorta. In the present study, phenoxybenzamine produced concentration-dependent, noncompetitive inhibition of the responses to both agonists in rat aorta, and the pA2' values for phenoxybenzamine were 8.12 +/- 0.23 and 7.74 +/- 0.27 against (-)-dobutamine and (-)-norepinephrine, respectively, which are not significantly different from each other (p greater than 0.05). In addition, the phasic and tonic components of the response to (-)-norepinephrine, which are mediated by the mobilization of intracellular calcium and the translocation of extracellular calcium, respectively, are also inhibited to the same extent by phenoxybenzamine. The results do not support the hypothesis of two alpha 1-adrenoceptor subtypes in rat aorta, one of which being coupled to the translocation of extracellular calcium, and the other to the mobilization of intracellular calcium. Rather, the results support our previous hypothesis that a single alpha 1-adrenoceptor subtype exists in vascular smooth muscle, and this alpha 1-adrenoceptor is coupled to two distinct signal transduction processes, one of which elicits the mobilization of intracellular calcium, and the other opens membrane calcium channels to permit the influx of extracellular calcium.

Animals↗

PubMed2001

Mechanism of action of angiotensin II in human isolated subcutaneous resistance arteries.

1. Human isolated subcutaneous arteries were mounted in a myograph and isometric tension measured. In some experiments, intracellular calcium [Ca(2+)]i was also measured using fura-2. 2. Angiotensin II (100 pM - 1 microM) increased [Ca(2+)]i and tone in a concentration-dependent manner. The effects of angiotensin II (100 nM) were inhibited by an AT1-receptor antagonist, candesartan (100 pM). 3. Ryanodine (10 microM), had no effect on angiotensin II-induced responses, but removal of extracellular Ca(2+) abolished angiotensin II-induced rise in [Ca(2+)]i and tone. Inhibition of Ca(2+) entry by Ni(2+) (2 mM), also inhibited angiotensin II responses. The dihydropyridine, L-type calcium channel antagonist, amlodipine (10 microM), only partially attenuated angiotensin II responses. 4. Inhibition of protein kinase C (PKC) by chelerythrine (1 microM), or by overnight exposure to a phorbol ester (PDBu; 500 nM) had no effect on angiotensin II-induced contraction. 5. Genistein (10 microM), a tyrosine kinase inhibitor, inhibited angiotensin II-induced contraction, but did not inhibit the rise in [Ca(2+)]i, suggesting that at this concentration it affected the calcium sensitivity of the contractile apparatus. Genistein did not affect responses to norepinephrine (NE) or high potassium (KPSS). 6. A selective MEK inhibitor, PD98059 (30 microM), inhibited both the angiotensin II-induced contraction and rise in [Ca(2+)]i, but had no effect on responses to NE or KPSS. 7. AT1 activation causes Ca(2+) influx via L-type calcium channels and a dihydropyridine-insensitive route, but does not release Ca(2+) from intracellular sites. Activation of tyrosine kinase(s) and the ERK 1/2 pathway, but not classical or novel PKC, also play a role in angiotensin II-induced contraction in human subcutaneous resistance arteries.

Amlodipine↗

PubMed1995

Molecular sieves: an alternative method of carbon dioxide removal which does not generate compound A during simulated low-flow sevoflurane anaesthesia.

Molecular sieves are used in industry to 'scrub' industrial gases. We examined, during simulated low-flow closed system anaesthesia, (1) the carbon dioxide adsorbing potential of molecular sieves and (2) the reactivity of the sieves compared to soda lime using sevoflurane as an indicator. A low-flow anaesthetic system containing 13X molecular sieves was connected to a model lung. End-tidal concentrations of CO2 were measured continuously at an O2 flow of 800 ml.min-1 and a CO2 flow of 200 ml.min-1. In the second study, sevoflurane (FE'sevo 1.7%) was added to the system after which samples were taken from the inspiratory limb of the anaesthetic system. This experiment was performed both during carbon dioxide removal with soda lime and with the molecular sieves. The samples were stored in gas-tight syringes and analysed by gas chromatography. The temperature of both absorbents was measured throughout the study. The molecular sieves adsorbed carbon dioxide (20%) efficiently for a period of 5 h. There was a gradual increase from the baseline of 4.4% to 4.5, 5.4, and 6.0% at 90, 180, and 300 min, respectively. When sevoflurane was added to the system, compound A was detected at the start of both experiments. However, when soda lime was used the concentrations of compound A increased 10-fold after 2.5 h compared with baseline values. No increase in compound A was observed when molecular sieves were used for carbon dioxide removal. The highest mean (SD) temperature of the molecular sieves was 41.5 (3.2) degrees C. Molecular sieves are effective adsorbents of carbon dioxide when used in a simulated low-flow, closed anaesthetic system.(ABSTRACT TRUNCATED AT 250 WORDS)

Adsorption↗