[Clinical experience in the management of dermatomycoses using the 1 per cent econazole-spray solution and the 1 per cent econazole-spray powder].
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Adult↗
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Results for “Econazole”
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Multiple effects of econazole on calcium signaling: depletion of thapsigargin-sensitive calcium store, activation of extracellular calcium influx, and inhibition of capacitative calcium entry.
The effect of econazole on intracellular calcium levels ([Ca2+]i) in Madin Darby canine kidney cells was investigated using fura-2 fluorimetry. Econazole increased [Ca2+]i dose-dependently at 5-50 microM. The Ca2+ signal consisted of an initial rise, a gradual decay and a sustained plateau. Extracellular Ca2+ removal partially reduced the econazole response. Mn2+ quench of fura-2 fluorescence confirmed econazole-induced Ca2+ influx. The econazole-sensitive intracellular Ca2+ store overlaps with that sensitive to thapsigargin, an inhibitor of the endoplasmic reticulum Ca2+ pump, because 25 microM econazole depleted the thapsigargin-sensitive store, and conversely, thapsigargin abolished the econazole response. Econazole (25-50 microM) partially inhibited capacitative Ca2+ entry induced by cyclopiazonic acid, another endoplasmic reticulum Ca2+ pump inhibitor, measured by depleting internal Ca2+ store in Ca(2+)-free medium followed by adding 10 mM CaCl2. Econazole induced capacitative Ca2+ entry itself. Pretreatment with La3+ (100 microM) partially inhibited 25 microM econazole-induced Mn2+ quench of fura-2 fluorescence, and La3+ immediately reduced 20 microM econazole-induced Ca2+ signal when added at the peak of the signal, suggesting that econazole induced Ca2+ influx via two separate pathways: one is sensitive to La3+, the other is not. La3+ enlarged 25 microM econazole-induced [Ca2+]i transient during the decay phase. The econazole response was not altered when the cytosolic level of inositol 1,4,5-trisphosphate was inhibited by the phospholipase C inhibitor U73122.
Animals↗
Effects of econazole on receptor-operated and depolarization-induced contractions in rat isolated aorta.
In our previous study, econazole caused a decrease in serum nitrite levels in septic mice in vivo, but it enhanced the mortality rate. The aim of the study was to investigate the in vitro effects of econazole on receptor-operated and depolarization-induced contractions on endothelium-intact and -denuded rat isolated aorta. Econazole (0.1, 1 and 10 microM) significantly inhibited receptor-operated (phenylephrine, Phe) and depolarization (KCl)-induced contractions of endothelium-intact or -denuded rings in a noncompetitive and concentration-dependent manner. Removal of endothelium changed the pD'2 values only for KCl-induced responses. The pD'2 values of L-type calcium channel blocker nifedipine were significantly higher than the econazole on Phe concentration-response curves in endothelium-intact and -denuded rings. Econazole caused a biphasic response in precontracted by Phe or KCl in endothelium-intact and -denuded rings, first a transient contraction following sustained relaxation. Removal of endothelium did not affect the contractile responses induced by Phe. The contractile responses induced by 10 microM econazole in the KCl-precontracted rings were antagonized by the treatment of alpha-adrenergic receptor antagonist, phentolamine (10 microM). Deendothelization was significantly increased the IC50 values of econazole obtained from Phe- and KCl-precontractions. The relaxations induced by 10 microM econazole in endothelium-intact rings precontracted with Phe or KCl were not changed by NO synthase inhibitor, L-N(G)-nitroarginine (100 microM). The IC50 values of econazole were significantly higher than nifedipine in endothelium-intact and -denuded rings. These results suggest that econazole is a noncompetitive antagonist on alpha1-adrenoceptor-mediated and depolarization-induced contractions in rat isolated aorta by inhibiting Ca2+ entry through L-type calcium channels, and the endothelium seems to modulate vascular responses induced by this agent. The vascular effects of econazole may limit the usage of this agent in septic shock.
Animals↗
Extracellular site for econazole-mediated block of Ca2+ release-activated Ca2+ current (Icrac) in T lymphocytes.
1. Standard whole cell patch clamp recording techniques were used to study the pharmacological characteristics and site of econazole-mediated inhibition of calcium release-activated calcium current (Icrac) in the human leukaemic T cell line, Jurkat. 2. Extracellularly applied econazole blocked Icrac in a concentration-dependent manner (IC50 approximately 14 microM). Block developed over a relatively slow timecourse of 30-60 s (10 microM), and only partially reversed over minutes. 3. Econazole dialysed from the pipette into the cytosol at concentrations ranging from 0.1 to 30 microM did not reduce Icrac, or quantitatively affect Icrac block by extracellularly applied econazole. 4. A less lipophilic quaternary iodide derivative of econazole was synthesized to retard absorption through the cell membrane. When applied extracellularly, this compound blocked Icrac in a concentration-dependent manner with onset kinetics comparable to econazole. 5. Results with intracellularly dialysed econazole and the quaternary econazole derivative provide convergent evidence that econazole blocks Icrac via an extracellular interaction. 6. The inability of intracellularly applied econazole to inhibit Icrac argues against the notion that econazole inhibits capacitative Ca2+ entry pathways secondary to its known inhibitory effects on cytochrome P-450.
Calcium↗
Functional effects of econazole on inducible nitric oxide synthase: production of a calmodulin-dependent enzyme.
1. We performed experiments to examine the effects of an anti-fungal imidazole compound, econazole, on the regulation and effects of lipopolysaccharide-inducible nitric oxide synthase (iNOS) activity in rat aortic rings and cultured J774 murine macrophage cells. 2. In endothelium-intact rings of thoracic aorta, phenylephrine caused a concentration-dependent contraction with EC50 of 1.9 +/- 0.15 x 10(-8) M (n = 5). Following incubation with lipopolysaccharide (LPS, 5 micrograms ml-1) for 8 h there was a right-shift in the concentration-response curve (EC50 3.1 +/- 0.28 x 10(-7) M, P < 0.05) with a depression in the maximum contraction from 1.44 +/- 0.25 g to 0.86 +/- 0.26 g (n = 4). Co-incubation of rings with econazole (1 x 10(-5) M) partially inhibited the LPS-induced loss of reactivity to phenylephrine (EC50 6.5 +/- 0.72 x 10(-8) M) and fully inhibited the reduction in maximum tension (1.49 +/- 0.19 g; n = 5). 3. In J774 cells, incubation with LPS (10 micrograms ml-1, 24 h) resulted in significant nitrite production that was inhibited by co-incubation with econazole (IC50 5.0 +/- 0.9 x 10(-6) M; n = 5). In cells stimulated with LPS, production of L-[3H]-citrulline from L-[3H]-arginine was 6.41 +/- 0.22 pmol mg-1 protein min-1 (n = 3). This was inhibited by 92 +/- 6% by addition of NG-monomethyl-L-arginine (L-NMMA, 1 x 10(-3) M; n = 3) to the homogenate but not by econazole (1 x 10(-5) M; n = 3). In contrast pretreatment of cells with econazole (1 x 10(-5) M) markedly reduced the LPS-induced [3H]-citrulline production (0.86 +/- 0.053 pmol mg-1 protein min-1; P < 0.01; n = 3). 4. In cells treated with LPS and econazole, L-[3H]-citrulline production was restored in a concentration-dependent manner by addition of calmodulin (1 x 10(-8)-3 x 10(-7) M) with an IC50 of 4.2 +/- 0.9 x 10(-8) M. 5. We have shown that econazole inhibits the functional and biochemical activity of iNOS in rat aortic rings and cultured J774 cells. Treatment of cells with econazole renders the NO synthase functionally inactive. In econazole-treated cells enzyme activity is restored by calmodulin suggesting that econazole may inhibit the binding of this essential co-factor to the enzyme following its production. These studies may have implications for the design of novel anti-inflammatory agents working through the L-arginine-nitric oxide pathway.
Animals↗
Enhanced econazole penetration into human nail by 2-n-nonyl-1,3-dioxolane.
This study determines the enhancing effects of 2-n-nonyl-1,3-dioxolane on the penetration of econazole, an antifungal drug, into the deeper layers of the human nail where fungal infection resides. Aliquots (10 microL) of Econail lacquer formulation containing 0.45 mg of [(14)C]-econazole with 18% 2-n-nonyl-1,3-dioxolane (test group) or without 2-n-nonyl-1,3-dioxolane (control group) were applied twice daily for 14 days to human nails that had been washed with ethanol before each morning's application. The hydration of the nail sample was well controlled to simulate normal physiological conditions. After 14 days of dosing, the inner ventral section of the nail plate was assayed for absorbed drug content, using a micrometer-controlled drilling and nail powder removal system. The mass balance values of [(14)C]-econazole in this study were 90.8 and 96.4% for the test and control groups, respectively. The weight-normalized econazole content in the ventral/intermediate nail plate center in the test group was 6-fold greater than that in the control (p = 0.008). The total econazole absorbed into the supporting bed cotton ball in the test group was nearly 200-fold greater than that in the control group (p = 0.008) over the 14-day period. The amount of econazole after dosing in the inner part of the human nail (potential diseased area) was 11.1 +/- 2.6 (SD) microg/mg of nail powder with 2-n-nonyl-1,3-dioxolane in the lacquer and 1.78 +/- 0.32 microg/mg without 2-n-nonyl-1,3-dioxolane (p = 0.008). The surface nail contained more econazole (p = 0.004), that is, nonabsorbed drug, where 2-n-nonyl-1,3-dioxolane was not part of the dosing solution. Econazole in the support bed under the nail (the total absorbed dose) was 47.5 +/- 22.0 mg in the lacquer with 2-n-nonyl-1,3-dioxolane and 0.2 +/- 0.1 mg in the lacquer without 2-n-nonyl-1,3-dioxolane (p = 0.008). Moreover the concentration in the deep nail layer in the test group is 14,000 times higher than minimum inhibitory concentration (MIC) believed necessary to inhibit the growth of infecting fungi (Dermatophytes species). In a subsequent study, [(14)C]-dioxolane did not penetrate the nail well. Therefore, the mechanism of enhancement of econazole penetration is at the formulation/nail interface.
Administration, Topical↗
Econazole: a review of its antifungal activity and therapeutic efficacy.
Econazole1 is a recently introduced imidazole antifungal agent which is very closely related structurally to another imidazole derivative, miconazole. For local application the nitrate salt of econazole is used, while in preliminary investigations of systemic use in a few patients econazole base has been administered orally or intravenously. In uncontrolled studies in large numbers of patients, econazole nitrate has been administered topically in the treatment of dermatomycoses due to a wide variety of fungi, and vaginally in the treatment of vaginal candidosis; but it has not been compared with any other antifungal drug in controlled therapeutic trials in mycoses of the skin and has only been compared with nystatin in a few patients with vaginal candidosis. Until adequate comparative studies are done the relative place of econazole in the treatment of dermatomycoses and vaginal condidosis, compared with traditional antifungal agents and with other imidazole derivatives such as miconazole or clotrimazole, cannot be clearly stated. Nevertheless, econazole nitrate is an effective antifungal drug. In dermatological studies about 90% of a large number of patients were cured, often after a relatively short treatment period (2 to 6 weeks, as occurs with other imidazole antifungal agents). The cure rate was only slightly lower (about 85%) in patients with severe mycoses of many years' duration than in those whose infections were of more recent onset. In vaginal candidosis a 3-day treatment regimen using a 150mg suppository once daily was only slightly less effective (85% mycological cure rate) than a 15-day regimen using a 50mg dose (suppository or cream) once daily (90% cure rate). A 3 to 5 day 'higher' dose regimen was slightly more effective than a standard 15-day regimen of nystatin vaginal inserts in a small group of patients with vaginal candidosis. The convenience of the higher-dose shorter term regimen would likely be an important advantage to most patients. Whether other agents useful in vaginal candidosis would be as effective as econazole were they to be used in this way, has not been determined. Topical or intravaginal econazole nitrate has usually been well tolerated, side effects being limited to local irritation in about 1 to 4% of patients in most studies.
Adult↗
[Effects of econazole and clotrimazole on TXB2 and PGE2 production in calcimycin-stimulated neutrophils and arachidonic acid-stimulated platelets].
The effects of econazole and clotrimazole which are used as antifungal agents, on TXB2 and PGE2 production in calcimycin (A-23187)-stimulated rat pleural neutrophils and arachidonic acid (AA)-stimulated washing rabbit platelets were examined by radioimmunoassay. Econazole and clotrimazole 0.05-100 mumol.L-1 inhibited TXB2 production both in rat pleural neutrophils and in rabbit platelets with a dose-dependent manner. The most potent inhibition was found in rabbit platelets. At the concentration of 50 mumol.L-1, econazole and clotrimazole were sufficient to inhibit TXB2 production in rabbit platelets by up to 99% and 98% respectively. Econazole and clotrimazole 0.05-5 mumol.L-1 also increased PGE2 biosynthesis in rabbit platelets. But econazole and clotrimazole 50 mumol.L-1 reduced the PGE2 production in rabbit platelets to 11% and 37% of the amounts of 5 mumol.L-1 econazole and clotrimazole respectively. The results suggest that econazole and clotrimazole at lower concentration may have a selective inhibitory effect on thromboxane synthetase, at higher concentration they also inhibit cyclooxygenase.
Animals↗
Econazole and clotrimazole in the treatment of vaginal candidiasis: a double blind comparative study.
OBJECTIVES: To compare the efficacy of treatment with econazole and clotrimazole in patients with vaginal candidiasis. DESIGN: A double blind study. Patients with vaginal candidiasis were randomly treated with vaginal depot preparations of econazole and clotrimazole. Efficacy after treatment by reduction of symptoms, a gynaecological examination and microbiological analysis of vaginal fluid. Adverse reactions were noted. SETTING: University gynaecological clinic at the de Soysa Hospital for Women, Colombo. PATIENTS: 102 patients microbiologically confirmed as having vaginal candidiasis. RESULTS: Two weeks after econazole treatment 19% still complained of a discharge and 7.5% had pruritus. The respective values for clotrimazole were 18% and 12%. The finding on gynaecological examination generally supported the reduction of symptoms. Microbiological assessment showed that 90.5% in the econazole group and 96% in the clotrimazole group became culture negative at two weeks after treatment. Adverse effects were similar in incidence and number for both treatment groups. Econazole was less acceptable to patients than clotrimazole. CONCLUSIONS: Econazole and clotrimazole are of equal efficacy for treatment of vaginal candidiasis. Econazole was less acceptable to patients.
Adolescent↗
Effects of econazole nitrate on yeast cells and mitochondria.
The inhibitory effect of econazole nitrate on the growth of yeast Saccharomyces cerevisiae is proportional to the concentration of the product. It depends on the phase of culture and on the number of cells present at the moment of econazole addition into the medium. The most important inhibition is obtained in the exponential phase of growth with a low concentration of cells. It is enhanced with cells which were previously in contact with the product. There is no adaptation of the yeast toward increased concentrations of econazole. The product penetrates the cells and attaches first to particular fractions, later to soluble fractions. The highest concentration of econazole nitrate in cells lies in the mitochondria. No product of econazole metabolism by S. cerevisiae was uncovered. Econazole nitrate does not slow down the in vivo activities of mitochondrial enzymes (cytochrome c oxidase, succinate dehydrogenase and phenylalanyl-tRNA synthetase), but inhibits the biosynthesis of mitochondrial membrane enzymes without affecting that of the synthetase, a matrix enzyme.
Chromatography, Thin Layer↗
Topical treatment of vaginal candidosis with sertaconazole and econazole sustained-release suppositories.
OBJECTIVE: To compare the efficacy and safety of sertaconazole and econazole sustained-release suppositories in the treatment of vulvovaginal candidosis. STUDY DESIGN: 369 women with symptoms and signs of vulvovaginitis were enrolled in this multicenter, randomized, double-blind study. After clinical examination and vaginal sampling, 183 women were treated with a 300-mg sertaconazole suppository and the other 186 with a 150-mg econazole suppository. They were evaluated 1 week after treatment and those who were clinically uncured received a second suppository and were re-assessed 1 week later. All women were evaluated 1 month after the last administration. At each follow-up visit, clinical efficacy was assessed and a vaginal sampling was performed for microscopic examination and culture. RESULTS: Of the 369 women included, only the 310 who had a positive culture for a strain of Candida were taken into account for efficacy analysis: 150 in the sertaconazole group and 160 in the econazole group. One hundred and five women (49 in the sertaconazole group and 56 in the econazole group) were not clinically cured after 1 week and received a second suppository. There were no differences between the two groups for the rates of clinical recovery (disappearance of signs and symptoms) and mycological recovery (negative culture), 1 week after the first application (62.1 and 67.7%, respectively), 1 week after the second application for women treated twice (72.3 and 80.6%, respectively) and for all patients 1 month after the last application (65.3 and 62.0%, respectively). Among the patients cured 1 week after the last application, the mycological recurrence rate after 1 month was significantly higher in the econazole group (32.7 vs. 19.8%, P=0.035). There was a trend towards better efficacy of sertaconazole after the first application, whereas the two treatments had similar efficacy in women treated twice. There were no serious adverse events and only local irritation was reported, without any statistically significant difference between the two groups. CONCLUSION: Single topical administration of sertaconazole and econazole had similar efficacy and safety but the former is associated with a lower rate of mycological recurrence one month after achieving a negative culture.
Administration, Intravaginal↗
Evaluation of in vitro activity of ciclopirox olamine, butenafine HCl and econazole nitrate against dermatophytes, yeasts and bacteria.
BACKGROUND: In many instances, a cutaneous fungal infection may exist concomitantly with bacterial involvement. In this study we compared the in vitro activity of three antifungal agents against the dermatophytes, yeasts and bacteria recovered most commonly from cutaneous mycoses and bacterial infections. METHODS: Using a microdilution method adapted from the National Committee for Clinical Laboratory Standards (NCCLS), we determined the minimum inhibitory concentrations (MICs) of ciclopirox olamine, econazole nitrate and butenafine HCl against a panel of dermatophyte fungi and yeasts (n = 39) and bacterial isolates (n = 45). RESULTS: All three antifungals demonstrated comparable activity against the dermatophytes tested, with a MIC range of 0.03-0.25 micro g/ml for ciclopirox, < 0.001-0.25 micro g/ml for econazole and 0.03-0.25 micro g/ml for butenafine. For yeasts, ciclopirox showed activity against all isolates, with an MIC range of 0.001-0.25 micro g/ml, whereas econazole had a broader range of 0.125-> 0.5 micro g/ml. Butenafine displayed limited activity against the yeast Candida albicans and no activity against Malassezia furfur. For the antibacterial activity studies, ciclopirox demonstrated activity against all isolates tested with a range of 0.06-2 micro g/ml, while econazole showed activity against Gram-positive bacteria only, with a MIC range of 0.004-0.25 micro g/ml. Butenafine HCl had a limited activity against bacterial isolates tested, showing activity against beta-hemolytic Streptococcus Group A and Corynebacterium only. Neither econazole nitrate nor butenafine HCl demonstrated activity against any of the Gram-negative strains evaluated in this study. CONCLUSIONS: The data suggest that ciclopirox olamine has the broadest in vitro activity, in comparison to econazole and butenafine HCl, against bacteria, yeasts and bacteria. These findings may have implications in the use of these antimycotics in the treatment of mixed cutaneous infections where bacteria or yeasts are present in addition to dermatophytes.
Antifungal Agents↗
Hepatoprotective and therapeutic effects of tetramethylpyrazine on acute econazole-induced liver injury.
2,3,5,6-Tetramethylpyrazine (TMP) is well known as a true calcium antagonist. The aim of this study was to investigate the hepatoprotective and therapeutic effects of TMP on acute econazole-induced liver injury. The hepatological effect of various concentrations of TMP was first assessed by the biochemical assays of SGOT and SGPT and then by hepatohistological microscopic examination. The dose-response relationship of liver injury induced by various doses of econazole was observed simultaneously from serum biochemical assay of SGOT and SGPT, and also from hepatohistological microscopic examination, by determination of the hepatoprotective effects of various concentrations of TMP on SGOT and SGPT elevation induced by a hepatotoxic dose of econazole (300 mg/kg). The inhibitory effect of various concentrations of TMP or vitamin E (positive control, 0.5 mM in vitro, 0.69 mM in vivo) on FeCl 2 -induced (in vitro) or econazole-induced (in vivo) lipid peroxidation was also investigated. The superoxide scavenging activity of various concentrations of TMP in econazole-damaged rat liver homogenate was assessed by the cytochrome C reduction method. Results showed that the hepatoprotective effect of TMP might be, at least in part, due to its inhibitory ability on membrane lipid peroxidation and free radical formation, or due to its free radical scavenging ability. Improvement of serum transaminases and MDA levels in rat liver homogenate, hepatohistological microscopic examination, and assessment of free radical scavenging activity by the cytochrome C reduction method were used to detect hepatoprotective and therapeutic effects of TMP on acute econazole-induced liver injury.
Acute Disease↗
Three-day therapy of vaginal candidiasis with clotrimazole vaginal tablets and econazole ovules: a multicenter comparative study.
The activity and tolerance of 200 mg clotrimazole vaginal tablets and 150 mg econazole vaginal ovules were compared in the treatment of vaginal candidiasis in a controlled multicenter (3 centers) study. Treatment was allocated according to a randomized list and each investigator treated 20 patients per group. Duration of therapy was 3 days. Follow-up investigations were carried out approximately 1 and 4 weeks after commencement of treatment. The results were analyzed for 54 patients treated with clotrimazole and 57 with econazole; 9 patients were excluded from the analysis because of insufficient data. At the first follow-up examination, 1 week after starting therapy, 93.7% of patients on clotrimazole and 83.7% of patients on econazole had negative cultures. The success of therapy, as judged by the clinicians, was 95.8% for clotrimazole and 88.0% for econazole. For the first and fourth week combined reviews, 86.0% of clotrimazole patients and 77.8% of econazole patients had negative cultures and the success of therapy was 88.4% for clotrimazole and 80.0% for econazole. These differences were not statistically significant but there was a clear numerical superiority for clotrimazole. Tolerance was good in all the patients and no side-effects were observed. One can conclude that the treatment of vaginal candidiasis with a 200-mg vaginal tablet of clotrimazole over 3 days is highly effective and comparable with other established treatment regimes.
Adolescent↗
Three-day therapy of vaginal candidiasis with clotrimazole vaginal tablets and econazole ovules: a multicentre comparative study.
The activity and tolerance of 200 mg clotrimazole vaginal tablets and 150 mg econazole vaginal ovules were compared in the treatment of vaginal candidiasis in a controlled multicentre (3 centres) study. Treatment was allocated according to a randomized list and each investigator treated 20 patients per group. The duration of therapy was 3 days. Follow-up investigations were carried out approximately 1 week and 4 weeks after commencement of treatment. The results were analyzed for 54 patients treated with clotrimazole and 57 with econazole: 9 patients were excluded from the analysis because of insufficient data. At the first follow-up examination, 1 week after starting therapy, 93.7% of patients on clotrimazole and 83.7% of patients on econazole had negative cultures. The success of therapy, as judged by the clinicians, was 95.8% for clotrimazole and 88.0% for econazole. For the first and fourth week combined reviews, 86.0% of clotrimazole patients and 77.8% of econazole patients had negative cultures and the success of therapy was 88.4% for clotrimazole and 80.0% for econazole. These differences were not statistically significant but there was a clear numerical superiority for clotrimazole. Tolerance was good in all the patients and no side-effects were observed.
Adolescent↗
An imidazole derivative (Econazole) as an antifungal agent in cell culture systems.
Econazole, an imidazole derivative, was tested as an antifungal agent in different cell culture systems. In comparison with Fungizone, Econazole has the following advantageous properties: higher stability, higher solubility, better antifungal activity against contaminants of cell cultures and a wider range between minimal inhibitory to cytotoxic concentration with Aspergillus fumigatus, Candida albicans and Penicillium sp., activity against gram-positive bacteria and lower price. Econazole exerts no antiviral effect and can therefore be used for virus isolation from heavily contaminated material. The antagonistic effect of serum on the antifungal effect of Econazole and Fungizone was comparable as was the inhibitory effect of both antimycotics on Mycoplasma growth. In view of the above mentioned properties Econazole lactic acid can be recommended as an antifungal agent for cell culture systems at a concentration of 1 microgram per ml.
Amphotericin B↗
Histamine release from rat mast cells induced by econazole.
1. Econazole released histamine from rat mast cells in vitro. This response was not affected by the addition of calcium or by prior treatment of mast cells with EDTA or cromoglycate. 2. Rat mast cells treated with econazole were stained by the vital dye trypan blue. 3. The intradermal injection of econazole increased vascular permeability. This response was antagonized by chlorpheniramine and cyproheptadine. 4. Our results demonstrate that econazole releases histamine by the "nonselective" mechanism. It is suggested that econazole inflammatory effects may be due to histamine release from mast cells.
Animals↗
Econazole, miconazole and SK & F 96365 inhibit depolarization-induced and receptor-operated contraction of guinea-pig isolated trachea in vitro.
Econazole, miconazole, SK & F 96365 and nifedipine inhibited Ca2+- and depolarization-induced and receptor-operated contraction of guinea-pig isolated trachea. Econazole, miconazole and SK & F 96365 inhibited histamine- and methacholine-induced tracheal contraction more than nifedipine. Nifedipine was more potent in inhibiting KCl-induced contraction. Nifedipine, salbutamol and theophylline, but not econazole, miconazole or SK & F 96365, relaxed KCl, histamine-, and methacholine-precontracted trachea. It appears that in the guinea-pig tracheal smooth muscle, econazole, miconazole and SK & F 96365 behave differently from nifedipine, theophylline and salbutamol. Econazole, miconazole and SK & F 96365 are thus introduced as novel antagonists of receptor-operated airway smooth muscle contraction.
Animals↗