Search PubMed⌕ Search

Biomedical subjects

P J Henry

Publications and source records attributed to P J Henry.

At least 19 recordsLinked to original sources
PubMed1995

Receptors for endothelin-1 in asthmatic human peripheral lung.

[125I]-endothelin-1 ([125I]-ET-1) binding was assessed by autoradiography in peripheral airway smooth muscle and alveolar wall tissue in human non-asthmatic and asthmatic peripheral lung. Levels of specific binding to these structures were similar in both non-asthmatic and asthmatic lung. The use of the receptor subtype-selective ligands, BQ-123 (ETA) and sarafotoxin S6c (ETB), demonstrated the existence of both ETA and ETB sites in airway smooth muscle and in alveoli. In airway smooth muscle from both sources, the great majority of sites were of the ETB subtype. Quantitative analyses of asthmatic and non-asthmatic alveolar wall tissue demonstrated that 29-32% of specific [125I]-ET-1 binding was to ETA sites and 68-71% was to ETB sites. Thus, asthma was not associated with any significant alteration in the densities of ETA and ETB receptors in peripheral human lung.

Adolescent↗
PubMed1995

Potentiation by endothelin-1 of cholinergic nerve-mediated contractions in mouse trachea via activation of ETB receptors.

1. We have previously shown that endothelin-1-induced contraction of mouse isolated tracheal smooth muscle was mediated via both ETA and ETB receptors. In the current study, we have investigated endothelin-1-induced potentiation of cholinergic nerve-mediated contractions in mouse isolated trachea and have characterized pharmacologically the endothelin receptors mediating this response. 2. Electrical field stimulation (EFS; 70 V, 0.5 ms duration, 10s train, 0.1-60 Hz) of mouse isolated trachea caused frequency-dependent, monophasic contractions (magnitude of contraction of 60 Hz was 56 +/- 4% Cmax (n = 6), where Cmax is the contractile response to 10 microM carbachol). EFS-induced contractions were abolished by either 0.1 microM atropine or 3 microM tetrodotoxin, but were not affected by 1 microM hexamethonium, indicating that they were induced by stimulation of postganglionic cholinergic nerves. In contrast, contractions induced by exogenously applied acetylcholine were inhibited by atropine, but not by either tetrodotoxin or hexamethonium. 3. The ETB receptor-selective agonist, sarafotoxin S6c, caused marked concentration-dependent potentiation of EFS-induced contractions in mouse isolated tracheal segments. At 0.1 nM, sarafotoxin S6c exerted no direct contractile effect, but significantly increased a standard EFS-induced contraction of 20% Cmax by 8 +/- 2% Cmax (i.e. 1.4 fold, n = 5, P < 0.05). At higher concentrations, 10 nM sarafotoxin S6c induced a large, transient contraction (peak response of 74 +/- 2% Cmax at 10 min; 3 +/- 2% Cmax at 45 min) and enhanced the standard EFS-induced contraction by 30 +/- 4% Cmax (i.e. 2.5 fold, n = 5, P < 0.01). In contrast, 10 nM sarafotoxin S6c did not enhance contractile responses to exogenously applied acetylcholine(n = 6).4. Endothelin-1 also modulated EFS-induced contractions. At 0.1 nM, endothelin-1 exerted no direct contractile effect, but significantly increased the standard EFS-induced contraction of 20%Cmax, by 7 +/- 2%Cma, (i.e. 1.35 fold, n = 5, P<0.05). At 1 nM, endothelin-l induced a small, sustained contraction(16 +/- 3%Cmo) and increased the standard EFS-induced contraction by 19 +/- 2%Cmax (i.e. 1.95 fold,n = 5, P <0.01). Finally, 10 nM endothelin-1 induced a large, sustained contraction (98 +/- 8%Cma), but the EFS-induced contraction was significantly reduced from 20%Cmax to 6 +/- 4%Cmax (n = 6, P <0.05).In contrast, in the presence of 3 microM BQ-123 (ETA receptor-selective antagonist), 1O nM endothelin-1 induced a transient contraction mediated via ETB receptors (peak response of 59 +/- 10%Cmax at 10 min;8 +/- 2%Cmax at 45 min). Under these conditions, the standard EFS-induced contraction was increased by 26+/- l%Cmax (i.e. 2.3 fold, n = 6, P<0.01).5. The potentiation of EFS-induced contractions produced by 1 nM endothelin-1 was not mediated by ETA receptors, since 3 microM BQ-123 did not diminish this effect (n = 6). Furthermore, 1 nM endothelin-1 did not potentiate EFS-induced contractions in preparations in which the function of the ETB receptor effector system had been attenuated by desensitization (n = 6).6. In summary, endothelin-1 potentiates cholinergic nerve-mediated contractions in mouse isolated trachea, apparently by activating prejunctional ETB receptors. This neuronal pathway offers an additional mechanism through which endothelin-1 may elevate bronchomotor tone.

Acetylcholine↗
PubMed1995

Rehabilitation of the edentulous mandible with osseointegrated dental implants: 10 year follow-up.

Long-term retrospective studies on the efficacy of implant retained bridgework are relatively few. In this study, 10 year follow-up results are reported on the rehabilitation of the edentulous mandible with osseointegrated implant anchored bridges. Fifteen patients were closely maintained and monitored using the conventional indices used in longitudinal periodontal research, together with serial intraoral periapical and extraoral panoramic radiographs. The need for prosthetic maintenance and the effects of the treatment on soft tissues, supporting bone, opposing dentition and the behavioural aspects of such rehabilitation are discussed. Based on the reviewed results of the study and numerous other investigations, the treatment of mandibular edentulism with fixed bridges supported by osseointegrated implants ad modum Brånemark is a highly effective method, giving predictable long-term results.

Adult↗
PubMed1995

Osseointegrated implants for single tooth replacement in general practice: a 1-year report from a multicentre prospective study.

The single tooth implant is a treatment option for the replacement of missing single teeth and in many cases is the treatment of choice. It is, however, an expensive treatment requiring a co-ordinated approach to the surgical and restorative aspects of treatment. In this study, a group of dentists in general and restorative dental practice and with no previous experience in implant surgery underwent an intensive training course in all aspects of implant treatment for single teeth. Using a system of simplified instrumentation with a strict adherence to protocol, the group installed and restored single tooth implants ad modum Brånemark in a wide range of clinical situations. At the one year follow-up period following crown insertion, the success rate of treatment compared favourably with results reported from centres using the specialist team approach to treatment. The results of this study indicate that further consideration should be given to the training of general dentists so that improved delivery of dental health care can be provided at a more economic level.

Adolescent↗
PubMed1995

Endothelin-1 receptor density, distribution, and function in human isolated asthmatic airways.

The potent bronchoconstrictor and mitogenic actions of the peptide endothelin-1 (ET-1) on airway smooth muscle may contribute significantly to the bronchial obstruction observed in asthma. However, the status of the receptor-effector systems that mediate these actions of ET-1 in asthmatic airways is currently unknown. Thus, we have used quantitative autoradiographic and isometric-tension recording techniques to evaluate the density, distribution, and function of the specific receptors that mediate the actions of ET-1 in both asthmatic and nonasthmatic airways. Here, we report that similar numbers of specific binding sites for [125I]-ET-1 exist in asthmatic and nonasthmatic airways, with the greatest densities located in airway smooth muscle in both tissue types. The ETB-receptor subtype constituted approximately 82% and 88% of these receptors for ET-1 in asthmatic and nonasthmatic human bronchial smooth muscle, respectively, and mediated contraction in response to this peptide. In addition, a component of ET-1-induced contraction appeared to be mediated by a non-ETB, BQ-123-resistant mechanism. Furthermore, a small population of ETA sites was identified that did not mediate contraction, but which may have a role in ET-1-induced prostanoid release and airway smooth-muscle proliferation. Interestingly, bronchial smooth muscle from asthmatic lung was significantly less sensitive to the contractile effects of ETB receptor activation, consistent with desensitization of this receptor subtype in response to the increased production and release of ET-1 that occurs in this disease.

Adolescent↗
PubMed1992

Influence of age on epithelium-dependent responsiveness of guinea-pig and rat tracheal smooth muscle to spasmogens.

The current study describes the influence of age and the presence of the epithelium on guinea-pig and rat tracheal airway smooth muscle sensitivity to the spasmogens histamine, acetylcholine, carbachol and potassium. In guinea-pig trachea from animals aged 2-52 weeks the potency of each of these spasmogens decreased with increased animal age. In contrast, no age-dependent changes in the potency of acetylcholine, carbachol or potassium were seen in rat trachea. Removal of the tracheal epithelium was associated with significant increases in the potencies of histamine and acetylcholine in guinea-pig trachea and of acetylcholine in rat trachea, but not of carbachol or potassium in either species. For histamine in guinea-pig trachea, the largest potency increase (4.6-fold) occurred in tissue from 6-week-old animals, with the smallest increases in tissue from the youngest (2 weeks) and the oldest (52 weeks) animals. Thus, although the sensitivity of airway smooth muscle to this spasmogen fell between 2 and 12 weeks of age, the effect of epithelial removal on sensitivity to histamine was apparently increased during this period. Further studies are required to assess the reasons for increased histamine and acetylcholine potency in airway smooth muscle after epithelial ablation.

Acetylcholine↗
PubMed1992

Endothelin-1-induced [3H]-inositol phosphate accumulation in rat trachea.

1. The effects of endothelin-1 (ET-1) and of the muscarinic cholinoceptor agonist, carbachol, on [3H]-inositol phosphate ([3H]-InsP) accumulation and smooth muscle contraction were determined in rat isolated tracheal tissue. 2. ET-1 (1 microM) and carbachol (10 microM) induced significant accumulation of [3H]-InsPs in myo-[2-3H]-inositol-loaded rat tracheal segments. Several components of the tracheal wall including the airway smooth muscle band, the cartilaginous region and the intercartilaginous region generated significant levels of [3H]-InsPs in response to ET-1 and carbachol. Following stimulation with ET-1, a greater proportion of tracheal [3H]-InsPs were generated in the intercartilaginous region (49%) than in either the airway smooth muscle band (25%) or cartilaginous region (26%). However, when the respective weights of these regions is taken into account, ET-1-induced accumulation of [3H]-InsPs was greatest in the airway smooth muscle band. The tracheal epithelium did not appear to generate [3H]-InsPs in response to ET-1 or modulate either basal or ET-1-induced accumulation of [3H]-InsPs in rat tracheal segments. 3. In the rat tracheal smooth muscle band, ET-1 caused a time- and concentration-dependent accumulation of [3H]-InsPs. Concentrations of ET-1 as low as 10 nM produced significant accumulation of [3H]-InsPs (1.23 +/- 0.10 fold increase above basal levels of 295 +/- 2 d.p.m. mg-1 wet wt., n = 3 experiments). At 10 microM, the highest concentration ?tsed, ET-1 produced similar levels of [3H]-InsP accumulation (7.03 +/- 0.55 fold above basal levels, t = 5) to that produced by a maximally effective concentration of carbachol (10 microM; 7.97 +/- 0.31 fold increase above basal levels, n = 4). ET-1-induced accumulation of [3H]-InsPs was not significantly affected by indomethacin (5 microM), nordihydroguaiaretic acid (NDGA, 10 microM), WEB 2086 (10 microM) or phosphoramidon (10 microM).4. ET-1 also produced concentration-dependent contractions of epithelium-denuded rat tracheal ring preparations. The mean concentration of ET-1 producing 50% of the maximum contractile response to carbachol (EC50) was 31 nm (95% confidence limits, 20-49 nM, n = 12). The presence of an intact tracheal epithelium, indomethacin (5 microM), WEB 2086 (10 microM) and phosphoramidon (10 microM) had no significant effect on the mean EC50 for ET-1-induced contraction (n = 5). In contrast, NDGA (10 microM) inhibited ET-1- induced contractions (4.0 fold increase in mean EC50, P < 0.001, n = 5). However, this effect of NDGA did not appear to be related to inhibition of leukotriene synthesis via lipoxygenase since the leukotriene antagonist SKF 104353 did not affect ET-1-induced contractions (n = 5) and moreover, leukotriene C4 and leukotriene D4 did not contract rat isolated tracheal smooth muscle preparations (n = 4).5. The threshold concentrations of ET-1 that produced increases in smooth muscle contraction and [3H]-InsPs accumulation were similar, although the EC50 for [3H]-InsP accumulation was 2.9 fold greater than that for smooth muscle contraction. For carbachol, the EC50 for [3H]-InsP accumulation (mean ECQO = 5.0 microM, 1.2-21 microM, n = 4) was 25 fold greater than that for smooth muscle contraction(mean EC50 = 0.20 miicroM, 0.17-0.24 microM, n = 12).6. It seems likely that ET-1 has a direct effect on InsP generation in rat tracheal smooth muscle and that this is largely responsible for the spasmogenic actions of this peptide.

Animals↗
PubMed1991

Effect of respiratory tract viral infection on murine airway beta-adrenoceptor function, distribution and density.

1. The effects of a respiratory tract viral infection on beta-adrenoceptor density, distribution and function were investigated in murine airways. 2. Following intranasal inoculation of CBA/CaH mice with influenza A/PR-8/34 virus, the virus proliferated rapidly in trachea (peak titres 2 days post-inoculation) and lung (peak titres 4-6 days post-inoculation). Respiratory tract viral infection was associated with a significant increase in lung weight (88% higher than control mice at day 6 post-inoculation) that was related temporally to the development of peripheral lung inflammation and consolidation. 3. Analysis of specific binding of [125I]-cyanopindolol to beta-adrenoceptors revealed that on days 2, 4 and 8 post-inoculation with virus, mouse isolated tracheal sections contained, on average, 40% more beta-adrenoceptors than tracheal sections from time matched control mice. Subsequent quantitative autoradiographic studies demonstrated that this increase in total tracheal beta-adrenoceptors was due primarily to a 90% increase in the density of beta-adrenoceptors in the tracheal epithelium in virus-infected mice. 4. In contrast, virus-infection had no significant effect on the density of beta-adrenoceptors in tracheal airway smooth muscle, although within 2 days of inoculation with virus, mouse tracheal smooth muscle segments were approximately 2 fold less sensitive to the beta-adrenoceptor agonist, noradrenaline (mean pD2 = 6.57 +/- 0.04, n = 24) and to the adenylyl cyclase-activator forskolin (mean pD2 = 6.78 +/- 0.04, n = 12) compared to segments from control mice (mean pD2 = 6.84 +/- 0.06 for noradrenaline; mean pD2 = 7.03 +/- 0.07 for forskolin). Similar values were obtained 8 days post-inoculation. At day 2, but not day 8 post-inoculation with virus, relaxation responses to theophylline were also marginally attenuated compared with controls.5. Mouse isolated tracheal segments obtained 2 days after virus inoculation and segments from timematched control mice were equisensitive to the spasmogenic actions of the muscarinic cholinoceptor agonist, carbachol. However, tracheal segments from mice inoculated with virus were less responsive to carbachol on day 4 (mean pD2 = 6.45 + 0.04, n = 8) and day 8 (mean pD2 = 6.45 +/- 0.02, n = 12) compared to control preparations (day 4, mean pD2 = 6.73 +/- 0.06, n = 8; day 8, mean pD2= 6.65 +/- 0.04, n = 12, P < 0.05). In contrast, endothelin-l-induced contractions of tracheal smooth muscle were notaffected by virus-infection.6. These data demonstrate that respiratory tract viral infection can produce significant tissue-selective changes in airway /beta-adrenoceptor density as well as small reductions in airway smooth muscle muscarinic cholinoceptor and /beta-adrenoceptor function.

Animals↗
PubMed1991

Endurance of jaw elevator muscles during cementation of a single molar crown.

Muscle activity of four jaw-closing muscles was monitored in 19 healthy subjects by EMG, under conditions associated with cementation of a crown restoration. Each subject performed two maximum voluntary contractions (MVC), each of two minutes duration, separated by a thirty-minute time interval. There was no visual feedback of muscle activity. Local analgesia, psychologic reinforcement and actual cementation were other conditions tested. All muscles fatigued as a function of time. For this experimental procedure the ipselateral muscles demonstrated less endurance than contralateral muscles. Psychologic reinforcement did not alter muscle activity. The effect of local analgesia was inconclusive and requires further investigation.

Adult↗
PubMed1991

Osseointegrated implants for single tooth replacement: a 1-year report from a multicenter prospective study.

One hundred seven dental implants were inserted to support single tooth restorations in 92 patients participating in a prospective multicenter investigation. Only three implants (2.8%) were lost after 1 year of clinical function. Most of the remaining restorations were esthetically successful by using modified components. The gingival condition was healthy around the single crowns and coincided well with the clinical situation around the permanent teeth. The most obvious problem experienced during the first year was related to loose abutment screws. Twenty-six percent of the screws retaining crowns were retightened during the observation period, but the frequency of loose screws had a tendency to decrease as the study progressed.

Adult↗
PubMed1990

Contractile effects and receptor distributions for endothelin-1 (ET-1) in human and animal airways.

ET-1 caused concentration-dependent, sustained contraction of all airway preparations tested and was most potent in mouse trachea, with rat trachea, human bronchus and guinea-pig trachea approximately 5, 10 and 70 fold less sensitive respectively. Human non-asthmatic and asthmatic bronchi were approximately equi-sensitive to ET-1. Quantitative light microscopic autoradiography demonstrated high levels of specific [125I]-ET-1 binding sites in airway smooth muscle of rat trachea greater than human asthmatic bronchus = human non-asthmatic bronchus greater than mouse trachea much greater than guinea-pig trachea. High levels of specific ET-1 binding were also revealed in peripheral airways and in alveolar wall tissue in human, rat and mouse lung. In a limited sample of asthmatic airway smooth muscle ET-1 receptor function and density was not elevated.

Animals↗
PubMed1990

Nitrate tolerance induced by nicorandil or nitroglycerin is associated with minimal loss of nicorandil vasodilator activity.

In the current study, the vasodilator and tolerance-inducing actions of a recently developed organic nitrate vasodilator, nicorandil, were compared to nitroglycerin (NTG) in an isolated coronary artery preparation. The order of potency for relaxing U46619-constricted bovine-isolated coronary artery rings was NTG greater than isosorbide dinitrate (ISDN) greater than nicorandil. NTG was approximately 250-fold more potent than nicorandil (mean EC50 values for relaxation; 0.044 and 11.2 microM, respectively; n = 6-8). Coronary artery rings preexposed for 60 min to NTG (30 microM) were subsequently markedly less responsive to the relaxant effects of NTG (7.5-fold increase in mean EC50 value, 68.4% decrease in Emax; p less than 0.001) and ISDN (14.1-fold increase in mean EC50 value; p less than 0.001), although only marginally less responsive to nicorandil (1.75-fold increase in mean EC50 value; p less than 0.05). Thus, the coronary artery relaxant actions of nicorandil were significantly less affected by NTG-induced tolerance than were the relaxant actions of the related organic nitrate compounds, NTG and ISDN. To compare the tolerance-inducing actions of NTG and nicorandil, the relaxant actions of a series of nitric oxide (NO)-containing vasodilators were determined in control coronary artery rings and in rings preexposed for 60 min to either 30 microM NTG or 5,000 microM nicorandil. Quantitatively, similar changes in coronary artery ring responsiveness were produced by tolerance induced by NTG and nicorandil; marked attenuation of responsiveness to NTG and to the nonnitrate compound 3-morpholinosydnonimine (SIN-1), but only marginal attenuation of responsiveness to nicorandil and NO.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Relationship between endothelin-1 binding site densities and constrictor activities in human and animal airway smooth muscle.

1. Endothelin-1 (ET-1) binding site densities and constrictor activities were compared in airway smooth muscle preparations of human, guinea-pig, rat and mouse. 2. The mean contractile response to 0.3 microM ET-1 (measured as the % maximum response to 10 microM carbachol, % Cmax +/- s.e.mean) and the mean concentration of ET-1 producing 30% Cmax (95% confidence limits) were respectively; 85.9 +/- 5.4% and 3.4 nM (2.4-5.0) for mouse trachea (n = 11), 88.8 +/- 4.7% and 18.2 nM (11.2-25.2) for rat trachea (n = 6), 71.0 +/- 7.1% and 35.2 nM (5.4-231) for human bronchus (n = 3), and 32.3 +/- 3.0% and 241 nM (125-460) for guinea-pig trachea (n = 6). 3. Light microscopic autoradiography revealed specific [125I]-ET-1 binding sites localized to the smooth muscle band, with very low levels of binding associated with cartilage, submucosal and epithelial cells. 4. Quantitative autoradiographic analyses of the concentration-dependence of specific [125I]-ET-1 binding (0.1-2 nM) to smooth muscle revealed similar dissociation constants but markedly different specific binding site densities for the various animal species. The order of densities of specific [125I]-ET-1 binding sites was rat trachea (69.0 +/- 11.2 amol mm-2) greater than human bronchus (42.7 +/- 17.5 amol mm-2) greater than mouse trachea (28.7 +/- 2.6 amol mm-2) greater than guinea-pig trachea (8.3 +/- 1.8 amol mm-2). 5. A positive relationship between [125I]-ET-1 binding site density and ET-1 constrictor activity was observed in airway smooth muscle preparations from rat, human and guinea-pig. The greater sensitivity of mouse trachea to the constrictor actions of ET-1 was not dependent on the release of cyclo-oxygenaseor epithelium-derived constrictor substances, but may have been due to an inter-species difference in the receptor-effector system for ET-1.

Adult↗
PubMed1990

Beta 1-adrenoceptors mediate smooth muscle relaxation in mouse isolated trachea.

1. The relaxant effects to the beta-adrenoceptor agonists isoprenaline, adrenaline, noradrenaline, RO363, procaterol and fenoterol were investigated in carbachol-contracted mouse isolated tracheal preparations. 2. The order of potencies for those beta-adrenoceptor agonists that induced full relaxation of carbachol-contracted mouse tracheal preparations was isoprenaline greater than RO363 greater than noradrenaline = adrenaline greater than fenoterol. The EC50 value of isoprenaline for relaxation was 46 nM. The beta 1-adrenoceptor-selective agonist, RO363 was ten times more potent than the beta 2-adrenoceptor-selective agonist, fenoterol. The highly beta 2-adrenoceptor-selective agonist procaterol was a partial relaxant and induced only 28 +/- 4% relaxation. 3. Relaxations induced by noradrenaline and isoprenaline were not significantly affected by the neuronal uptake inhibitor, cocaine (10 microM) or by the extraneuronal uptake inhibitor, deoxycorticosterone acetate (25 microM) respectively. The alpha-adrenoceptor agonist methoxamine induced no observable elevation of mouse tracheal smooth muscle tone. 4. Schild plots for the beta-adrenoceptor antagonists, atenolol and betaxolol (beta 1-adrenoceptor-selective) and ICI 118,551 (beta 2-adrenoceptor-selective) were linear, with slope values approaching unity. Mean pA2 values derived for atenolol, betaxolol and ICI 118,551 for antagonism of beta-adrenoceptor-mediated relaxation were 7.1, 8.4 and 7.2, respectively. These data were independent of the use of isoprenaline or noradrenaline as the agonist. 5. These findings indicate that beta-adrenoceptor-mediated relaxations of mouse isolated trachea occur predominantly through activation of beta 1-adrenoceptors.

Animals↗
PubMed1990

Distribution of beta 1- and beta 2-adrenoceptors in mouse trachea and lung: a quantitative autoradiographic study.

1. Binding and quantitative autoradiography were used to detect [125I]-iodocyanopindolol (I-CYP) associated with beta 1- and beta 2-adrenoceptors in mouse tracheal epithelium and airway smooth muscle as well as in lung parenchymal tissue. 2. Specific I-CYP binding to slide-mounted tissue sections of both trachea and parenchyma was of high affinity (KD = 49.0 pM, n = 3, trachea; KD = 118.9 pM, n = 3, parenchyma) and saturable, involving single populations of non-interacting binding sites (Hill coefficient nH = 1.00 +/- 0.02, trachea; nH = 0.99 +/- 0.03, parenchyma). 3. Direct measurement of tissue radioactivity also showed that specific I-CYP binding was competitively inhibited in the presence of the beta-adrenoceptor antagonists (-)-propranolol (non-selective), CGP 20712A (beta 1-selective) and ICI 118,551 (beta 2-selective). Analysis of the competition binding curves for the two selective antagonists revealed mixed populations of beta 1- and beta 2-adrenoceptors in the approximate proportions 33% and 67% respectively in mouse trachea and 28% and 72% respectively in mouse lung parenchyma. 4. Densities of autoradiographic grains derived from specific I-CYP binding to alveolar wall tissue and to tracheal epithelium and airway smooth muscle were quantified by a computer-assisted image analysis system, which allowed the construction of competition binding curves in the presence of the selective beta-adrenoceptor antagonists CGP 20712A and ICI 118,551. Analysis of these data demonstrated that in alveolar wall, beta 1- and beta 2-adrenoceptors co-existed in the proportions 18% and 82%, respectively. 5. Quantitative autoradiographic analyses also showed that beta 1- and beta 2-adrenoceptors were differentially distributed in tracheal epithelium and airway smooth muscle. The beta 2-adrenoceptor subtype accounted for 71% of all beta-adrenoceptors in epithelium. Conversely, beta l-adrenoceptors which mediate relaxant responses of mouse trachea to beta,-adrenoceptor agonists (Henry & Goldie, 1990), accounted for 69% of all beta-adrenoceptors in the airway smooth muscle.

Adrenergic beta-Antagonists↗
PubMed1990

Oxide thickness and surface contamination of six endosseous dental implants determined by electron spectroscopy for chemical analysis: a preliminary report.

Electron spectroscopy and argon ion etching were used to determine the depth and composition of the oxide layers of six competitive dental implant systems. To minimize problems associated with analyzing the active oxide layers, the implants were removed from their original packaging in an oxygen-free environment. The majority of the six implant systems were found to have similar oxide thickness in the range of 20 to 34 A. Some variation was found in the extent of non-oxide surface contamination.

Corrosion↗
PubMed1989

Determinants of in vitro nitroglycerin tolerance induction and reversal: influence of dose regimen, nitrate-free period, and sulfhydryl supplementation.

The influence of dose regimen on the induction and reversal of tolerance to nitroglycerin (NTG) is not well understood despite the current widespread clinical use of both sustained and intermittent modes of NTG administration. In an isolated coronary artery preparation both the NTG preexposure concentration and the duration of the NTG preexposure period were positive and independent determinants of the extent of NTG tolerance induction. During a "nitrate-free" or washout period, NTG tolerance was at least partially reversible. The apparent rate of NTG tolerance reversal during a "nitrate-free" period was not dependent on the absolute degree of NTG tolerance induced or on the dose regimen used to induce NTG tolerance. In this isolated vascular preparation, sulfhydryl (SH) supplementation with 1 mM N-acetylcysteine produced no significant augmentation of NTG-induced relaxations in either NTG tolerant or non tolerant tissues. N-acetylcysteine was ineffectual in attenuating the development of NTG tolerance in coronary artery preparations incubated in either Krebs bicarbonate buffer or in 10% human plasma. We conclude that in this model the NTG preexposure concentration, the duration of the NTG preexposure period, and the duration of the "nitrate-free" period are critical and independent determinants of the extent of NTG tolerance but that NTG tolerance is not significantly attenuated by SH supplementation.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗