6,963 publications from this institution
Case 1 A 58-year-old man was admitted to our coronary care with troponin negative unstable angina. His risk factors included, being an exsmoker for a year, treated hypertension and dyslipidaemia. Medication on admission was aspirin and a statin. ECG showed Twave inversion laterally. Nine years previously he had a bare metal stent implanted in his circumflex artery following a lateral infarction the preceding year. Angiography done during his acute presentation revealed an in-stent restenosis in the previously treated circumflex artery and a diffusely diseased marginal branch. The left anterior decending coronary (LAD) was normal and the right coronary artery (RCA) had a non-flow limiting lesion in the mid-vessel with a fractional flow reserve (FFR) of 0.79. Intravascular ultrasound (IVUS) of the circumflex artery was performed using a 20 MHz Eagle eye IVUS catheter (Volcano Therapeutics, Rancho Cordova, CA, USA). The length of the stented segment was 30mm and had a minimal luminal area (MLA) 4.6 mm2. Neo-intimal formation was visible throughout the stent (Figure 1). This gave a neointimal hyperplasia (NIH) volume of 80.3 mm3. The NIH on virtual histology had a tissue composition of necrotic core (NC) 13.6%, (0.08 mm2, 2.4 mm3), calcified tissue 16.8%, (0.10 mm2, 3.0 mm3), fibrofatty 5.8%, (0.03 mm2, 1.04 mm3), fibrotic tissue 63.9%, (0.38 mm2, 11.5 mm3). Distal to the MLA at distance of 18 mm IVUS revealed an eccentric soft neo-intimal ruptured plaque1,2 (Figure 1C) within the stent. The necrotic core was 22% with remnant plaque burden of 54% at the plaque rupture site (Figure 1 C’). Just distal to ruptured plaque the vessel wall was intact and the plaque burden was higher 65% with no necrotic core in contact with the lumen (Figure 1D”). This ruptured lesion was subsequently managed with a drug eluting stent (DES) that also covered the MLA. The histological findings of a similar plaque rupture are illustrated in Case 2.
Cyclooxygenase products modulate the expression of nitric oxide synthase (NOS) in certain cell types. We determined the effect of prostaglandins (PG) E2 and F2alpha on exhaled nitric oxide (NO) concentrations measured by chemiluminescence. Inhaled PGE2 and PGF2alpha significantly reduced exhaled NO. After the highest dose of PGE2 (100 micrograms), NO concentrations fell from 6.9 +/- 0.5 ppb to 4.0 +/- 0.8 ppb (p < 0.001), and from 22.9 +/- 2.0 ppb to 12.3 +/- 1. 2 ppb (p < 0.001), whereas after PGF2alpha, it fell from 6.5 +/- 0.6 ppb to 3.0 +/- 0.5 ppb (p < 0.001), and from 26.0 +/- 3.4 ppb to 11. 5 +/- 1.4 ppb (p < 0.001) in normal (n = 7) and asthmatic (n = 8) subjects, respectively. Although the prostaglandins did not change FEV1 in normal subjects, PGE2 caused an increase in asthmatics (from 3.6 +/- 0.3 L to 3.8 +/- 0.4 L, p < 0.05) and PGF2alpha caused a transient reduction in FEV1 from 4.0 +/- 0.2 L to 3.5 +/- 0.2 L (p < 0.05). To further determine the relationship between bronchoconstriction and exhaled NO levels, we examined the effect of inhaled methacholine which did not change exhaled NO concentrations in normal and asthmatic subjects despite a greater than 20% fall in FEV1 in asthmatics. Therefore, PGE2 and PGF2alpha reduce exhaled NO, an effect not related to airway caliber changes but which may result from an inhibition of nitric oxide synthase (NOS), particularly inducible NOS (iNOS).
Nonadrenergic, noncholinergic (NANC) nerves, which cause relaxation of airway smooth muscle, have been described in several species including man. Stimulation of efferent vagus nerves during cholinergic and adrenergic blockade induces a pronounced bronchodilation in the cat. In more recent studies in man, capsaicin inhalation or mechanical irritation of the larynx, under conditions of cholinergic and adrenergic blockade, have been shown to cause a transient bronchodilator response. There is some evidence that neuropeptides such as vasointestinal peptide (VIP) or peptide histidine methionine (PHM) may be the neurotransmitter of NANC nerves, but this is not conclusive. Nitric oxide may be another neurotransmitter. In mild asthma, the NANC bronchodilator response is similar to that observed in normal subjects; on the other hand, a reduction in VIP immunoreactivity has been reported in more severe patients. The contribution of NANC dilator nerves in pathophysiological situations is not known, but their effect may be modulated during allergic responses. Use of antagonists or inhibitors of putative neurotransmitters, and molecular biological techniques will be useful in defining both the physiological and pathophysiological roles of NANC inhibitory nerves in the airways.
"Neuropeptides in the Respiratory Tract: Part II." American Review of Respiratory Disease, 144(6), pp. 1391–1399
1 We examined the effect of various pharmacological agents on the acute bronchoconstrictor response and airway microvascular leakage in a model of guinea-pig sensitization to trimellitic anhydride (TMA) a cause of low molecular weight occupational asthma in man. 2 Guinea-pigs were given intradermal injections of 0.1 ml of 0.3% TMA in corn oil; 21–28 days later, anaesthetized guinea-pigs were challenged with TMA conjugated to guinea-pig albumin by tracheal instillation. Changes in lung resistance were measured and airway microvascular leakage was quantified by measuring the extravasation of Evans blue dye into the airway tissue. 3 Sensitized guinea-pig (n = 9 in each group) were pretreated with chlorpheniramine (2.5 mg kg−1, i.v.), WEB 2086 (10 μg kg−1, i.v.), BW 4AC (50 mg kg−1, i.p.), nedocromil sodium (2% aerosol for 60 s) or vehicle alone. 4 Pretreatment with chlorpheniramine inhibited both the acute bronchoconstrictor response and the increase in airway microvascular leakage. WEB 2086 and nedocromil sodium partially inhibited the bronchoconstrictor response but had no significant effect on airway microvascular leakage. BW 4AC caused a non-significant reduction of the bronchoconstrictor response and airway microvascular leakage. 5 These results indicate that both the bronchoconstrictor response and the airway microvascular response in this model of sensitization is mediated to a large extent by histamine. PAF but not 5-lipoxygenase products also partially mediates the bronchoconstrictor response but not the airway microvascular leakage. Nedocromil sodium partially inhibits the bronchoconstrictor response only.
Abstract : A collaborative study has been made of samples of pyrotechnic compositions (delays, coloured smokes and a percussion primer) by a number of laboratories. A variety of techniques have been used to characterize the ignition/ignition transfer behaviour of the compositions. These include temperature of ignition, heat of reaction, burning rate, time to ignition, safety tests and DSC/DTA analysis. This report presents the data collected by each laboratory during this investigation.
A geometrically nonlinear model is developed to investigate the buckling behaviour of plates with a pre-existing delamination under uniaxial compression. The Rayleigh-Ritz procedure, based on trigonometric out-of-plane displacement functions, is used in conjunction with potential energy principles to describe the buckling and postbuckling response. The formulation is enhanced with the introduction of a discrete cohesive zone model to allow the delamination to grow under further loading. Different cases are investigated with residual capacities of the plates being evaluated in the neighbourhood of a transitional depth of delamination, where the postbuckling behaviour changes from thin film to mixed mode to global buckling. The model is validated with the commercial finite-element code Abaqus and criteria are proposed such that the component may be exploited beyond the critical loads.
The purpose of this study was to assess the early changes in stenosis geometry after insertion of intravascular stents in human coronary arteries. Morphologic changes were evaluated by quantitative coronary angiography (using automated edge detection) and by calculation of the theoretical pressure decrease across the dilated and stented stenosis from the Poiseuille and turbulent resistances assuming a coronary blood flow of either 1 or 3 ml/s. Twenty-six patients* were studied before and after angioplasty, as well as immediately after stent implantation. The stented coronary artery was the left anterior descending artery in 19 cases, the circumflex artery in 2 cases, the right coronary artery in 2 cases and a coronary artery bypass vein graft in 3 cases. After stent implantation, an additional increase in minimal luminal cross-sectional area of the dilated vessel was observed, suggesting that the self-expanding stainless steel endoprosthesis used in this study has a dilating function in addition to its stenting role.
1. Almitrine at a dose of 0·5 mg h−1 kg−1 given intravenously over 2 h had no effect on resting ventilation in normal males. 2. There was a small, but insignificant, rise in the hypercapnic drive to breathe as compared with placebo. 3. A large rise in the hypoxic drive to breathe was seen in response to almitrine. 4. These findings support the claim that almitrine has its action on ventilation via the peripheral chemoreceptors. 5. No correlation between blood levels of almitrine and the rise in hypoxic response was seen.
