To determine functional and anatomic changes in the first 24 hours after coronary angloplasty, we studied at random 15 patients (9 men, mean age 60 years) who underwent coronary angioplasty of 16 coronary arteries. Quantitative coronary angiography and coronary flow reserve measurements from digitized coronary angiograms were performed before, immediately after, and 24 hours after coronary angioplasty. Calculated were the minimal luminal diameter, obstruction area, and percentage diameter stenosis from two preferably orthogonal projections. Prior myocardial infarction in the myocardial region of interest was present in four patients. Seven patients had multivessel disease. Collateral vessels supplying the compromised flow region were observed in three patients. Six patients had refractory unstable angina pectoris. After coronary angioplasty, anglographically visible dissection was noted in six patients, whereas side branch occlusion was observed in one. Minimal luminal diameter before, immediately after, and 24 hours after was 0.93 ± 0.18 mm, 1.53 ± 28 mm, and 1.53 ± 0.21 mm, respectively; obstruction area was 0.70 ± 0.26 mm2, 1.92 ± 0.69 mm2, and 1.87 ± 0.51 mm2, respectively; diameter stenosis was 60.4 ± 8.0%, 36.8 ± 11.4%, and 37.6 ± 5.3%, respectively. The coronary flow reserve (lower limit of normal with this technique 3.4) was essentially the same before and immediately after coronary angioplasty (1.26 ± 0.59 vs 1.30 ± 0.42, p = NS) with a slight improvement to 1.78 ± 0.90 (p < 0.05) 1 day later. Coronary artery dimensions correlated poorly with coronary blood flow reserve before and after angioplasty. We conclude that on average no changes in minimal luminal diameter, obstruction area, and percentage diameter stenosis occurred in the first 24 hours after coronary angioplasty, although there were individual variations, and coronary flow reserve measurements from digitized coronary angiograms were only minimally improved 1 day after coronary angioplasty and correlated poorly with quantitative measurements of coronary artery dimensions. Therefore it is suggested that coronary flow reserve measurements from digitized coronary angiograms in the setting of coronary angioplasty have little value in unselected patients with conditions known to disturb coronary flow reserve.
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Uptake of 3H-prazosin (3H-PZ), a potent alpha-adrenoceptor antagonist, and 3H-dihydroalprenolol (3H-DHA), a potent beta-antagonist, was measured in rat heart and lung after intravenous injection. 3H-PZ binding was inhibited in a dose-dependent manner by phentolamine with maximum displacement at 5 mg/kg which represented 50–70% of the total binding. 3H-DHA was inhibited by increasing doses of l-propranolol with maximum displacement at 1 mg/kg (30–70% of total binding), whereas d-propranolol was approximately 100 times less potent, confirming stereospecificity of binding. These radioligands appeared to label adrenoceptors in vivo. The distribution of both radioligands in heart, lung and blood vessels was investigated.
Definitions Burden of COPD - Epidemiology, Economic, and Social burden Risk Factors - Environmental Exposures and Host Factors Pathophysiology Biochemistry/Immunology: Inflammation, Oxidative Stress, Proteases Pathophysiology: Chronic Bronchitis, Obstructive Bronchiolitis, Emphysema, Vascular Disease Asthma Compared to COPD Clinical Consultation: Symptoms and Signs Investigations Diagnosis, Classification, Clinical Progression of COPD Special Types of COPD, Differential Diagnosis, Severity of COPD Disease Progression, Respiratory Failure, Cor Pulmonale, Death Smoking Cessation and Reduction of Risk Factors Pharmacotherapy - Drug Therapy of COPD Management of Stable COPD Management of Exacerbations of COPD Pulmonary Rehabilitation Oxygen Therapy and Ventilatory Support Surgery Future Trends in Therapy
Nitric oxide can be detected in the exhaled air of animals and normal human subjects, is increased in patients with asthma and bronchiectasis, and may be modulated by inhaled corticosteroids. Nitric oxide may provide a noninvasive means of monitoring inflammation in the respiratory tract and the measurement of exhaled nitric oxide has attracted increasing interest. However, interpretation of exhaled nitric oxide measurements may be difficult and there is a wide variation in the reported levels of nitric oxide in exhaled air, suggesting that technical factors are important.