Public-health impact of outdoor air pollution for 2nd air pollution management policy in Seoul metropolitan area, Korea

OBJECTIVES: Air pollution contributes to mortality and morbidity. We estimated the impact of outdoor air pollution on public health in Seoul metropolitan area, Korea. Attributable cases of morbidity and mortality were estimated. METHODS: Epidemiology-based exposure-response functions for a 10 microg/m3 increase in particulate matter (PM(2.5) and PM(10)) were used to quantify the effects of air pollution. Cases attributable to air pollution were estimated for mortality (adults > or = 30 years), respiratory and cardiovascular hospital admissions (all ages), chronic bronchitis (all ages), and acute bronchitis episodes (< or =18 years). Environmental exposure (PM(2.5) and PM(10)) was modeled for each 3 km x 3 km. RESULTS: In 2010, air pollution caused 15.9% of total mortality or approximately 15,346 attributable cases per year. Particulate air pollution also accounted for: 12,511 hospitalized cases of respiratory disease; 20,490 new cases of chronic bronchitis (adults); 278,346 episodes of acute bronchitis (children). After performing the 2nd Seoul metropolitan air pollution management plan, the reducible death number associated with air pollution is 14,915 cases per year in 2024. We can reduce 57.9% of death associated with air pollution. CONCLUSION: This assessment estimates the public-health impacts of current patterns of air pollution. Although individual health risks of air pollution are relatively small, the public-health consequences are remarkable. Particulate air pollution remains a key target for public-health action in the Seoul metropolitan area. Our results, which have also been used for economic valuation, should guide decisions on the assessment of environmental health-policy options.

Changes in Cytosolic Ca2+ Concentration of Single Rabbit Coronary Artery Smooth Muscle Cell during Ischemic Cardioplegic Period

BACKGROUND: No-reflow is a specific type of vascular damage occuring when removal of coronary occlusion dose not lead to restoration of coronary flow. There are three major explanations for the no-reflow phenomenon such as endothelial cell edema, microvascular plugging by platelets or thrombi and coronary occlusion by ischemic contracture of the myocardium. But detailed mechanisms of no-reflow phenomenon are not known. The objects of this study are to elucidate the possibility whether elevation of cytosolic Ca2+ concentration during ischemic cardioplegic period is mechanism of no-reflow phenomenon or not. METHODS: Changes in cytosolic Ca2+ concentration were measured under varying experimental condition. Free [Ca2+] in the cytosole [Ca2+]i of single rabbit coronary artery cells was measured with fluorescent Ca2+ indicator, Fura-2. RESULTS: Resting [Ca2+]i was 134.2+/-34 nM (n=43). When single cells were perfused with cardioplegic or ischemic cardioplegic solution, [Ca2+]i was significantly increased and degree of [Ca2+]i elevation was further augmented by ischemic cardioplegic solution. Pretreatment of sarcoplasmic reticulum emptying agent (20mM caffeine) had no effect on cardioplegia-induced [Ca2+]i change, but application of Ca2+ channel blocker (5x10-7M nifedipine) or an antagonist of Na+/Ca2+ exchange (5mM Ni2+ ) partially (nifedipine) or completely (nickel) inhibited the [Ca2+]i elevation. Pretreament of caffeine had no effect on ischemic cardioplegia-induced [Ca2+]i change, but application of nifedipine or nickel partially inhibited the [Ca2+]i elevation. Magnitude of ischemic cardioplegia-induced [Ca2+]i elevation was dependent on the Ca2+ concentration of perfusate from 0 to 2.5mM. When Ni2+ was added to reperfusion solution, recovery of ischemic cardioplegia-induced [Ca2+]i elevation was very rapid compared with control. CONCLUSIONS: From the above results, it may be speculated that ischemic cardioplegia-induced [Ca2+]i elevation may act as one of the mechanism of no-reflow phenomenon in rabbit coronary artery.

Effect of Propranolol on Gallamine-induced Tachycardia during Halothane Anesthesia / 대한마취과학회지

That gallamine causes tachycardia during general anesthesia is well known, but the efficacy of its anticholinergic action or an adrenergic beta blocking action remains to be determined. Twelve patients were subjected to this study, in which under halothane anesthesia small doses of propranolol. an adrenergic beta-blocker, was administered. In all cases bradycardia resulted and the greatest decrease was noted five minutes after intravenous injection of propranolol(0. 5 1. 0mg). At the height of bradycardia, gallamine 80 mg was administered intravenously. In all cases gallamine produced a significant increase of heart rate over the level before the injection of propranolol, but not so much as without propranolol pretreatment. But fifth minute values after propranolol expressed as 100 per cent, (per cent change in heart rate after propranolol followed by gallamine,) and after gallamine were similar effectively. This study suggested that gallamine-induced tachycardia is modified, but its anticholinergic action is not impaired by propranolol, and that gallamine-induced tachycardia is caused by anticholiaergic action of gallamine.

Anaphylactoid Reaction induced by Muscle Relaxants / 대한마취과학회지

Severe bronchospasm, hypotension and skin rash were observed in a 23 year-old woman after injection of gallamine iodide. Her past history revealed no asthmatic and allergic diathesis. Initial administration of succinylcholine induced a mild degree of bronchspasm and urticaria-like skin rash, which were intensified in severity after gallamine injection under the anesthetic state. Administration of hydrocortisone 500mg I.V. and antihistaminic(Avil), 100pmg I.M., produced successful relief of bronchospasm with circulatory embarrassment. A review was done as to histamine libration and bronchospasm due to succinylcholine, gallamine, d-tubocurarine, thiopental and atropine. The value of intradermal skin rash test was discussed.