Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Comprehensive investigation is necessary for determining the cause of death in cases with positive drug screens. We investigated the case of a male who reportedly expired from an acute asthma attack. He had limited access to both therapeutic drugs and drugs of abuse because he was a state prisoner. His autopsy was remarkable because the weights of his right and left lungs were 690 and 760 g, respectively. His upper airway was clear of debris. There was an abundant amount of blood and frothy fluid in the pulmonary parenchyma. There were no focal lesions. The pulmonary vasculature was unremarkable. Microscopic evaluation of the lung tissue showed that the bronchi contained dense inflammatory infiltrates consisting mostly of eosinophils and a few lymphocytes and plasma cells. Basement membrane thickening was evident in the bronchi, and mucous plugs were identified in some of the bronchial lumina. A morphine concentration of 80 ng/mL was found in the blood. Theophylline and albuterol were detected in trace amounts. The opinion of the coroner was that the patient died of an acute asthma attack, and the presence of morphine may have contributed to his death. A careful review of his medical history and the mechanisms of drug-induced asthma revealed that the etiology of his death was more likely due to heroin abuse and noncardiogenic pulmonary edema. Episodic exacerbations of his chronic asthma were a contributing factor in his demise. However, in and of itself, asthma was not responsible for his death. Pertinent information associated with this case is presented, along with additional findings of toxicological screens and other evidence demonstrating that his asthma treatment did not contribute to his death. In addition, opiate-induced asthma, as well as other drug-induced diseases that can contribute to mortality in patients who abuse narcotics, is reviewed.
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PMID:The role of pharmacology and forensics in the death of an asthmatic. 892 50

The effect and mechanism of action of adenosine on the pulmonary circulation of rabbits were studied. Adenosine (10(-5)-10(-3) M) produced a concentration-dependent decrease in pulmonary arterial tension of precontracted pulmonary arterial rings. Removal of endothelium (denuded) augmented the adenosine-induced vasodilation in the pulmonary arterial rings. Theophylline (5 x 10(-5) M), an adenosine receptor antagonist, reduces the vasodilation induced by adenosine in intact and denuded rings. Pretreatment of the pulmonary rings with the cyclooxygenase inhibitor indomethacin (5 x 10(-6) M) significantly attenuated the adenosine-induced relaxation in denuded but not in the intact pulmonary arterial rings. Methylene blue (5 x 10(-5) M), a guanylate cyclase inhibitor, significantly reduced the relaxation induced by adenosine in both the intact and the denuded arterial rings. Adenosine significantly attenuated the pressor responses of serotonin and acetylcholine in the intact and denuded rabbit's pulmonary arterial rings. The results of this study indicate that adenosine induces pulmonary vasodilation and that functional endothelium is not required to evoke this dilation. In addition, guanylate cyclase activity and the generation of cGMP is essential for adenosine to induce vasodilation in the rabbit lung. Furthermore, the results of this study may suggest that adenosine could be used to reduce the severity of pulmonary hypertension and possibly pulmonary edema.
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PMID:Effect of adenosine on pulmonary circulation of rabbits. 1021 84