19 research outputs found

    Can Exhaled Carbon Monoxide Be Used as a Marker of Exposure? A Cross-Sectional Study in Young Adults

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    Carbon monoxide (CO) poisoning is a major public health issue worldwide. People are exposed to CO in their daily lives, with one of the common sources of CO being cigarette smoking. Inhalation of CO leads to elevated carboxyhaemoglobin (COHb) levels in the blood and also in exhaled CO concentration. Several factors have been shown to affect COHb concentration and COHb half-life. However, factors affecting exhaled CO concentration and exhaled CO half-life are not well understood. The present study aimed to investigate the potential factors related to baseline exhaled CO concentration and exhaled CO half-life among smokers. A cross-sectional study was conducted between 26 January and 30 June 2019, and young adults were recruited into the study. A total of 74 participants (mean age: 27.1 years, 71.6% males and 28.4% females) attended the study. They were invited to complete a questionnaire, including demographic, physiological, and behavioural factors. Then, exhaled CO measurements were taken. These measurements were taken before and after smoking a single cigarette for smokers and only once for non-smokers. The average baseline exhaled CO concentration was 6.9 ± 4.9 ppm for smokers and 1.9 ± 0.5 ppm for non-smokers. The mean of exhaled CO half-life was around 273.3 min (4.6 h) for smokers. No difference was seen in exhaled CO half-life between light smokers and heavy smokers in the smoking group. Gender and cigarettes smoked weekly affected baseline exhaled CO in smokers. Even though height seemed to positively associate with exhaled CO half-life, the relationship disappeared when adjusting by gender and weight. Therefore, exhaled CO could be used as a marker of CO exposure, but we cannot ignore the factors mentioned in the study. For future study, considering factors related to smoking habits and smoking style are recommended as these may affect total inhaled CO

    Chronic overcirculation-induced pulmonary arterial hypertension in aorto-caval shunt.

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    Pulmonary arterial hypertension is a common complication of congenital heart defects with left-to-right shunts. Current preclinical models do not reproduce clinical characteristics of shunt-related pulmonary hypertension. Aorto-caval shunt was firstly described as a model of right ventricle volume overload. The pathophysiology and the possible determination of pulmonary arterial hypertension of different periods of shunt exposure are still undefined. A method to create standardized, reproducible aorto-caval shunt was developed in growing rats (260±40 g). Three groups of animals were considered: shunt exposure for 10 weeks, shunt exposure for 20 weeks and control (sham laparotomy). Echocardiography and magnetic resonance revealed increased right ventricular end diastolic area in shunt at 10 weeks compared to control. Hemodynamic analysis demonstrated increased right ventricular afterload and increased effective pulmonary arterial elastance (Ea) in shunt at 20 weeks compared to control (1.29±0.20 vs. 0.14±0.06 mmHg/μl, p=0.004). At the same time point, the maximal slope of end-systolic pressure-volume relationship (Ees) decreased (0.5±0.2 mmHg/ml vs. 1.2±0.3, p<0.001). Consequently, right ventricular-arterial coupling was markedly deteriorated with a ≈50% decrease in the ratio of end-systolic to pulmonary artery elastance (Ees/Ea). Finally, left ventricular preload diminished (≈30% decrease in left ventricular end-diastolic volume). Histology demonstrated medial hypertrophy and small artery luminal narrowing. Chronic exposure to aorto-caval shunt is a reliable model to produce right ventricular volume overload and secondary pulmonary arterial hypertension. This model could be an alternative with low mortality and high reproducibility for investigators on the underlying mechanisms of shunt-related pulmonary hypertension
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