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Les infrastructures urbaines sont souvent particulièrement remarquables en Inde du fait de leurs défauts (coupure, fluctuation importante, état délabré, etc.), ainsi que de leur rythme de construction soutenu (grands projets de dépollution, métro, ponts autoroutiers, etc.). Dans cet article, je m’intéresse au réseau d’assainissement de la ville de Varanasi, devenu depuis les années 1980 un symbole de ces difficultés de gestion urbaine, notamment à cause du déversement quotidien de centaines de millions de litres d’eaux usées sans traitement dans le Gange, et ce malgré des investissements massifs (Alley, 2014). En me concentrant sur le personnel technique qui gère et entretient les stations d’épuration et de pompage désavouées, je tente d’analyser à la fois leur vision et analyse des dysfonctionnements, et le rôle des dynamiques sociales, professionnelles et institutionnelles dans la pérennité de l’échec. Urban infrastructures are often particularly visible in India, both due to their recurrent failures and to the rhythm of their construction. In this article, we look at the wastewater treatment system of Varanasi, which has become since the 1980s, a symbol of the difficulties of urban planning in contemporary India, as millions of litters of wastewater flow untreated into the river Ganges despite large investments (Alley, 2014). By focusing on the technical workers who operate and maintain these infrastructures, we try to decipher their vision and analysis of the situation and the role of social, professional and institutional dynamics in the perpetuation of failure.

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We tested the influence of L-propionylcarnitine (LPC) in modifying mechanical stunning during reflow. Nineteen adolescent anesthetized swine were extracorporeally perfused at control coronary flows for 20 min, supplemented with excess fatty acids (average values 1.1 +/- 0.1 mumol/ml), and subjected to 45 min regional ischemia (-60 delta % decrease in anterior descending flow) followed by 35 min reperfusion. Responses in 10 placebo hearts were compared with those obtained from 9 animals treated with 50 mg/kg LPC at 0 min perfusion and 40 mg/kg at 40 min perfusion. Ischemia in placebo hearts caused a 62.6 delta % decrease in active shortening in anterior descending bed, which failed to recover (-41.4 delta % from control values) during reflow. Conversely, in LPC-treated hearts, decreases in active shortening (-38.6 and -11.6 delta %) during ischemia and reflow, respectively, were significantly smaller (P less than or equal to 0.05). This improved motion was associated with greater rates of myocardial oxygen consumption but similar levels of fatty acid oxidation and fatty acid intermediates. Thus LPC significantly reversed mechanical stunning in myocardial ischemia/reperfusion protocols, presumably because of its positive inotropic properties. This derivative, otherwise innocuous in nature, could represent an attractive new treatment choice for future clinical use.