The monitoring of pH and PaCO2PaCO2 could

have added important missing information. Sixth, we did not analyze the atelectatic lung. In conclusion, considering that tidal volumes calculated on the basis of two healthy lungs are twice as great in their impact when delivered to a single lung, our results suggest that a high tidal volume that would be appropriate to two-lung ventilation should be avoided when changing into OLV. In addition, the use of 5 cm H2O PEEP associated with a protective tidal volume could be useful to maintain arterial oxygenation without inducing a possible inflammatory/remodeling response. The authors would like to express their gratitude to Mr. Antonio Carlos Quaresma for animal care and skilful technical PARP assay assistance. This work was supported by The Centers of Excellence Program (PRONEX-FAPERJ), The Brazilian Council for Scientific and Technological Development (CNPq/MCT), and The Carlos Chagas Filho Rio de Janeiro State Research Supporting Foundation (FAPERJ). “
“The neural mechanisms involved in the control of breathing buy A-1210477 must be responsive to challenges affecting O2, CO2, and pH levels in the body, such as exercise, sleep, hypercapnia and hypoxia (Feldman et al., 2003 and Nattie, 2006). The physiological process by which blood gases are detected, called chemoreception, depends on chemical sensors present in the aortic or carotid body

(peripheral chemoreceptors) and within the central nervous system (CNS) (central chemoreceptors) (Ballantyne and Scheid, 2001, Feldman et al., 2003, Guyenet, 2008 and Loeschcke, 1982). The peripheral chemoreceptors, located mainly in the carotid body in the rat, detect changes in the partial Vasopressin Receptor O2 pressure (PO2PO2) or the CO2 pressure (PCO2PCO2) in the arterial blood and send signals through the glossopharyngeal nerve to the commissural region of the nucleus of the solitary tract

(commNTS) (Blessing, 1997, Campanucci and Nurse, 2007, Colombari et al., 1996, Finley and Katz, 1992, Sapru, 1996 and Smith et al., 2006). Similar to the hypoxia, the intravenous (iv) injection of low dose of potassium cyanide (KCN) activates the peripheral chemoreceptors producing tachypneic, pressor and bradycardic responses that are abolished by the bilateral ligature of the carotid body arteries (Braga et al., 2007, Franchini and Krieger, 1993, Haibara et al., 1999 and Moreira et al., 2006). The pressor and bradycardic responses to i.v. KCN are also abolished by electrolytic lesions of the commNTS (Colombari et al., 1996). Under anesthesia, the activation of breathing and the rise in sympathetic nerve discharge (SND) caused by carotid body stimulation are blocked by the injection of glutamatergic antagonists into the commNTS, which suggests that the primary afferent neurons are likely glutamatergic (Sapru, 1996). Detection of an increase in PCO2PCO2 by central and peripheral chemoreception acts to maintain stable arterial PCO2PCO2 (Feldman et al., 2003 and Smith et al., 2006).