2007
DOI: 10.1203/pdr.0b013e318098721a
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Ventilatory Response to Hypoxia during Endotoxemia in Young Rats: Role of Nitric Oxide

Abstract: Administration of Escherichia coli endotoxin attenuates the ventilatory response to hypoxia (VRH) in newborn piglets, but the mechanisms responsible for this depression are not clearly understood. Nitric oxide (NO) production increases during sepsis and elevated NO levels can inhibit carotid body function. The role of endothelial NO on the VRH during endotoxemia was evaluated in 26 young rats. Minute ventilation (V E ) and oxygen consumption (VO 2 ) were measured in room air (RA) and during 30 min of hypoxia (… Show more

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Cited by 17 publications
(14 citation statements)
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“…This is associated with an attenuated ventilatory response to hypoxia, both before and after carotid sinus nerve transection [17] . This is consistent with prior data that endotoxemia impairs the ventilatory response to hypoxia in rat pups [18] , and that prostaglandin-mediated respiratory inhibition may be implicated [19] . In summary, as seen in figures 3 and 4 , we speculate that immature or impaired respiratory control and resultant intermittent hypoxia may initiate a proinflammatory and/or prooxidant cascade that, in turn, may further inhibit respiratory neural output and aggravate the problem.…”
Section: Intermittent Hypoxia As a Proinflammatory Stresssupporting
confidence: 93%
“…This is associated with an attenuated ventilatory response to hypoxia, both before and after carotid sinus nerve transection [17] . This is consistent with prior data that endotoxemia impairs the ventilatory response to hypoxia in rat pups [18] , and that prostaglandin-mediated respiratory inhibition may be implicated [19] . In summary, as seen in figures 3 and 4 , we speculate that immature or impaired respiratory control and resultant intermittent hypoxia may initiate a proinflammatory and/or prooxidant cascade that, in turn, may further inhibit respiratory neural output and aggravate the problem.…”
Section: Intermittent Hypoxia As a Proinflammatory Stresssupporting
confidence: 93%
“…We recognize that our model comprising intrapulmonary LPS exposure may initiate inflammation that is compartmentalized to the lung, initiate a blood-borne proinflammatory response, or both. Prior studies have employed injection of E. coli, endotoxin, LPS, or recombinant IL-1β via the intraperitoneal route to simulate neonatal sepsis in rat pups (Ladino et al, 2007, Olsson et al, 2003). As IL-1β does not readily cross the blood brain barrier, a likely mechanism for the resultant apnea was thought to be IL-1β-induced activation of the cyclooxygenase-2 pathway and release of prostaglandin E2 which can cross the blood brain barrier with resultant respiratory depression (Hofstetter et al, 2007).…”
Section: Discussionmentioning
confidence: 99%
“…The possibility that such differences also contribute to the opposite effects of inflammation induced by LPS versus inspired hypoxia on chemoreflexes (inhibiting vs. facilitating, respectively), remains to be tested. In a number of animal species, the hypoxic or hypercapnic ventilatory responses are actually attenuated by systemic inflammation (Fernández et al, 2008; Ladino et al, 2007; McDeigan et al, 2003). …”
Section: Cns Inflammation and Neuroplasticitymentioning
confidence: 99%