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Assessment of Respiratory Function in Conscious Mice by Double-chamber Plethysmography
Published on: July 10, 2018
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[PARTICIPATION OF NO-ERGIC MECHANISMS IN REALIZATION OF RESPIRATORY EFFECTS OF PRO-INFLAMMATORY CYTOKINE
Rossiiskii Fiziologicheskii Zhurnal Imeni I.M. Sechenova
|March 19, 2016
Summary
Nitric oxide (NO) mechanisms modulate vagal respiratory reflexes during inflammation. Blocking NO-synthase with L-NAME prevented IL-1beta
Area of Science:
- Neuroscience
- Respiratory Physiology
- Inflammation Research
Context:
- Pro-inflammatory cytokine Interleukin-1 beta (IL-1beta) influences physiological processes.
- Nitric oxide (NO) plays a role in neural and vascular functions.
- Understanding IL-1beta's respiratory effects is crucial for managing inflammatory conditions.
Purpose:
- To investigate the role of NO-ergic mechanisms in mediating respiratory effects of IL-1beta.
- To examine how inhibiting NO-synthase affects breathing patterns and the Hering-Breuer reflex during IL-1beta administration.
Summary:
- Intravenous IL-1beta administration increased respiratory rate, tidal volume, and lung ventilation in rats.
- Inhibition of NO-synthase using N-nitro-L-arginine methyl ester (L-NAME) abolished the IL-1beta-induced enhancement of the Hering-Breuer inspiratory-inhibitory reflex.
- Breathing pattern changes induced by IL-1beta were not affected by L-NAME.
Impact:
- NO-ergic mechanisms are involved in modulating vagal respiratory reflexes during acute systemic inflammation.
- Increased IL-1beta may enhance the inspiratory-inhibitory reflex strength via increased NO synthesis and subsequent glutamate-ergic transmission in pump neurons.
- Findings suggest a link between NO, IL-1beta, and respiratory reflex control in inflammation.
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