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Author (up) Martel, E.; Ponchon, P.; Champeroux, P.; Elghozi, J.L.; Renaud De La Faverie, J.F.; Dabire, H.; Pannier, B.; Richard, S.; Safar, M.; Cuche, J.L. isbn  openurl
  Title Mechanisms of the cardiovascular deconditioning induced by tail suspension in the rat Type Miscellaneous
  Year 1998 Publication Abbreviated Journal  
  Volume Issue Pages H1667-H1673  
  Keywords Mechanisms, cardiovascular, cardiovascular deconditioning, tail suspension, rat, Animal, Blood Pressure/physiology, Cardiovascular Deconditioning/physiology, Catecholamines/blood, Heart Rate/physiology, Hindlimb Suspension, Male, Rats, Rats, Wistar, Rec  
  Abstract The aim of the present work was to obtain insights into the pathophysiology of cardiovascular deconditioning (CVD) induced by tail suspension (TS) in the rat: during TS, when central venous pressure (CVP) has been normalized (E. Martel, P. Champeroux, P. Lacolley, S. Richard, M. Safar, and J. L. Cuche. J. Appl. Physiol. 80: 1390-1396, 1996), and during simulated orthostatism (SO), when transient episodes of hypotension and bradycardia are disclosed, bradycardia with SO represents a response that seems peculiar to the rat compared with humans. According to basic physiology, a reduced activity of the sympathetic system induced by increased CVP was suspected but was not supported by data obtained through spectral analysis of blood pressure (BP) and heart rate (HR) variability or measurements of plasma catecholamine concentration during TS. Nonetheless, indirect evidence was obtained. During SO, plasma catecholamine concentration was lower in TS rats than in controls, suggesting a reduced synthesis of catecholamines, itself secondary to reduced activity of the sympathetic system. Furthermore, after 48 h of TS, the number of binding sites and affinity of alpha-receptors in rat aorta were increased, compatible with a reduced level of neurotransmitter in the synaptic cleft. A second series of experiments was carried out to study hypotension and bradycardia in TS rats during SO. Hypersensitivity of serotonergic mechanisms was suspected. Two 5-HT3 receptor antagonists (ondansetron and MDL-72222) blocked hypotension and restored tachycardia, basic features of orthostatic adaptation of the circulatory system. Response to the 5-HT3 receptor agonist was measured through dose-response curves of BP and HR after injection of 2-methylserotonin. After low doses, hypotension (10 micrograms/kg) and bradycardia (3 and 10 micrograms/kg) were significantly greater in 48-h TS rats than in controls. Thus CVD in the rat induced by TS appears to implicate at least two mechanisms: reduced activity of the sympathetic system and hypersensitivity of serotonergic mechanisms.  
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  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title Journal Article  
  Series Volume 274 Series Issue 5 Pt 2 Edition  
  ISSN ISBN 0363-6135 Medium  
  Area Expedition Conference  
  Notes Approved no  
  Call Number refbase @ user @ Martel1998 Serial 9212  
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