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Autonomic control of heart period in duodenal ulcer patients insights from spectral analysis of heart rate variability
Authors:Lucini D  Cerchiello M  Basilisco G  Cainelli M  Bianchi P A  Fiorelli G  Malliani A  Pagani M
Affiliation:Centro Ricerca sulla Terapia Neurovegetativa, Medicina Interna I, Ospedale L. Sacco, CNR, Università di Milano, Italy.
Abstract:
Beyond the fundamental pathogenetic importance of Helicobacter Pylori a possible additional role of vagal innervation in favouring or modulating the clinical history of duodenal ulcer (DU) has been suggested by old studies employing invasive methodologies. Aim of this study was to assess whether vagal prevalence in autonomic modulation was present in healed DU patients (n=20) as compared to controls,(n=50), using a validated non-invasive methodology, based on spectral analysis of cardiovascular variability. This approach provides markers of the sympathetic and vagal modulations of the SA node, respectively by way of the normalized low frequency (LF(RR)) and high frequency (HF(RR)) components of RR interval variability; LF/HF ratio furnishes a marker of sympatho-vagal balance. In addition, sham feeding (SF) provided a means to assess, in DU patients, neurally mediated acid secretion, as the SF acid output (SAO) to basal acid output (BAO) ratio (SAO/BAO). Results showed that LF(RR) was smaller in DU patients than in controls (40.3+/-3.9 vs. 52.3+/-2.3 normalized units, nu; P<0.05). On the contrary, HF(RR) was greater (52.1+/-3.7 vs. 35.7+/-2.3 nu; P<0.05). Conversely the LF component of SAP variability, a marker of sympathetic vasomotor modulations, and the index alpha, a measure of baroreflex control of the SA node, as well as respiratory patterns, were similar in the two groups. SAO/BAO ratio was significantly correlated with markers of autonomic control of the SA node (r = -0.67, P<0.0083 with HF(RR)). In conclusion results suggest an enhanced vagal modulation of heart period in DU patients at rest, that appears linked to indices of neurally mediated gastric acid secretion response.
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