Electron Microscope Study of Atrophy by Denervation in Red and White Muscles of Rat

Franzini, C; Pellegrino, C

doi:10.1016/b978-1-4832-2795-5.50246-x

Cited by 2 publications

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“…Achalasia has a widespread effect on the body. Extraesophageal denervation has been found in the stomach [ 9 ], the vagal trunk and the dorsal motor nuclei [ 10 – 16 ]. Functional and motor abnormalities have been observed in the stomach [ 17 – 22 ], the gallbladder [ 19 ], and the small bowel [ 23 , 24 ].…”

Section: Introductionmentioning

confidence: 99%

Cardiovascular dysautonomia in Achalasia Patients: Blood pressure and heart rate variability alterations

et al. 2021

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Achalasia is a disease characterized by the inability to relax the esophageal sphincter due to a degeneration of the parasympathetic ganglion cells located in the wall of the thoracic esophagus. Achalasia has been associated with extraesophageal dysmotility, suggesting alterations of the autonomic nervous system (ANS) that extend beyond the esophagus. The purpose of the present contribution is to investigate whether achalasia may be interpreted as the esophageal manifestation of a more generalized disturbance of the ANS which includes alterations of heart rate and/or blood pressure. Therefore simultaneous non-invasive records of the heart inter-beat intervals (IBI) and beat-to-beat systolic blood pressure (SBP) of 14 patients (9 female, 5 male) with achalasia were compared with the records of 34 rigorously screened healthy control subjects (17 female, 17 male) in three different conditions: supine, standing up, and controlled breathing at 0.1 Hz, using a variety of measures in the time and spectral domains. Significant differences in heart rate variability (HRV) and blood pressure variability (BPV) were observed which seem to be due to cardiovagal damage to the heart, i.e., a failure of the ANS, as expected according to our hypothesis. This non-invasive methodology can be employed as an auxiliary clinical protocol to study etiology and evolution of achalasia, and other pathologies that damage ANS.

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