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Postprandial hypotension: hemodynamic differences between multiple system atrophy and peripheral autonomic neuropathy

M Hirayama1, H Watanabe, Y Koike

  • 1Department of Neurology, Nagoya University School of Medicine, Japan.

Journal of the Autonomic Nervous System
|April 1, 1993
PubMed
Summary

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Postprandial hypotension (PPH) involves systemic vasodilation and a failure of compensatory increases in cardiac output and vascular resistance. This study investigated hemodynamic changes after glucose ingestion in patients with autonomic dysfunction.

Area of Science:

  • Cardiovascular Physiology
  • Autonomic Nervous System Function
  • Gastrointestinal Physiology

Background:

  • Postprandial hypotension (PPH) is a common condition, particularly in older adults and those with autonomic dysfunction.
  • The precise mechanisms underlying PPH, especially the roles of systemic vasodilation and impaired compensatory responses, require further elucidation.

Purpose of the Study:

  • To investigate the hemodynamic mechanisms contributing to postprandial hypotension (PPH) after oral glucose ingestion.
  • To compare hemodynamic responses in patients with multiple system atrophy (MSA) and peripheral autonomic neuropathy (PN) against normal controls.

Main Methods:

  • Hemodynamic investigations were conducted following oral glucose ingestion in 10 MSA patients, 3 PN patients, and 16 healthy controls.
  • Measurements included blood pressure (BP), heart rate (HR), cardiac output (CO), lower leg blood flow (LBF), and portal blood flow (PBF).

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  • Impedance plethysmography and B-mode pulse Doppler were utilized for flow measurements.

    • Main Results:

    • Normal subjects showed increased portal blood flow (PBF) and cardiac output (CO) post-ingestion, with minimal changes in BP, lower leg blood flow (LBF), and vascular resistance (LVR).
    • MSA patients exhibited significant BP drops, lack of HR and CO increase, but increased PBF, LBF, and decreased LVR.
    • PN patients showed a transient BP decrease, with PBF and LVR changes similar to MSA, and a greater CO increase than controls.

    Conclusions:

    • Systemic vasodilation, likely mediated by gastrointestinal vasodilatatory peptides, plays a significant role in PPH.
    • The failure to adequately increase cardiac output and lower leg vascular resistance contributes substantially to the development of PPH in autonomic dysfunction.