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Related Experiment Videos

Microcirculatory functions in systemic sclerosis: additional parameters for therapeutic concepts?

H P Albrecht1, D Hiller, O P Hornstein

  • 1Department of Dermatology, University of Erlangen-Nürnberg, Germany.

The Journal of Investigative Dermatology
|August 1, 1993
PubMed
Summary
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Progressive systemic sclerosis (PSS) impairs skin microcirculation, causing "hyperemic hypoxia." Calcitonin therapy improved oxygen levels and blood flow, suggesting vascular benefits in PSS patients.

Area of Science:

  • Dermatology
  • Vascular Biology
  • Rheumatology

Background:

  • Progressive systemic sclerosis (PSS) is characterized by microvascular dysfunction.
  • Cutaneous microcirculation plays a crucial role in thermoregulation and oxygen delivery.
  • Understanding PSS-related vascular changes is vital for therapeutic development.

Purpose of the Study:

  • To investigate the functional reactivity of cutaneous microcirculation in PSS patients.
  • To assess the impact of calcitonin therapy on microcirculatory parameters and prostacyclin levels in PSS.
  • To explore the role of vascular factors in PSS pathogenesis.

Main Methods:

  • Simultaneous measurement of red blood cell flux and cutaneous oxygen tension (pcuO2) during hyperemic challenges (arterial occlusion, local heating).

Related Experiment Videos

  • Assay of serum 6-keto-prostaglandin 1 alpha (PGF1 alpha) levels.
  • Evaluation of a 10-day intravenous calcitonin infusion in PSS patients.

    • Main Results:

    • PSS patients exhibited reduced initial pcuO2, inversely proportional to flux and PGF1 alpha.
    • Hyperemic responses were significantly blunted in PSS, indicating "hyperemic hypoxia."
    • Calcitonin infusion led to increased pcuO2, temporary rises in PGF1 alpha and flux, and improved clinical symptoms.

    Conclusions:

    • Calcitonin therapy demonstrates a beneficial effect on cutaneous microcirculation in PSS.
    • The therapy may act partly through increasing endogenous prostacyclin release.
    • Disturbed dermal vessel reactivity and elevated PGF1 alpha levels highlight vascular involvement in PSS pathogenesis.