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Alpha-thrombin-induced pulmonary vasoconstriction.

M J Horgan1, J W Fenton, A B Malik

  • 1Department of Physiology, Albany Medical College of Union University, New York.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|November 1, 1987
PubMed
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Thrombin causes pulmonary vasoconstriction and edema by activating cyclooxygenase metabolites. The enzyme's proteolytic site is essential for these effects, highlighting thrombin's role in lung injury.

Area of Science:

  • Pulmonary Circulation
  • Vascular Pharmacology
  • Biochemistry

Background:

  • Thrombin is a key enzyme in hemostasis and inflammation.
  • Its direct effects on pulmonary vasculature are not fully understood.
  • Pulmonary edema and vasoconstriction can lead to severe respiratory compromise.

Purpose of the Study:

  • To investigate the direct effects of alpha-thrombin on pulmonary vasomotor tone.
  • To elucidate the mechanisms underlying thrombin-induced pulmonary vasoconstriction and edema.
  • To determine the role of thrombin's enzymatic activity in these responses.

Main Methods:

  • Isolated perfused guinea pig lungs.
  • Administration of alpha-thrombin and modified thrombins.
  • Measurement of pulmonary arterial pressure (Ppa), pulmonary capillary pressure (Ppc), and lung weight.

Related Experiment Videos

  • Assessment of thromboxane B2 concentration.
  • Pharmacological inhibition of cyclooxygenase and thromboxane synthase pathways.

    • Main Results:

    • Alpha-thrombin caused dose-dependent increases in Ppa and Ppc, indicating vasoconstriction.
    • Pulmonary edema and increased lung weight were observed post-thrombin injection.
    • Modified thrombins lacking specific sites did not induce these effects.
    • Inhibition of cyclooxygenase or thromboxane synthase blocked thrombin-induced vasoconstriction and edema.
    • Hirudin, a thrombin antagonist, also inhibited these responses.

    Conclusions:

    • Thrombin induces pulmonary vasoconstriction, primarily in postcapillary vessels.
    • This response is mediated by cyclooxygenase-derived metabolites.
    • Pulmonary edema formation is dependent on cyclooxygenase pathway activation.
    • The serine proteolytic site of alpha-thrombin is critical for its pulmonary vasoconstrictor and edemogenic effects.