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Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues
Published on: June 3, 2019
[Mast cell and blood coagulation functions during prolonged noradrenaline administration]
Biulleten' Eksperimental'Noi Biologii I Meditsiny
|December 1, 1989
Summary
Long-term noradrenaline injection in dogs reduces connective tissue mast cells, increasing young forms and heparin release. This suggests heparin acts as an unspecific adaptogen, influencing hemostasis.
Area of Science:
- Pharmacology
- Histology
- Hematology
Background:
- Connective tissue mast cells play roles in various physiological processes.
- Noradrenaline is a key neurotransmitter and hormone involved in stress responses.
- Heparin is a crucial anticoagulant and biologically active substance.
Purpose of the Study:
- To investigate the effects of prolonged noradrenaline administration on mast cells in dogs.
- To analyze changes in mast cell morphology and degranulation.
- To correlate these cellular changes with alterations in the coagulation system.
Main Methods:
- Sustained intravenous infusion of noradrenaline (0.56 microgram/kg/min for 2 hours daily over six days) in canine subjects.
- Histological examination of connective tissue to quantify mast cell populations and assess morphology.
- Measurement of free heparin levels and assessment of anticoagulant activity in the hemostasis unit.
Main Results:
- A significant decrease in the total number of connective tissue mast cells was observed.
- A shift in mast cell population towards younger forms, with a reduction in mature cells.
- Evidence of marked mast cell degranulation, formation of cell clusters, and increased free heparin levels.
- Activation of the anticoagulant system, indicating a functional change in hemostasis.
Conclusions:
- Prolonged noradrenaline exposure alters mast cell populations and induces degranulation in dogs.
- The observed increase in free heparin levels suggests its release from degranulating mast cells.
- Released heparin likely contributes to the observed activation of anticoagulant hemostasis, acting as an unspecific adaptogen.
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