Related Experiment Videos
Catecholamine effects on pulmonary blood vessels in strangulation.
1Department of Forensic Medicine, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Zeitschrift Fur Rechtsmedizin. Journal of Legal Medicine
|January 1, 1987
Summary
Asphyxia from strangulation increases plasma noradrenaline, causing pulmonary vasoconstriction. This occurs as noradrenaline invades endothelial cells in pulmonary arteries and capillaries, leading to congestion.
Area of Science:
- Cardiovascular Physiology
- Pulmonary Circulation
- Asphyxia Research
Background:
- Pulmonary congestion is a critical outcome of asphyxia.
- The role of noradrenaline in asphyxia-induced pulmonary vasoconstriction requires further elucidation.
Purpose of the Study:
- To investigate the mechanism of pulmonary vasoconstriction during asphyxia induced by strangulation.
- To determine the role of noradrenaline uptake in pulmonary endothelial cells.
Main Methods:
- Utilized fluorescence histochemistry, peroxidase-anti-peroxidase (PAP) immunocytochemistry, and autoradiography in guinea pigs.
- Quantified noradrenaline uptake in pulmonary arteries and capillaries via radioassay.
- Examined myoendothelial junctions in constricted arteries.
Main Results:
- Strangulation led to significantly higher noradrenaline uptake in pulmonary arteries and capillaries compared to controls.
- Invasive noradrenaline was observed within myoendothelial junctions of constricted arteries.
- Increased plasma noradrenaline levels were noted following asphyxia.
Conclusions:
- Pulmonary vasoconstriction in strangulation-induced asphyxia is mediated by increased plasma noradrenaline.
- Asphyxia causes noradrenaline to invade pulmonary endothelial cells, triggering vasoconstriction.
- Myoendothelial junctions play a role in this noradrenaline-mediated vasoconstrictive process.