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Hypothermic circulatory arrest causes multisystem vascular endothelial dysfunction and apoptosis
W A Cooper1, I G Duarte, V H Thourani
1Cardiothoracic Research Laboratory, Carlyle Fraser Heart Center of Crawford Long Hospital, and Emory University School of Medicine, Atlanta, Georgia 30365, USA.
The Annals of Thoracic Surgery
|April 6, 2000
Summary
Deep hypothermic circulatory arrest (DHCA) causes endothelial dysfunction in cerebral microvessels, renal arteries, and pulmonary veins. DHCA also leads to duodenal apoptosis, potentially contributing to organ failure.
Area of Science:
- Cardiovascular Research
- Organ Transplantation
- Surgical Critical Care
Background:
- Deep hypothermic circulatory arrest (DHCA) is linked to multiple organ failure.
- Endothelial dysfunction and apoptosis are potential mechanisms underlying organ damage.
- The impact of DHCA on various organ systems requires further investigation.
Purpose of the Study:
- To investigate the effects of DHCA on endothelial function in brain, kidney, and lung vasculature.
- To assess the incidence of apoptosis in different tissues following DHCA.
- To elucidate the role of endothelial dysfunction and apoptosis in post-DHCA organ failure.
Main Methods:
- Pigs underwent either DHCA (18°C for 60 minutes) or normothermic cardiopulmonary bypass (CPB).
- Endothelial function was evaluated using vasorelaxation responses to bradykinin and acetylcholine.
- Apoptosis was assessed via DNA laddering in duodenal tissue.
Main Results:
- DHCA impaired endothelial relaxation in small cerebral arteries, renal arteries, and pulmonary veins.
- Apoptosis was significantly higher in duodenal tissue after DHCA compared to controls.
- In vivo transcranial vasorelaxation responses to acetylcholine remained similar between groups.
Conclusions:
- DHCA induces endothelial dysfunction in specific vascular beds, including cerebral microvessels, renal arteries, and pulmonary veins.
- DHCA is associated with duodenal apoptosis.
- Endothelial dysfunction and apoptosis following DHCA may contribute to multisystem organ failure.