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Cutaneous venodilation in response to systemic hypoxemia in dogs
The Journal of Surgical Research
|January 1, 1984
Summary
Systemic hypoxemia causes saphenous vein dilation in dogs via neural pathways involving the vagus nerves and carotid chemoreceptors. This reflex may impair cardiac output during hypoxemia.
Area of Science:
- Cardiovascular Physiology
- Neuroscience
- Respiratory Physiology
Background:
- The role of cutaneous veins in cardiovascular adjustments to hypoxemia is not fully understood.
- Systemic hypoxemia can trigger complex physiological responses affecting blood flow distribution.
Purpose of the Study:
- To investigate the participation of the saphenous vein in the cardiovascular response to systemic hypoxemia.
- To determine the neural mechanisms underlying hypoxemia-induced changes in saphenous vein tone.
Main Methods:
- Experiments were conducted on chloralose-anesthetized, paralyzed, and ventilated dogs.
- The saphenous vein was perfused at constant flow, and responses to 10% oxygen inhalation were measured.
- Neural pathways were interrupted by vagotomy, carotid chemoreceptor denervation, or lumbar sympathetic chain section.
Main Results:
- Systemic hypoxemia induced a significant decrease in saphenous vein perfusion pressure, indicating vasodilation.
- Arterial pressure increased slightly during hypoxemia.
- Hypoxemia-induced saphenous vein dilation was abolished by interrupting afferent (vagus/carotid) or efferent (sympathetic) neural pathways.
Conclusions:
- Systemic hypoxemia elicits a neurally mediated dilation of the saphenous vein in anesthetized dogs.
- This reflex is dependent on intact vagus nerves and/or carotid chemoreceptors.
- Saphenous vein dilation during hypoxemia may be a decompensatory mechanism, potentially compromising cardiac output.