P: Regional circulation Flashcards
Resting coronary blood flow:
around 225ml/min
What is active hyperemia?
vasodilatory metabolites released when levels of O2 in coronary myocytes becoming insufficient.
Mediators of active hyperemia and their respective mechanisms?
adenosine and nitric oxide.
Reduction in [ATP]I results in an opening of K channels + hyperpolarisation –> relaxation of vascular smooth muscle.
Direct effect of sympathetic nerves on blood vessels :
Vasoconstricts via alpha adrenergic receptors on coronary VSM
Indirect effect of sympathetic nerve activity:
increased cardiac activity produces metabolic vasodilatory metabolites –> increases coronary blood flow. So indirectly causes vasodilation.
Myocardial infarction:
- Decreased cardiac output
- Pulmonary oedema from buildup of blood
- Fibrillation of heart
- Rupture of heart
Basal high SN activity:
- Maintains degree of vasoconstriction
- Binds to a and adrenergic receptors on VSM
- Modulated by baroreceptors
Carotid artery occlusion
- Reduces baroreceptor firing
- Increases SN activity immediately reducing muscle blood flow
- Contributes large increase in MAP
Release of carotid artery
- Increases baroreceptor firing
- Vasodilation caused by reduced SN activity increase muscle blood flow
- Reduction in MAP
Vasodilatory metabolites
Adenosine, K+, CO2, lactic acid. Increase blood flow in active muscle.
VSM in exercising skeletal muscle in response to adrenaline concentration changing:
At start of exercise, low adrenaline concentrations only bind to B1 and B2 receptors, causing vasodilation and increased blood flow to skeletal muscle.
As exercise gets more intense, adrenaline starts binding to a-adrenergic receptors, producing vasoconstrictor effects.
ACh relation to nitric oxide
- Ach can trigger nitric oxide release from endothelial cells
- Activates endothelial nitric oxide synthase
- Endothelial mediated regulation of blood flow
Early stage of exercise
- Ach from neuromuscular junction may also diffuse to local blood vessels promoting NO production, VSM relaxation + vasodilation
- Metabolites in actively contracting muscle induce dilation in microcirculation promoting a pressure gradient with upstream feed arteries.
- Increase in blood flow elevates shear stress, release of NO and further vasodilation
Nitric Oxide during exercise
- NO can cause function sympatholysis –> vasoconstrictor activity blunted as NO inhibits noradrenaline release + opposes a2-mediated constriction of VSM
- Skeletal muscle fibres contain neuronal NOS which increase NO release during contraction which can promote local vasodilation.
Cutaneous circulation:
- Arterioles feed blood into capillaries which loop under epidermis
- Blood flows into complex venous plexus which acts as blood reservoir
- Specialised shunts, arteriovenous anastomoses feed blood into plexuses directly from subcutaneous arteries.