Some feedback to the next layer of questions:
Local and Autonomic Control of the Vasculature Smooth muscle surrounds each blood vessel, and the tension of these cells controls the radius of the vessel.
Vasoconstriction is caused by contraction of the smooth muscle cells, and vasodilatation occurs passively, powered by BP as the vascular muscle relaxes.
Vessel tone is controlled by local factors and autonomic mechanisms. All of these are short-term corrections to changes in blood pressure.
This is most likely what we visual with MOXY as we can see
In the long term, control of blood pressure is determined by fluid balance--fluid intake vs fluid output. Thus, the kidneys are the most important organs in control of BP.This is not visual with MOXY tHb reactions ( too slow)
The fluctuation is due to BP changes and adjust ments and in sports with big % of muscle mass involved teh blood pressure si needed to balance the “ weakness” of the heart as it can ‘t maintain the O2 demand from all the involved muscles and the central governor has to make some “decisions” on where is what needed to survive.
The non-involved muscle will be the one we see the most fluctuations .
Smaller arteries and arterioles have a basal tone, that is the muscle is always partially contracted at rest. This is necessary to provide for vasodilation, which can only be accomplished by relaxing the muscles. That means that tissues capable of large increases in blood flow (such as skeletal muscle) have a high basal tone. Basal tone is slight in most veins.
Local control of blood vessels:
Local temperature: Especially important in the skin. High ambient temperatures cause cutaneous arterioles and veins to dilate.
TSI % in NIRS, which are based on a stable tHb show some interesting variation. If we use a NIRS, who takes skin O2 information and pair it up with MOXY , who takes muscle SmO2 we will see that whne Skin flow goes up SmO2 drops and when Skin flow drops SmO2 goes up.
See test we showed with compression garments. Cold causes vasoconstriction, which conserves heat and safeguards core temperature.
External pressure compresses the vessels and impairs blood flow. May be caused in muscle by muscle contraction (myocardial or skeletal), or in skin by sitting, kneeling, or lying.
All this can be nicely demonstrated using MOXY. The interesting question is often what overrules what.
Autoregulation--the relative constancy of tissue perfusion in the face of pressure changes. Independent of the nervous system. Vessels respond directly to changes in arterial pressure. A rise in pressure evokes arteriole vasoconstriction (and increased vascular resistance), while a fall in pressure evokes vasodilation (and reduced resistance). Account for near-constancy of blood flow. A change in arteriole radius takes 30 to 60 seconds to develop fully, so a sudden change is pressure elicits an initial brief change in flow (Increased pressure, increased blood flow). Keeps capillary pressure stable. Myogenic mechanism--an increase in vascular pressure causes vascular smooth muscle to contract; reduced pressure causes muscle relaxation.
Endothelium-derived relaxing factor (NO)--released in response to shear stress to cause vasodilation.
A balance between autoregulation and EDRF is largely responsible for regulation of vessel diameter.
Local hypoxia causes vasodilation of arterioles
Carbon dioxide causes vasodilation
Extracellular K+, which can double in contracting muscle, causes vasodilation
Autacoids, vasoactive chemicals that are produced locally, released locally, and act locally (in effect, local hormones); they include histamine, which participates in inflamation. Histamine (a derivative of the amino acid, histadine) is released in response to trauma and allergic reactions. It dilates arterioles and contricts veins.
Reactive hyperaemia--after inadequate blood flow (i.e., from compression of skin), the blood flow immediately after release is much higher than normal. Vasodilator metabolites accumulate. Resupplies oxygen and nutrients to ischemic tissue very rapidly.
Increased blood flow (caused by an increase in arterial pressure), vasodilator products of tissue metabolism are washed out and their interstitial concentration declines, increasing vessel tone.
Neural vasoconstrictor regions are tonically active (averaging approx 1 impulse per second at rest) contributing to basal tone. Reflexes that enhance this activity result in more frequent impulses (as high as 10 per second) to the terminals containing norepinephrine, which is released and elicits constriction.
Affects both arteries and veins, but has most important effects on small arteries and arterioles. Capillary pressure is reduced by arteriole vasoconstriction.
Skin responds more profoundly to sympathetic activation--Skin more sensitive to sympathetic stimulation and also has lower basal sympathetic tone than most other tissues, so greater change is possible.
If sympathetic outflow is generalized, results in rise in BP (by increased peripheral resistance and increased cardiac output).
Circulating catecholamines (E, NE from adrenal) have similar but less profound effects.
Parasympathetic fibers generally not found on arterioles. Parasympathetic innervation of arterioles in salivary glands
Baroreflex--vasodilation caused by fall in sympathetic activity
Baroreceptors are stretch receptors located in the carotid sinuses (where internal and external carotids split) and in the aortic arch. Impulsed from them travel up the 9th and 10th nerves to the NTS. Stim of NTS inhibits sympathetic outflow to peripheral vessels (depressor effect) -- (also causes bradycardia via parasympathetic mechanisms, which also lead to reduced BP).
Baroreceptors are also located in heart and pulmonary vessels.
Provide short-term adjustment, but long term changes in blood pressure are achieved by changing the fluid balance (via the kidneys).
The baroreceptors in the heart and pulmonary circulation also has a diuretic effect on the kidneys to decrease blood volume.
Hypothalamus is sensitive to changes in brain temp, and shunt blood to skin to diffuse heat or away from skin to concerve heat.
Forebrain--Emotional responses often elicit vasodilatory and depressor responses (blushing, fainting).
Pain also effects BP. Cutaneous pain raises BP, while visceral pain lowers it.
Lung stretch receptors--Inflation of lungs causes systemic vasodilation, while deflation causes vasoconstriction.
The brain and heart are controlled primarily by intrinsic factors. Thus, in acute hemorhage, when there is massive sympathetic discharge to contrict vessels, blood flow to the brain and heart are not greatly reduced.
In the skin, external vascular control is dominant.
In skeletal muscle, both are prominent--at rest, external (sympathetic) vasoconstrictor tone is dominant. In anticipation of, and at the start of exercise, blood flow to leg muscles increases. After the onset of exercise, vasodilation occurs as a result of local increase in metabolites. Vasoconstriction occurs in inactive tissues as a result of general sympathetic discharge, but constrictor impulses reaching vessels of active muscles are overridden by local metabolic effect. This allows increased blood flow where needed and shunts blood away from areas that don't need it