Special peripheral circulations

10% CO

Goal of maintaining temperature homeostasis

2 types of vessel

1. Arterioles
2. Basal tone present
3. AV Anastomoses

• No basal tone
• When dilated → act as low resistance pathway to increase skin blood flow
• Constricts when cold
• Countercurrent mechanism exists between the arteries and veins which allows direct heat exchange (Vein returning cool blood, Arteries delivering warm blood)

Intrinsic regulation

Capillaries have a myogenic mechanism (not so for anastomoses)

Locally medited vasodilation when warm, vasoconstriction when cool

Prolonged cold causes cell damage, releases vasoactive mediators and causes vasodilation, "reactive hyperaemia"

Extrinsic regulation

SNS when cold -> NA -> vasoconstriction of both vessel types

SNS when warm -> ACh (exclusive to skin!) -> vasodilation and sweating

Hypothalamus -> blushing, blanching in response to emotion (embarrassment, arousal, fear).

15% CO

$$\text{Cerebral blood flow} = 50\text{ml}\text{min}^{-1}100\text{g}^{-1} = 700\text{mL}\text{min}^{-1} = 15\% CO$$

$$\text{Cerebral blood flow} = \frac{CPP}{\text{Cerebral vascular resistance}} = \frac{MAP - \text{min}(CVP, ICP)}{CVR}$$

Myogenic mechanism maintains cerebral blood flow at around 50ml/min for a MAP of 60 to a MAP of 160.

Neurovascular coupling: increased neuronal activity is sensed by one pole of astrocytes, which release potassium onto cerebral vessels from their other pole. The potassium ramps up the Na/K ATPase pump on the smooth muscle, causing hyperpolarization and vasodilation.

CO2 and low plasma pH cause cerebral vasodilation via endothelial cells producing eNOS \(\to\) NO release

Oxygen: A fall in PaO2 or a rise in oxygen requirements will cause adenosine formation -> vasodilation; also induce eNOS \(\to\) NO

Temperature: Fever increases cerebral blood flow

Viscosity: increases CVR, decreasing CBF.

From the Coeliac, SMA, and IMA.

Arterioles and venules in the villi form a countercurrent exchange, facilitating rapid absorption.

This also allows for shunting of O2 from the arteriole to the venule at the bases of the villi. This is exaggerated at low flow rates -> necrosis of villi.

Local:

Weak myogenic mechanism

Weak adenosine-mediated autoregulation in response to hypoxia

Extrinsic:

Gastrin, CCK, and absorbed glucose all vasodilate in response to food ingestion

\(\alpha_1\) receptors abound; potent vasoconstriction of both arterioles and capacitance vessels in response to catecholamines

30% CO

Unique dual inflow: 75% flow from portal vein, 25% hepatic artery (but the artery delivers 50% of the DO2).

These combine to form sinuoids.

• Large pressure drop over the resistance arterioles such that the pressure in the sinusioid is only ~10mmHg. Changes in venous pressure are transmitted directly to the sinusoids.
• Highly permeable - fenestrated with reflection coefficient 0

Local regulation:

Portal vein resistance is not under local regulation; portal vein flow is largely determined by splanchnic arterial flow

Hepatic arterioles

• myogenic mechanism (maintains flow for MAP 80-180),
• hepatic arterial buffer response, i.e. they increase flow inversely with portal flow changes. Adenosine constantly produced by GIT. Normally the portal vein washes away adenosine. If portal flow falls, adenosine accumulates, vasodilating the hepatic arterioles.

Extrinsic regulation:

Portal vein resistance is deceased by VIP and ACh following a meal

The portal system and arterial system vasoconstrict in response to catecholamines, increasing stressed volume

Somatostatin \(\to\) portal vein constriction

Physiological determinants:

Portal vein flow \(\propto\) splanchic arterial flow

\(\Delta\)P from sinusoids is to CVP is small \(\to\) raised CVP or TR severely impacts flow; inspiration \(\to \ \downarrow)ITP \(\to \ \downarrow\)CVP \(\to \ \uparrow\)hepatic blood flow

\(\downarrow\)CO or MAP reduce both arterial and portal blood flow

Umbilical artery, from the internal iliacs, carry deoxygenated blood to the placenta.

Umbilical vein returns oxygenated and nutrient-containing blood

Half goes through the liver (for nutrition), half to the IVC via the ductus venosus.

Ductus venosus, lower extremity, and post-hepatic blood then all join in the IVC.

Mostly ductus venosus blood travels in a jet to the foramen ovale, into the LA and thence the LV.

The remaining IVC blood mixes with the coronary sinus and SVC blood in the RA and is ejected into the pulmonary artery. Only 10% goes to the lungs (which are heavily vasoconstricted because of HPV). This 10% ultimately joins the foramen ovale blood in the LV. The remainder travels to the arch of the aorta via the ductus arteriosus.

The LV blood supples only the head, upper limbs, and left coronary artery. The RV (by way of the ductus arteriosus) supplies the rest of the body, and pumps twice as much blood as the LV.

During birth:

Stretch of the umbilical vessels triggers vasoconstriction.

Once flow through the umbilical vein ceases, the ductus venosus also closes.

From asphyxia during birth:

Respiratory center triggered and neonate inhales, filling the lungs with air

Pulmonary vascular resistance falls precipitously

Flow to the LA increases, flow to the RA (previously from umbilical vein) decreases

This snaps the foramen ovale valve closed

Over the next 2 days:

Ductus arteriosus closes in response to high oxygen tension

This is caused by FALLING levels of PGE2

Ibuprofen promotes closure, while PGE1 keeps the thing open