Listen to the recording. Repeat each medical term during the pause in the recording. Mind the stress.
| active (arterial) hyperemia | () |
| arteriole | |
| blood flow | |
| blood vessel | |
| capillary bed | |
| coin stacks | ( ) |
| elasticity | |
| embolus (pi.: emboli) | |
| endogenous/vascular ischemia | / |
| hematogenous/obturationischemia | / |
| inflow | |
| ligature | 1) ; 2) , (, ), ; , (, ), |
| metarteriole | , , |
| microcirculation | |
| microcirculatory bed | |
| mixed/combined hyperemia | |
| outflow | |
| passive (venous) hyperemia, congestion | () , |
| plasma capillary | |
| precapillary | ; |
| rheologic | , |
| rouleaux | (pl rouleau, .) ( ) |
| sludge of erythrocytes | |
| sphincter | , ( , ) |
| stasis | ( ) |
| terminal | , ; ; , |
| thoroughfare, preferencial channel | , |
| thrombus (pl. trombi) | (.: ) |
| tissue-type/compression ischemia | / |
| true | |
| venule | |
| viscosity |
Without looking into the text listen to the recording.
Say what information you have gathered. Listen to the text again.
Now, read the text silently, trying to grasp all the details of thecontents.
Then, read it simultaneously with the speaker, trying to catch upwith the tempo.
After that read the text aloud, trying to imitate the intonation.
MICROCIRCULATION is the movement of blood in small blood vessels not more than 100 mcm in diameter: arterioles, terminal arterioles with precapillary sphincters, metarterioles (with the thoroughfare, i.e. preferenciai channel), true capillaries, plasma capillaries, postcapillaryvenules (8-30 mcm), collective venules (30-50 mcm), and muscle venules (50-100 mcm). A metarteriole branches from the middle part of the arteriole, passing through the capillary bed to the venule. It is wider than a true capillary and is surrounded in the first half (the proximal part) of its way through the capillary bed with smooth muscle cells. A proximal part of the metarteriole gives rise to numerous true capillaries. The precapillary sphincters of the arteriole and metarteriole control the entry of blood into the capillaries. The distal segment of the thoroughfare receives capillaries from the microcirculatory bed, but no sphincters are present where the afferent capillaries enter the thoroughfare. The thoroughfare, or principal channel, is characterized by low resistance to blood flow.
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The changes occurring in microcirculation are referred to as hyperemia and ischemia. Hyperemia is a phenomenon of increased blood filling in an organ or in a portion of tissue. There are several variations of hyperemia: arterial, venous and mixed type.
Arterial hyperemia (Latin: fluxio, active hyperemia) is a dynamic increase of blood filling in a portion of tissue due to enhanced inflow of blood through arteries. Outflow is also increased here in accordance with the enhanced inflow, as well as the linear and volume velocities of blood flow. In this case the number of blood capillaries, partial pressure of oxygen in blood, and oxygen supply of the tissue are increased, too.
Venous hyperemia (Latin: congestio, passive hyperemia. congestion) develops due to obstructed venous drainage of blood, whereas the inflow remains normal. Practically, the etiology of venous hyperemia is limited to mechanical obstruction to drainage inside the veins (thrombi or emboli), or to external pressure (ligature, tumor, etc). In the case of venous hyperemia the blood flow is slowed down. Postcapillaryvenulesand capillaries appear distinctly enlarged above the area obstructing the outflow. The linear and volume velocities of the blood flow are decreased. Partial pressure of oxygen in venous blood is low. Oxygen supply of the tissue is poor.
Mixed (combined) hyperemia results from a combination of venous and arterial types, in which case obstructed venous drainage of blood takes place simultaneously with increased inflow. It may occur as transient state from active hyperemia to congestion.
Ischemia is characterized by the decrease of blood flow within an organ or tissue on account of decreased or inadequate inflow through the arteries. Ischemia may be hematogenous (obturation), endogenous (vascular) and tissue-type (compression). Progressive slowing down of blood flow in the case of venous hyperemia or ischemia may result in complete cessation of blood flow and, thus, cause congestive, or ischemic stasis. Stasis (genuine, or capillary) may also develop due to changes in the rheologic properties of blood within microvessels (viscosity and elasticity).
Stasis is preceded by pre-static phenomena: jerk-like or pendulum-like blood motions, sludge of erythrocytes, forming of coin stacks (rouleaux), etc.
The biophysics of blood microcirculation during pre-static phenomena and stasis was thoroughly investigated by Alexander LeonidovichChizhevsky (see his biography).
Answer the questions.
1. What type of blood movement is referred to as microcirculation?
2. What types of blood vessels provide for microcirculation?
3. Which part of the metarteriole gives rise to numerous true capillaries?
4. Which sphincters control the entry of blood into the capillaries?
5. Which segments of the thoroughfare (principal channel) receive capillaries from the microcirculatory bed?
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6. What resistance to blood flow is characteristic of the thorough fare?
7. What two main types of abnormality occur in microcirculation?
8. What is hyperemia?
9. What variations of hyperemia may be distinguished?
10.What peculiarities are characteristic of arterial or active hyperemia?
11.What causes venous or passive hyperemia (congestion)?
12.What combination gives rise to mixed or combined hyperemia?
13.What is ischemia characterized by?
14.What variations of ischemia exist?
15.What processes may cause congestive or ischemic stasis?
16.By what kind of pre-static phenomena is stasis preceded?
17.What is rouleaux phenomenon? (use the text)
