- •13. Disturbances of the peripheral blood circulation
- •13.1. Name the main forms of the local disturbances of blood circulation:
- •13.2. What is arterial hyperemia?
- •13.3. What functional changes and clinical attributes characterize arterial hyperemia?
- •13.4. What factors can be a cause of arterial hyperemia? What mean the physiological and pathological arterial hyperemia?
- •13.5. Name the main mechanisms of the pathological arterial hyperemia development.
- •13.6. What is the essence of the neurotonic mechanism of development of the arterial hyperemia ?
- •13.7. Explain the neuroparalytic mechanism of development of the arterial hyperemia.
- •13.8. What humoral factors can be the cause of development of arterial hyperemia?
- •13.9. What is the role of endothelium of blood vessels in development of arterial hyperemia?
- •13.10. Name possible outcomes of arterial hyperemia.
- •13.11. What is venous hyperemia?
- •13.12. What factors can be the cause of venous hyperemia?
- •13.13. What attributes display venous hyperemia?
- •13.14. What local and common violations can be consequence of venous hyperemia?
- •13.15. What is ischemia?
- •13.16. What attributes are typical for ischemia?
- •13.17. Name the main types of ischemia depending on the reason and mechanisms of its occurrence.
- •13.18. How are defined the character of metabolic, functional and structural disturbances in a tissue in case of its ischemia?
- •13.19. What consecutive stages characterize the pathogenesis of alterations in ischemic tissues?
- •13.20. What is stasis?
- •13.21. Name the main variants of stasis and their reasons.
- •13.22. What is the thrombosis?
- •13.23. Name three major factors, promoting thrombosis formation (Virhov’s triad).
- •13.24. What phases is the process of blood clot forming consists of? What is their essence?
- •13.25. What negative consequences can thrombosis formation in pathology have?
- •13.26. What is embolism?
- •13.27. What kinds of embolism are assigned?
- •13.28. Name principal causes of embolism exogenous.
- •13.29. Name the principal causes of embolism of endogenous origins.
- •13.31. What is the essence of a phenomenon called "sludge"?
- •13.32. How the exchange of water between plasma of blood and an interstitial liquid is carried out?
- •13.33. How does hydrostatic and oncotic pressure of blood and an intercellular liquid changes influence on intensity of processes of a filtration-reabsorption of water in capillaries?
- •13.34. What is the insufficiency of lymphokinesia? Name its main forms.
13.7. Explain the neuroparalytic mechanism of development of the arterial hyperemia.
Neuroparalytic arterial hyperemia develops at the discontinuance of pulsation on sympathetic adrenergic nerves possessing vasoconstrictive activity. In experiment on animals it is modelled with the help of surgical interventions and pharmacological methods. It is frequently applied section of sympathetic adrenergic fibers and nerves. So, on cutting sympathetic fibers of the sciatic nerve expansion of vessels of the leg of frog (A. Valter experience) is observed, and on removal of cervical unit of the sympathetic trunk reddening and rise in temperature of the ear of the rabbit on the side of operation (K. Bernar experiment) happen.
There are different pharmacological methods of modeling of arterial hyperemia of neuroparalytic type: violations of formation, deposition and releasing of catecholamines by the endings of sympathetic nerves (application of sympatolytics), blockade of α-adrenoreceptors of vascular smooth muscles by corresponding adrenoceptor antagonists, blockade of transmission of nervous impulses in sympathetic nodes by ganglionic blocking agents.
13.8. What humoral factors can be the cause of development of arterial hyperemia?
Arterial hyperemia of myoparalytic type can develop as a result of activity of three groups of humoral factors: 1) increasing of concentration of CO2, inorganic ions (potassium, hydrogen) and deficiency of oxygen; 2) metabolites (a lactic acid, organic acids of pentose cycle, ADP, AMP, adenosine); 3) biologically active substances – BAS (histamine, serotonin, kinins, and prostaglandins).
The specified factors cause expansion of vessels, acting directly on smooth muscles of the vascular wall, or intermediately, through influence on endothelium of vessels.
13.9. What is the role of endothelium of blood vessels in development of arterial hyperemia?
As a result of action of a lots of local humoral factors, in particular, biologically active substances, endothelial cells of vessels release the substance which has name the factor of relaxation of endothelial origin (according to the last researches, it is the nitrogen oxide (II), formed from aminoacid arginine). This factor of relaxation acts on smooth muscle cells of the vascular wall and causes their hyperpolarization. It leads to the reduction of basal tonus of blood vessels and their expansion under the influence of blood pressure.
13.10. Name possible outcomes of arterial hyperemia.
In most cases arterial hyperemia is accompanied by increase in the metabolism and amplification of activity of body that is the adaptation to action of the raised functional loading.
However adverse consequences are possible also. At arteriosclerosis, for example, sharp expansion of a vessel can be accompanied by break of its wall and hemorrhage in the tissue. Especially frequently the similar phenomenon is observed in the brain.
13.11. What is venous hyperemia?
Venous hyperemia is increase of blood flow of the organ or the site of tissue as a result of the complicated outflow of blood on veins.