Ischemic heart disease

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Primary and secondary prevention. The concept of "coronary heart disease" indicates that the disease is the result of an inadequate supply of blood cells attack and transport to him oxygen from the surrounding world. Coronary heart disease can occur due to lack of oxygen in the air, or small blood red blood cells, or in breach of the mechanisms of development of oxygen. But the main reason for myocardial ischemia is, of course, atherosclerosis of coronary vessels.
Atherosclerosis of the coronary arteries experiencing severe disorders of blood supply to the heart muscle. Some changes occur, when this process affects a small branch artery, other changes come, when the atherosclerotic process of sealing and the second one major coronary artery. In the first case, the blood supply is compensated, and infarction almost feels oxygen deficit in the second case, on the contrary, there are signs of severe hypoxia, dramatically affects its contractile function.
No less serious and complicating circumstances leading to hypoxic condition of myocardium are stress factors. Under their influence increases production of hormones and increases the need heart of oxygen. Due to obstacles in the system of myocardium blood supply and increase the number of adrenaline (as a result of emotional stress) greatly increases the need heart of oxygen (Fig. 3).
Stimulation of the cerebral cortex, under emotional stress is passed to the hypothalamus, where the release of norepinephrine () from nerve cells. Activating noradrenergic elements (NAHE), norepinephrine causes the excitation of the sympathetic centers and thereby leads to increased activity of sympathetic-adrenal system. This leads to increased adrenaline (A) of the cerebral napochechnikov layer. The blood enriched with adrenaline, which cross the blood-brain barrier (BBB) penetrates into certain parts of the limbic-reticular system and hypothalamus. Causes the activation of the adrenergic elements (AE) of the Central nervous system and simultaneous excitation of serotonergic (SE) and cholinergic (HAE) elements of the brain. The increase in their activity stimulates (+) education releasing factor (P), which, flowing down in the pituitary, contributes to the enhanced getting the blood of adrenocorticotropic hormone (ACTH). Under the influence of this hormone in the adrenal cortex increases the synthesis of corticosteroids (CS); easily penetrating into the hypothalamus, corticosteroids according to the law of feedback retard (-) education releasing factor and, therefore, their content in the blood begins to decrease. But long-term and life-threatening stress impacts the COP associated with a particular protein blood - interacted (T). Connection KS+T delayed the blood-brain barrier. In the brain ceases to provide information on the content of the COP in the blood, which leads to the violation of the law feedback and loss of regulatory functions.
Stress influence through the cerebral cortex and the reticular formation cause changes (Kassil) in subcortical centers and contribute to the development of vascular dystonia. In these conditions, these processes lead to even greater ischemia and development of angina pectoris or myocardial infarction. Of course, the development of these diseases is much more complicated than the imbalance between demand and supply of the heart muscle oxygen.
When a small hypoxia on the first stage there is a protective reaction - vascular wall begins to produce adenosine, which enters the blood and provides sossoudorasshiratee effect. This, in turn, improves coronary blood supply. Important role in these processes becomes neurohumoral regulation link, as included with sympathetic nerve fibers vascular constrictors, improves coronary flow. However, under the influence of emotional stress increases the level of vasopressin, which increases coronary artery spasm.