Neuroendocrine reactions during stress

NetworkThe nerve
endocrine
reaction during the second section of stress When the body is strongly stimulated, there will be a series of neuroendocrine reactions based on acerbic nerve excitement, increased cedar phenolamine secretion and increased hypotuitary, pituitary-adrenal cortogenic secretion, to adapt to strong stimulation, improve the body's ability to resist disease. Therefore, neuroendocrine reactions during stress are the physiological basis for systemic nonse specific reactions during disease (Tables 8-1).Table 8-1 Stresses
Hormones
and Neurotransmitter ChangesHormone and Neurotransmitter ChangesHormone and Delivery Increased Secretion Secretion of Inhibited Cerestaphenolamine (Adrenaline, Dethyroid, Dopamine)Adrenal Corticosteroid Release Factor (CRF)Adrenal Corticosteroids (ACTH)Glucosin (adrenal glands) β-endorphins, growth hormone, oxytocinglucoglytin anti-diuretic hormone nephrine, angiotensin, aldehydetissues
hormones: prostatin, thrombocytopenia, peptides cellular factors
: interleaving-1insulin, the concentration of plasma epinephrine, epinephrine, and dopamine increased rapidly during stress of the intersecting nerve-adrenal myelin reaction As to when the concentration of these hormones returns to normal, the situation varies from stress to stress. For example, the plasma cerpamine has returned to normal for more than an hour after the athletes have been playing. However, more than half a month after a large area of burns, the discharge of catethamidophenolamine in the patient's urine is still 7 to 8 times that of normal people.stress, the sensory nerve-adrenal myelin response is both defensive and detrimental to the body.1. Defensive significance is mainly manifested in the following five aspects.(1) faster heart rate, increased heart contraction, increased total external resistance: it is conducive to improving the heart's output per beat and per minute, improve blood pressure. (2) Redistrictation of blood: sensing - adrenal myelin system excited, skin, abdominal visceral;(3) bronchid clenching: it is beneficial to improve the breathing of the depulation and provide more oxygen to the blood. (4) promotes glycogen decomposition, raises blood sugar, promotes fat decomposition, and increases free fatty acids in plasma, thus ensuring an increase in the energy demand of the stress-timing body. (5) acetaminophenolic has a role in the secretion of many hormones (Table 8-2). Increased secretion of cerviolamine is an important cause of many hormone changes during stress. Table 8-2 Effects of acetaminophen on hormone secretion Hormone effects the actH promotes β, α (? ) Gluatic glu promotes β, α (? Insulin promotes α growth promotes α thyroxine promotes β thyroxine promotes β calcitonin promotes β nephrine Β Promotes erythrin promotes β gastric progenin promotes β 2. Adverse aspects of the body (1) external small blood vessels contraction, microcirculation irrigation flow is small, resulting in tissue isoemia. (2) cerial phenolamine promotes plateplate aggregation, which can cause tissue isemia in small blood vessels. (3) excessive energy consumption. (4) increases the oxygen consumption of the heart muscle. stress generally mainly causes the excitement of the intersecting nerve, but sometimes also causes the side-sensing nerve excite to dominate. For example, a sudden emotional stimulation can sometimes cause a person's heart rate to slow down and blood pressure to drop. II. Adrenal glucocorticoid response 1. Increased glucocorticoid secretion during stress The concentration of plasma glucocorticoids (glucocorticoids, GC) increases almost innocular to stress. The response was rapid and the increase was large. For example, in patients with extensive burn shock, plasma cortisol (hydrocortison or cortisol) content can be as high as 3 to 5 times normal (952 to 1600nmol/L (34.5 to 58.0 μg/dl) and normal plasma content is 69 to 276nmol/L (2.5 to 10 μg/dl). At the same time, the lipid and
vitamin
C content of adrenal cortogenic cells decreased, the adrenal glands were hypertrophic, the outer blood erythroid erythroid particles
cell count
decreased, and the excret of 17-hydroxysteroids in urine increased. The 2nd, together with the above plasma cortisol concentration, has dropped to near normal, and if there are complications after surgery, plasma cortisol continues to rise (Figure 8-1). In patients with extensive burns, plasma cortisol can be maintained at high levels for up to 2 to 3 months. Deaths, in the dying stage of plasma cortisol and extremely high. Figure 8-1 (1) 5 patients with postoperoperial complications
Concentration of plasma cortisol before and after surgery Figure 8-2 (2) 1 case of pneumonia after surgery
Concentration of plasma cortisol before and after surgery (quoted from Gill GV, et al Brit J Surg 62:441, 1975) 2. The increased secretion of glucosal hormones during stress is achieved through the interaction of the hypothyroids-pituitary frontal leaves-adrenal cortology. The adrenal corticosteroid release factor (corticotropin releasing factor, CRF) secreted by the hypotheroidal brain circulates through the pituitary veins into the pituitary frontal leaf, stimulating the release of ACT, which acts on the adrenal corticophyll, promoting the secretion of cortisol, which in turn inhibits the release of CRF and ACTH, i.e. negative feedback regulation mechanisms. The lower masculine brain is controlled by various parts of the brain, which mainly accept fibers from the limbic system, and below which are mainly affected by the mesh structure of the brain trunk. Fiber-regulated mood responses from the amygdala of the limbic system, such as stressogens such as anger, fear, and anxiety, significantly increase ACTH secretion through this channel. Stress principles such as trauma and drastic humidity changes can be transmitted through the outer receptor to the impulse, causing the excitement of the updram system of the brain-dry mesh structure, which causes the hypothyroidism and stimulates the release of ACTH (Figure 8-2). Figure 8-2 Regulation of glucodermal hormone secretion during stress (from Yanggang, 1980) The physiological significance of increased glucoticoid secretion during stress GC secretion is one of the most important reactions to stress, which stimulates an extremely important role in the body's anti-harmful pyrethroids. Animal experiments have shown that after the adrenal glands are removed, animals can survive under suitable conditions, but if severely stimulated, they are prone to failure and death. Injection of glucoticoids into animals that have their adrenal glands removed can restore the animal's ability to resist damage. A large number of clinical observations also proved that the resistance of the corresponding kinesiogens was significantly reduced in patients with low adrenal cortical function. The mechanism of GC secretion increases during stress, the mechanism of increasing the body's resistance to stimulation is not completely clear, there are four aspects already known: (1) glucoticoids promote
protein
decomposition and glycogen, which can replenish the reserves of hepatic glycogen; (2) glucoticoids can increase cardiovascular sensitivity to theophenolamine. When the adrenal cortique is insulable, the vascular smooth muscle becomes extremely insensitive to epinephrine, which is prone to decreased blood pressure and circulatory failure. (3) has been shown that pharmacological concentrations of glucosal hormones have the effect of stabilizing lysosome membranes and preventing or reducing leakage of lysase-based enzymes. This avoids or mitigates the damage caused by hydrolyzed enzymes to cells and others. However, whether the concentration of glucoticoids during stress has this effect has yet to be discussed. (4) inhibits the generation, release and activation of chemical media. Physiological concentrations of glucoticoids inhibit the production, release and activation of many chemical media. For example, prostatin (PGs), white triene (LTs), thrombosis (Tx), refractive peptides, 5-serotonin, fissinogen activators, collagenase, and lymph factors. When combined with in-cell GC subjects, GC induces a protein with a molecular weight of 40 to 50 kD, called macrocortin or lipoprotein (lipomodulin). It inhibits the activity of phospholipase A
2
, thus reducing the release of peanut tyrenic acid, thereby reducing the production of PGs, LTs and Tx. Because these chemical media are produced too much during stress, GC can inhibit the production of these media, so there can be no strong inflammation, perverted reaction, etc.