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The relationship of the cardiovascular system of the mother and fetus

A special place is occupied by the pathology of pregnancy, leading to a violation of the utero-placental and placental-fetal circulation and pathology of the umbilical cord (H. Plat et al., 1984; P.S. Gurevich, 1989).

As you know, during pregnancy a new vascular bed develops - uterine-placental circulation. The blood flow in the uterus changes, and if the non-pregnant uterus is supplied with two uterine arteries extending from the internal iliac arteries, then the uterine arteries are connected to the arteries of the ovaries to provide blood circulation to the pregnant uterus. On each side of the uterus, an anastomosis develops between the main branch of the uterine artery and the tubal branch of the ovarian artery, which originates from the thoracic aorta below the renal arteries. The arterial line formed on each side of the uterus is the source of an abundant network of small arteries that branch in a plane parallel to the surface, penetrate the uterine wall and extend to the endometrium, ending in an intervillous space. This newly formed vasculature contributes to an unusual increase in uterine blood flow. During pregnancy, smooth muscle hypertrophy occurs in the uterine arteries, which makes possible a characteristic increase in the internal radius without changing the wall thickness and an increase in capacity for the development of tension (KKGriendling et al., 1985).

The volume of circulating blood in the mother during pregnancy increases from approximately 3500 to 5000 ml or 40%. An increase in blood volume is determined already at the 10th week of pregnancy and reaches peak values ​​by about the 30th week (LDLongo, 1983). This increase is due to an increase in plasma volume of 50%, which is more than 25% higher than the volume of red blood cells, and causes slight anemia during pregnancy. It is believed that an increase in plasma volume occurs due to the combined action of estradiol and progesterone on the increasing production of renin by stimulating the secretion of aldosterone and, in turn, the retention of sodium and water by the kidneys (LDLongo, 1983). The erythropoietic effect of progesterone, prolactin and chorionic somatomammotropin leads to an increase in the volume of red blood cells in the blood (LDLongo, 1983). It is still unknown why an increase in the erythrocyte volume cannot reach a correspondence with an increasing plasma volume during a long pregnancy period (L.G. Moore, 1995).

An increase in blood volume accompanies an increasing minute volume of the heart. An increase in cardiac output begins in the early stages of pregnancy and reaches a plateau (MMLees et al., 1967) or decreases in the last 3 months. to levels characteristic of non-pregnant women (K. Ueland et al., 1964). It is believed (MVHart et al., 1985) that estrogen and / or progesterone are involved in a preparatory process by which cardiac output increases before an increase in uterine blood flow occurs.
Births themselves cause a significant increase in cardiac output and are accompanied by a large shift in body fluids (L.G. Moore, 1995).

Despite an increase in cardiac output, systemic blood pressure decreases in early pregnancy, showing a tendency to return to the level characteristic of non-pregnant women in the later stages. The decrease in pulmonary and systemic blood pressure against the background of an increased cardiac output occurs due to a decrease in vascular resistance, which, in turn, is due to three factors (L.G. Moore, 1995): a creation of a new uterine-placental circulation, an increase the diameter of existing vessels and in the reduction of contractility in response to vasoconstrictive stimuli, including for norepinephrine (GLMoore, JTReeves, 1980; M. Cutaia et al., 1987), adrenaline, serotonin, histamine (M. Cutaia et al., 1987), angiotensin II (R. Abdul-Karim, NSAssali, 1961; LCChesley et . al., 1965; M. Cutaia et al., 1987), arginine-vasopressin (MSPaller, 1984), hypoxia (KIFuchs et al., 1982), stimulation of the sympathetic nervous system (J. Dogterom, W. DeJong, 1974; MKMcLaughlin et al., 1985) and other pressor agents. It is believed (L.G. Moore, 1995 and others) that reduced contractility is due to increased production of the first described in 1980 RFFurchgott, JWZawadzki and the so-called VERF (produced by the endothelium of the relaxing factor / factors), which is formed in response on the effect on the endothelium of various vasoconstrictive neurohumoral substances, such as acetylcholine, histamine, bradykinin, substance P, FAT (platelet activating factor), thrombin, etc. (REFurchgott, 1983; PM Vanhoutte et al., 1986). Under the influence of these substances, VERF, in turn, hyperpolarizes cell membranes, stimulates guanylate cyclase, and increases the formation of cyclic GMF to inhibit the contractility process (PMVanhoutte, 1987). A dilatation reaction that is absent in the uterine arteries of non-pregnant women develops simultaneously with pregnancy in parallel with an increase in estrogen levels (C. Bell, 1974).

The similarity of the effect of pregnancy on the vessels of the small and large circle suggests the participation of the main factors underlying the regulation of blood vessels. There is still not a sufficient understanding of the functional consequences of changes in vasoreactivity for maternal and fetal health. It is teleologically possible to consider reduced vasoreactivity as a means of ensuring low vascular resistance and maximum blood flow to the uteroplacental circulation. At the same time, it remains a mystery why reduced reactivity extends to the entire body, involving both systemic and pulmonary circulation (L.G. Moore, 1995).
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The relationship of the cardiovascular system of the mother and fetus

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