Морфологія (Dec 2016)
The development of the vascular component of rat atrial myocardium on the background of atrial surface-volume characteristics changes after the influence of acute prenatal hypoxia.
Abstract
Background. Intrauterine hypoxia leads to cardiovascular system abnormalities and fetal death that determine actuality in research of this problem nowadays. The previous researches were focused to the influence of hypoxia to the process of ventricular myocardium vasculogenesis, than antial myocardium blood vessels formation is still out of the scientist’s attention. Objective. Purpose of the work was to determine the changes of blood vessels formation during the stages of cardiogenesis after the influence of acute prenatal hypoxia. Methods. Embryo hearts were investigated on 14th, 16th and 18th days of prenatal ontogenesis, newborn rat hearts and the hearts of rats on 3rd, 14th and 30th day of postnatal ontogenesis. Animals were subdivided into two groups: 1st experimental group of animals was exposed to acute prenatal hypoxia and control group animals. Hypoxia modeling was conducted on pregnant females by injection of 1% sodium nitrite intraperitonealy in dose of 6 mg per 100 g of weight on the 13th embryonic day that lead to moderate hypoxia. Control animals were injected by 1 ml of 0.9% physiological solution of sodium chloride subcutaneously. During the work complex of histological, immunohistochemical and three-dimensional computer modeling methods were used. Results and conclusion. There were more rich blood vessels in atrial myocardium of newborn rats after the influence of acute prenatal hypoxia as compared to the norm. It is important to be admitted that atrial myocardial thickness, volume and surface area of the atria were stable. The arterioles of the 1st experimental group animals were concentrated inside atrial myocardium (intramural), than control group animals arterioles were found under the epicardium only. It was determined by previous research that hypoxia leads to increased diameter and amount of the vessels, and also to hypertrophy. It was compensatory response of the organism toward to increased myocardial thickness. In our experiment greater prevalence of the blood vessels after exposure of acute prenatal hypoxia was associated with the stimulating effect of hypoxia on vasculogenesis through HIF. Thus, greater prevalence of the blood vessels after exposure of acute prenatal hypoxia as compared to the norm is compensatory response of the organism to oxygen deficiency.
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