Structurally functional characteristic respiratory departments of the lungs at influence stress factors and oxytocinum
The aim of the study to determine the combined effect of chronic emotional-painful stress (DEC) and of Escherichia coli (E. coli) on the functional state of type II respiratory alveolocytes (А2) the lungs of rats. The study was conducted on male white rats. Animals were divided into 3 groups. Animals in group 1 intratracheally injected with 0.2 ml of sterile saline. In the second group of animals called DEC daily for 3 hours for 7 days and the next day after the end of stressing intratracheal suspension imposed daily agar culture of E. coli at a dose of 200 million microbial cells in 0.2 ml of saline. Animals of group 3 were exposed to the same type as the second group and after each session of stressing and contamination given intramuscularly to 0.02 IU of oxytocin (OT). Lungs were taken at 1 day after contamination, and subjected to the methods of light and electron microscopy, immunocytochemistry, morphometry. The results showed that when infected with chronic lung DEC occurred most pronounced changes of a destructive nature, with the maximum expression of MMP-9. In A2, the number and volume density of mitochondria (Vvmit) were reduced compared with control at 4.8±0,6 and 4.3±0,4, the number and volume density of lamellar bodies (Vv n t) decreased by 3.3±0,3 and 4.3±0,5 times, respectively. These changes indicate a reduction in adaptive-compensatory options A2 and reducing the synthesis and secretion of surfactant in the combined stress. In the lungs of animals treated with OT were observed less pronounced destructive changes, with minimal expression of MMP-9. In A2, the number of mitochondria and lamellar bodies and their Vvmit and Vv item that has been reduced compared with controls, but increased compared with the second group. The number of mitochondria was greater than 1.43±0,2 times, Vvmit 2.3±0,5, the number of lamellar bodies in the 2,2±0,4, Vv n t 3.6±0,7, which indicates the positive role of OT in the regulation of adaptive-compensatory processes in the A2, activation synthesis and secretion of pulmonary surfactant in adult rats.