Acute lung injury (ALI) is an acute progressive ischemic respiratory failure induced by various reasons. The alveolar-capillary injure is pathology fundament for ALI. Pulmonary vascular endothelial cells, as the important barrier for material exchange in and out vascellum, are main target for blood current shearing force and risk factor in blood. So they are more facility to contact with destructive stimulus earlier and are injuried. Recent researchs shown, intracellular pH (pHi) and activity of sodium-hydrogen exchanger isoform I (NHE1) are important for endothelial cells injury. As integral transmembrane proteins located in plasma membrane, NHE1 participate Na ~+/H~+ exchange in and out cells, and play significance effects on maintain water, electrolyte, acid-base balance and cell volume. Atrial natriuretic peptide (ANP), consisted of 28 amino acids, is an important regulator of the sodium and volume homeostasis. It has strong vasodilating, diuresis and natriuretic effects. Recent investigation showed that ANP protects pulmonary physiological functions against inflammatory states in ALI, but the mechanism is still unclear. In view of these, our experiments use rat pulmonary microvascular endothelial cells (PMVECs) as the research element, NHE1 inhibitor, 5-(N, N-hexamethylene)-amiloride (HMA) as instrument. Aim is to make it clear that 1 the effect of NHE1 on LPS-induced injury of rat PMVECs; 2 the therapeutical effect of ANP on LPS-induced injury of rat PMVECs; 3 whether ANP has therapeutic effects on injury of rat PMVECs through inhibiting NHE1. Method:...
|