Journal Home
Search for

Volume 84, Issue 6, Pages 375-379 (June 2008)


View previous. 8 of 14 View next.

The plasma angiotensin II level increases in very low-birth weight infants with neonatal chronic lung disease

Masakazu MiyawakiCorresponding Author Informationemail address, Takahiro Okutani, Ryuzo Higuchi, Norishige Yoshikawa

Received 15 June 2007; received in revised form 17 September 2007; accepted 7 October 2007.

Abstract 

Background

Angiotensin II (AII) has been reported to play an important role in organ fibrosis, and a local renin–angiotensin-system (RAS) has been demonstrated in the lungs. However, the relationship of the RAS to chronic lung disease of the newborn (CLD) remains obscure.

Objective

To investigate the plasma AII levels throughout the neonatal period in very low-birth weight (VLBW) infants and examine the possible factors that might affect the AII levels.

Study design

The study includes 20 VLBW infants. Blood samples were collected on days 0, 7, 21 and 35 and plasma AII levels were assayed using an enzyme immunoassay. The data were analyzed by a multiple linear regression analysis with the plasma AII level as the dependent variable and significant factors determined based on a univariate analysis as independent variables.

Results

The geometric mean of the plasma AII concentrations on days 0, 7, 21 and 35 was 51 pg/mL, 86 pg/mL, 132 pg/mL, and 50 pg/mL, respectively. On day 21, only CLD (p<0.01) had a highly significant association with the plasma AII level. On day 35, birth weight (p<0.05) and CLD (p<0.01) had a highly significant association with the plasma AII level. This analysis confirmed CLD to be the most significant factor associated with plasma AII level on days 21 and 35.

Conclusion

These findings suggest that higher levels of plasma AII in VLBW infants appear to be related to the development of CLD.

Division of Perinatal Medicine, NICU, Wakayama Medical University, 811-1 Kimiidera, Wakayama City, Wakayama 641-8509, Japan

Corresponding Author InformationCorresponding author. Tel.: +81 73 441 0633; fax: +81 73 444 9055.

PII: S0378-3782(07)00199-5

doi:10.1016/j.earlhumdev.2007.10.005


View previous. 8 of 14 View next.