[Effect of oxygen on L-arginine transport in pulmonary arteries in rats chronically exposed to hypoxia-hypercapnia].
OBJECTIVE
To investigate the effect of chronic hypoxia-hypercapnia and oxygen inhalation on L-arginine transport in rat pulmonary artery.


METHODS
Forty male Sprague-Dawley rats were randomly divided into four groups: normal control group (A), the group of 4-week hypoxia-hypercapnia after 4-week hypoxia (B), the group of 4-week oxygen inhalation (D) 4-week exposure to air (C) after 4-week hypoxia and 4-week hypoxia-hypercapnia. Changes in pulmonary artery L-arginine (L-Arg) transport, nitric oxide synthase (NOS) activity, plasma nitrite (NO(2)/NO(3)) concentration and L-Arg level in rats were measured.


RESULTS
(1) The mean pulmonary artery pressure (mPAP) and weight ratio of right ventricle to left ventricle plus septum (RV/LV + S) of B group were higher than those of A group (33% and 35%, respectively, P < 0.01), with the D group lower than C group (24% and 24%, respectively, P < 0.05). (2) At low (0.2 mmol/L) or high (5.0 mmol/L) concentration of L-Arg, the velocity of L-Arg transport in B group was lower than that in A group [(3.04 +/- 0.16 vs 4.62 +/- 0.55) micro mol x g(-1) x min(-1) and (8.12 +/- 0.14 vs 11.24 +/- 1.02) micro mol x g(-1) x min(-1), respectively, P < 0.01], and in D group higher than in C group [(4.30 +/- 0.18 vs 3.80 +/- 0.21) micro mol x g(-1) x min(-1) and [(12.31 +/- 0.65 vs 10.04 +/- 1.28) micro mol x g(-1) x min(-1), respectively, P < 0.01]. (3) The activity of pulmonary artery tNOS and iNOS in B group was significantly higher than that in C group [(3.82 +/- 0.42 vs 2.59 +/- 0.22) micro nmol x g(-1) x min(-1) and (3.07 +/- 0.30 vs 1.62 +/- 0.10) nmol x g(-1) x min(-1) respectively, P < 0.01], but cNOS in B group was lower than that in NC group [(0.75 +/- 0.16 vs 0.93 +/- 0.10) nmol x g(-1) x min(-1), P < 0.01]. The activity of tNOS and cNOS was not significantly different between D group and C group (P > 0.05); However, iNOS was lower in D group than in C group [(1.97 +/- 0.18 vs 2.25 +/- 0.17) nmol x g(-1) x min(-1), P < 0.05]. (4) Plasma NO(2)/NO(3) content of B group was decreased by 21%, compared with C group (P < 0.01); and D group was increased by 89% (P < 0.01), compared with C group. (5) Plasma L-Arg level was not significantly different among the four groups (P > 0.05).


CONCLUSIONS
The L-Arg transport injury of the pulmonary artery might be the key cause for the decrease of nitric oxide generation in rats with chronic hypoxia-hypercapnia induced pulmonary hypertension. Oxygen inhalation was found to improve L-Arg transport in the injured arteries.
Gong
Yong-sheng
YS
Institute of Cor Pulmonale, Wenzhou Medical College, Wenzhou 325003, China.
Fan
Xiao-fang
XF
Liu
Dao-hou
DH
Hu
Liang-gang
LG
Li
Ji-wu
JW
Tang
Chao-shu
CS
Pang
Yong-zheng
YZ
Jiang
Zhong-sun
ZS
D000818:Animals; D001120:Arginine / Q000097:blood*; D001692:Biological Transport; D006935:Hypercapnia / Q000378:metabolism / Q000628:therapy*; D000860:Hypoxia / Q000378:metabolism / Q000628:therapy*; D008297:Male; D009569:Nitric Oxide / Q000502:physiology; D019001:Nitric Oxide Synthase / Q000097:blood; D010102:Oxygen Inhalation Therapy; D011651:Pulmonary Artery / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
D009569:Nitric Oxide; D001120:Arginine; D019001:Nitric Oxide Synthase