PMID- 15465885
OWN - NLM
STAT- MEDLINE
DCOM- 20050524
LR  - 20161124
IS  - 8750-7587 (Print)
IS  - 0161-7567 (Linking)
VI  - 98
IP  - 2
DP  - 2005 Feb
TI  - NOS3 deficiency augments hypoxic pulmonary vasoconstriction and enhances systemic 
      oxygenation during one-lung ventilation in mice.
PG  - 748-52
AB  - Nitric oxide (NO), synthesized by NO synthases (NOS), plays a pivotal role in 
      regulation of pulmonary vascular tone. To examine the role of endothelial NOS 
      (NOS3) in hypoxic pulmonary vasoconstriction (HPV), we measured left lung 
      pulmonary vascular resistance (LPVR), intrapulmonary shunting, and arterial PO2 
      (PaO2) before and during left mainstem bronchus occlusion (LMBO) in mice with and 
      without a deletion of the gene encoding NOS3. The increase of LPVR induced by 
      LMBO was greater in NOS3-deficient mice than in wild-type mice (151 +/- 39% vs. 
      109 +/- 36%, mean +/- SD; P < 0.05). NOS3-deficient mice had a lower 
      intrapulmonary shunt fraction than wild-type mice (17.1 +/- 3.6% vs. 21.7 +/- 
      2.4%, P < 0.05) during LMBO. Both real-time PaO2 monitoring with an 
      intra-arterial probe and arterial blood-gas analysis during LMBO showed higher 
      PaO2 in NOS3-deficient mice than in wild-type mice (P < 0.05). Inhibition of all 
      three NOS isoforms with Nomega-nitro-L-arginine methyl ester (L-NAME) augmented 
      the increase of LPVR induced by LMBO in wild-type mice (183 +/- 67% in L-NAME 
      treated vs. 109 +/- 36% in saline treated, P < 0.01) but not in NOS3-deficient 
      mice. Similarly, systemic oxygenation during one-lung ventilation was augmented 
      by L-NAME in wild-type mice but not in NOS3-deficient mice. These findings 
      indicate that NO derived from NOS3 modulates HPV in vivo and that inhibition of 
      NOS3 improves systemic oxygenation during acute unilateral lung hypoxia.
FAU - Liu, Rong
AU  - Liu R
AD  - Dept. of Anesthesia and Critical Care, Massachusetts General Hospital, 55 Fruit 
      St., Boston, MA 02114, USA.
FAU - Evgenov, Oleg V
AU  - Evgenov OV
FAU - Ichinose, Fumito
AU  - Ichinose F
LA  - eng
GR  - HL-71897/HL/NHLBI NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
DEP - 20041001
PL  - United States
TA  - J Appl Physiol (1985)
JT  - Journal of applied physiology (Bethesda, Md. : 1985)
JID - 8502536
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
RN  - EC 1.14.13.39 (Nos3 protein, mouse)
SB  - IM
MH  - Animals
MH  - Bronchoconstriction
MH  - Hypertension, Pulmonary/etiology/*physiopathology
MH  - Hypoxia/complications/*physiopathology
MH  - Lung/*blood supply/*physiopathology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Nitric Oxide Synthase/*deficiency
MH  - Nitric Oxide Synthase Type II
MH  - Nitric Oxide Synthase Type III
MH  - Pulmonary Artery/*physiopathology
MH  - *Pulmonary Ventilation
MH  - Vascular Resistance
EDAT- 2004/10/07 09:00
MHDA- 2005/05/25 09:00
CRDT- 2004/10/07 09:00
PHST- 2004/10/07 09:00 [pubmed]
PHST- 2005/05/25 09:00 [medline]
PHST- 2004/10/07 09:00 [entrez]
AID - 00820.2004 [pii]
AID - 10.1152/japplphysiol.00820.2004 [doi]
PST - ppublish
SO  - J Appl Physiol (1985). 2005 Feb;98(2):748-52. doi: 
      10.1152/japplphysiol.00820.2004. Epub 2004 Oct 1.