PMID- 21340969
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20121002
LR  - 20110222
IS  - 1543-1894 (Print)
IS  - 1543-1894 (Linking)
VI  - 36
DP  - 2000
TI  - Nitric oxide synthase inhibitors.
PG  - 115-31
LID - 10.1385/1-59259-216-3:115 [doi]
AB  - In 1990, several studies reported that an enhanced formation of endogenous nitric 
      oxide (NO) contributes to the hypotension caused by endotoxin and tumor-necrosis 
      factor-alpha (TNFalpha) (1-3). In addition, it became apparent that this overproduction 
      of NO also plays an important role in the pathophysiology of the vascular 
      hyporesponsiveness to vasoconstrictor agents (also termed vasoplegia) (4,5). 
      Since then, many studies have reported on the effects and side effects of NO 
      synthase (NOS) inhibitors in animal models of shock. Prior to discussing the 
      pharmacology of various classes of NOS inhibitors, this chapter will briefly 
      introduce the physiological role(s) of NO as well as the various (beneficial as 
      well as detrimental) roles of NO in animal models of septic shock.
FAU - Siriwardena, D K
AU  - Siriwardena DK
AD  - Moorfields Eye Hospital, London, UK.
FAU - Tagori, H
AU  - Tagori H
FAU - Thiemermann, C
AU  - Thiemermann C
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Methods Mol Med
JT  - Methods in molecular medicine
JID - 101123138
EDAT- 2000/01/01 00:00
MHDA- 2000/01/01 00:01
CRDT- 2011/02/23 06:00
PHST- 2011/02/23 06:00 [entrez]
PHST- 2000/01/01 00:00 [pubmed]
PHST- 2000/01/01 00:01 [medline]
AID - 10.1385/1-59259-216-3:115 [doi]
PST - ppublish
SO  - Methods Mol Med. 2000;36:115-31. doi: 10.1385/1-59259-216-3:115.