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1 r warm ischemia by utilizing pharmalogically induced hypotension.
2 ce treated with MK 571 exhibited less sepsis-induced hypotension.
3 g and after a 10 min period of nitroprusside-induced hypotension.
4 independently associated with acetaminophen-induced hypotension.
5 ther than 2-AG is a major contributor to LPS-induced hypotension.
6 Intracoronary and intravenous VEGF165 induced hypotension.
7 1 receptors has been implicated in endotoxin-induced hypotension.
8 to be an effective vasopressor for milrinone-induced hypotension.
9 ich does not influence anandamide- or HU-210-induced hypotension.
10 of exercise may have contributed to exercise-induced hypotension.
11 ght to assess the incidence of acetaminophen-induced hypotension.
12 ing to avoid possible patient harm from drug-induced hypotension.
14 activity response to transient nitroprusside-induced hypotension (53.3 +/- 3.7 vs. 40.1 +/- 2.7 burst
16 roxide dismutase (SOD) mimetic, blocked IL-2-induced hypotension and allowed the dose of IL-2 to be i
17 iorated endotoxin (lipopolysaccharide [LPS])-induced hypotension and altered plasma cytokine levels.
19 t with the time course of lipopolysaccharide-induced hypotension and cardiovascular hyporeactivity in
20 ice, mast cells can degrade NT and reduce NT-induced hypotension and CLP-associated mortality, and op
25 in TG mice in response to both nitroglycerin-induced hypotension and phenylephrine-induced hypertensi
26 attenuates the early component of endotoxin-induced hypotension and reduces serum concentrations of
28 imation of the consequences of acetaminophen-induced hypotension, and assess the pathophysiologic mec
29 ining heparin and synthetically derived OSCS induced hypotension associated with kallikrein activatio
30 dose-dependent inhibition of beta-endorphin-induced hypotension, but not bradycardia, with a potency
31 ated in endotoxin (lipopolysaccharide (LPS))-induced hypotension, but the endocannabinoid involved an
32 zed rats subjected to 2 hours of hydralazine-induced hypotension contained tenfold more c-Fos-ir DNPI
36 mbin infusion effectively blocked bradykinin-induced hypotension in wild-type, but not in TAFI-defici
37 scular barrier function to ameliorate trauma-induced hypotension, offering a novel therapeutic opport
39 ed RVLM neurons after 2 hours of hydralazine-induced hypotension (to 73 +/- 2 mm Hg) in conscious rat
40 mide may be paracrine mediators of endotoxin-induced hypotension via activation of vascular CB1 recep
43 major hemodynamic finding was that endotoxin-induced hypotension was significantly attenuated by inte
45 itant administration of L-NAME inhibits VEGF-induced hypotension while most likely preserving VEGF-in
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