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1 intubated patients with sepsis-related acute circulatory failure.
2 er dysfunction with vascular leakage-induced circulatory failure.
3 ogressive, often dilated, cardiomyopathy and circulatory failure.
4 in postnatal death, most probably because of circulatory failure.
5 ns suggest that TF(-/-) embryos are dying of circulatory failure.
6 exceptional during the early phase of acute circulatory failure.
7 f Ramsay sedation scale >4]) and, in case of circulatory failure, a second set of measurements after
9 n = 90) presenting with sepsis-induced acute circulatory failure and considered for volume expansion.
11 tion of iNOS activity with L-NIL reduced the circulatory failure and liver injury, while selective in
12 -permeable radical scavenger (tempol) on the circulatory failure and MODS (kidney, liver, lung) cause
13 le(4,3-alpha)quinoxaline-1-one (ODQ), on the circulatory failure and multiple organ dysfunction syndr
14 , life-threatening condition associated with circulatory failure and multiple organ dysfunctions.
15 sms by which calpain inhibitor I reduces the circulatory failure as well as the organ injury and dysf
19 f endogenous nitric oxide contributes to the circulatory failure caused by endotoxin (lipopolysacchar
20 survival in a cohort of patients with severe circulatory failure correlated with their relative frequ
21 of norepinephrine tartrate) with persistent circulatory failure (defined by lactate > 2 mmol/L, olig
22 was significant liver damage resulting from circulatory failure during cardiopulmonary arrest before
24 might participate in the pathophysiology of circulatory failure during sepsis, and represent a poten
25 e heart failure and impending respiratory or circulatory failure especially in the presence of a diag
26 managing critically ill patients with acute circulatory failure, especially in the absence of cardia
29 y-five mechanically ventilated patients with circulatory failure for whom the decision to give fluid
31 ight ventricular assistance (and right-sided circulatory failure), hemodynamic indexes, percent trans
32 sferase and aspartate aminotransferase), and circulatory failure (hypotension) as well as the increas
35 physiological change determines whether CSF circulatory failure manifests as Alzheimer's disease (AD
36 types in ARDS that more closely aligned with circulatory failure mechanisms and mortality than curren
40 evious G1 ACLF, with liver, coagulation, and circulatory failure posing the highest increased risk.
41 utilized in the treatment of respiratory and circulatory failure refractory to conventional managemen
45 of the acute heart failure patient, such as circulatory failure, volume overload, renal insufficienc
46 early identification of patients at risk for circulatory failure with a much lower false-alarm rate t