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1 er body negative pressure (LBNP) to onset of cardiovascular collapse.
2 od pressure was a late indicator of imminent cardiovascular collapse.
3 ive production of inflammatory cytokines and cardiovascular collapse.
4 result of intense sympathetic activation of cardiovascular collapse.
5 acute lethal toxicity (ALT) characterized by cardiovascular collapse.
6 may induce severe neurological symptoms and cardiovascular collapse.
7 One control died from cardiovascular collapse.
8 vent perioperative adrenal insufficiency and cardiovascular collapse.
9 t the earliest signs of toxicity may prevent cardiovascular collapse.
10 in 5-min stages until the onset of impending cardiovascular collapse.
11 omplex constellation of findings with sudden cardiovascular collapse, acute left ventricular failure
12 ite aggressive measures for the treatment of cardiovascular collapse and cardiac arrest, the hypotens
15 ickle mouse model, intravenous hemin induced cardiovascular collapse and mortality within 120 minutes
18 emic blood pressure and delayed the onset of cardiovascular collapse during severe hypovolemic hypote
19 pedance threshold device at the same time of cardiovascular collapse during sham breathing (102 +/- 3
20 o the duration of LBNP exposure required for cardiovascular collapse in each subject (i.e., LBNP maxi
21 heterodimeric cytolytic protein that induces cardiovascular collapse in humans and native predators.
22 hat only excessive iNOS-derived NO underlies cardiovascular collapse in shock, our data strongly supp
24 ient increases in blood pressure followed by cardiovascular collapse in wild-type mice, but U-46619 c
25 factors associated with an increased risk of cardiovascular collapse included multisystem organ failu
26 TD may provide short-term protection against cardiovascular collapse induced by orthostatic stress or
27 nflammatory response syndrome with resulting cardiovascular collapse, ischemic damage to vital organs
28 used loss of pulsatile arterial pressure and cardiovascular collapse (mean arterial pressure, 32+/-8
29 highlights the recognition and treatment of cardiovascular collapse or cardiopulmonary arrest in an
30 al anaesthesia may be attributable to sudden cardiovascular collapse precipitated by ventricular arrh
32 sures that are early indicators of impending cardiovascular collapse resulting from progressive reduc
33 ts in cardiac arrest, hemorrhagic shock, and cardiovascular collapse secondary to a number of life-th
36 ere reductions in blood pressure, leading to cardiovascular collapse that can accompany septicemia.
37 marked severity and duration may progress to cardiovascular collapse unresponsive to volume replaceme
39 xiation from pulmonary edema and generalized cardiovascular collapse were the most likely pathogenic
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