ライフサイエンスコーパス: respiratory depression

1 (one case each of infection, migration, and respiratory depression).

2 ainkillers, like morphine, can be limited by respiratory depression.

3 Death results from respiratory depression.

4 s side effects, including potentially lethal respiratory depression.

5 ion, leading to motor effects, sedation, and respiratory depression.

6 apneas, and protects against hypoxia-induced respiratory depression.

7 drugs in these patients as they are prone to respiratory depression.

8 ciated with unwanted adverse effects such as respiratory depression.

9 n in buprenorphine-associated fatalities and respiratory depression.

10 potential treatment options for GHB-induced respiratory depression.

11 to be primarily responsible for GHB-induced respiratory depression.

12 overdose treatment strategies on GHB-induced respiratory depression.

13 areas, which resembles natural sleep without respiratory depression.

14 in ventilation that counteracts the hypoxic respiratory depression.

15 orphine-induced tolerance, constipation, and respiratory depression.

16 o play a role in mediating adenosine-induced respiratory depression.

17 therapeutic usefulness is their induction of respiratory depression.

18 cause of concerns about safety, particularly respiratory depression.

19 ot associated with an increased incidence of respiratory depression.

20 on with GHB or its analogs leads to coma and respiratory depression.

21 n blood oxygen levels caused by drug-induced respiratory depression.

22 ) sleep and to contribute to state-dependent respiratory depression.

23 sleep, and prevent cholinergically mediated respiratory depression.

24 in patients with pulmonary disease to avoid respiratory depression.

25 infants who suffer from frequent apnoeas and respiratory depression.

26 ermine the receptors involved in GHB-induced respiratory depression, a specific GABA(B) receptor anta

27 ng, potentially risky complications, such as respiratory depression and desaturation, still occur and

28 which lack circulating leptin, also exhibit respiratory depression and elevated PaCO2 (> 10 mm Hg; p

29 and sleep-like sedation without narcosis or respiratory depression and has relatively few cardiovasc

30 ldren to reduce pain and anxiety may produce respiratory depression and hypotension.

31 t of the trial, with particular reference to respiratory depression and hypotension.

32 induced side-effects, such as opioid-induced respiratory depression and itch, and P-glycoprotein modu

33 he reflexive component and is devoid of both respiratory depression and morphine-like reinforcing act

34 , adenosine contributes to the occurrence of respiratory depression and recurrent apneas.

35 nd cerebral venous blood are associated with respiratory depression and reduced organ blood flow.

36 xpected to decrease side effects, minimizing respiratory depression and reinforcing properties genera

37 ear to be safe, but the occurrence of severe respiratory depression and the ability to rescue remain

38 bativeness, a labile level of consciousness, respiratory depression, and death.

39 in adult dosages does not cause significant respiratory depression, and is generally safe for those

40 experienced deterioration of mental status, respiratory depression, and somnolence.

41 relevant to conditions in which hypoxia and respiratory depression are implicated, including apnoea

42 hine and related opioids-which include fatal respiratory depression-are thought to be mediated by mu-

43 hypochlorite- and hydrogen peroxide-induced respiratory depression as well as decreased oxidant-indu

44 e is comparably effective while avoiding the respiratory depression association with opioid administr

45 r general anaesthesia that prevents neonatal respiratory depression at birth.

46 ntricular tachycardia, deep vein thrombosis, respiratory depression, atelectasis, pneumonia, ileus, a

47 most research has focused on seizure-related respiratory depression, cardiac arrhythmia, cerebral dep

48 thanol levels that could put them at risk of respiratory depression, cardiac arrhythmias, seizures, r

49 0 mg/kg) were responsible for dose-dependent respiratory depression combining increased inspiratory (

50 -independent LTD along with life-threatening respiratory depression consequences in the newborn.

51 orphine, showed limited physical dependence, respiratory depression, constipation, and displayed no r

52 The rate of respiratory depression did not differ between groups.

53 fering should be anticipated, concerns about respiratory depression dismissed, and vigorous preemptiv

54 their ability to manage a rare, but critical respiratory depression episode.

55 ell as following acute poisoning with severe respiratory depression have been attributed to buprenorp

56 havioural disorder characterized by neonatal respiratory depression, hypotonia and failure to thrive

57 hese results suggest that leptin can prevent respiratory depression in obesity, but a deficiency in c

58 Leptin prevents respiratory depression in obesity.

59 the depression in suckling activity but not respiratory depression in vivo or brainstem LTD in vitro

60 Hybrid 13a did not result in significant respiratory depression, in contrast to an equipotent ana

61 10 nmol) also attenuated the hypotension and respiratory depression induced by morphine (50 or 100 nm

62 The initial vasodilation appears caused by respiratory depression-induced hypoxia and a subsequent

63 Respiratory depression limits provision of safe opioid a

64 Oxidant activation of airway neurons induces respiratory depression, nasal obstruction, sneezing, cou

65 ve effects ranging from sedation, confusion, respiratory depression, nausea, ileus, constipation, tol

66 amma-hydroxybutyrate (GHB) frequently causes respiratory depression, occasionally resulting in death;

67 tions are related to anesthetic drug-induced respiratory depression or airway obstruction leading to

68 ly 10- to 30-fold higher doses did not cause respiratory depression or cardiovascular adverse events

69 tent an analgesic than morphine, elicited no respiratory depression or physical dependence, and only

70 doses of benzodiazepines was associated with respiratory depression (OR 2.9, 1.4-6.1).

71 ed that Gly-Gln inhibits the hypotension and respiratory depression produced by central beta-endorphi

72 us findings that these agents can counteract respiratory depression produced by morphine overdose.

73 thin 10 min and for at least 1 hour, without respiratory depression requiring intervention.

74 associated with classical opiates, including respiratory depression, significant constipation, physic

75 antagonist injection enhanced the secondary respiratory depression, suggesting that a significant co

76 l other mu opioids, exhibits a threshold for respiratory depression that is well above its threshold

77 er, these data suggest that fentanyl-induced respiratory depression triggers brain hypoxia and subseq

78 Respiratory depression was not reported.

79 thadone- or buprenorphine-treated animals no respiratory depression was observed when ethanol was co-

80 on but in prolonged morphine-treated animals respiratory depression was observed when ethanol was co-

81 s of CSE lasting for longer than 60 min, and respiratory depression were analysed with logistic regre

82 of its adequate sedation and less prevalent respiratory depression when compared with opioid adminis

83 heretofore have been associated with opiate respiratory depression, which may have clinical applicat