ライフサイエンスコーパス: respiratory depression

1 rms such as dependence, substance abuse, and respiratory depression).

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

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

4 sleep, and prevent cholinergically mediated respiratory depression.

5 in patients with pulmonary disease to avoid respiratory depression.

6 cluding tolerance, withdrawal, delirium, and respiratory depression.

7 gnalling pathways resulting in analgesia and respiratory depression.

8 easured by conditioned place preference, and respiratory depression.

9 shallow, a side-effect called opioid-induced respiratory depression.

10 escalating unintentional death rates due to respiratory depression.

11 us, that are key mediators of opioid-induced respiratory depression.

12 rategy to reverse and prevent opioid-induced respiratory depression.

13 ajor factor contributing to fentanyl-induced respiratory depression.

14 iating the cause of overdose- opioid-induced respiratory depression.

15 eceptor system and induce potentially lethal respiratory depression.

16 of which could contribute to opioid-induced respiratory depression.

17 lecting a drop in blood oxygen levels due to respiratory depression.

18 hat cervical EES reversed the opioid-induced respiratory depression.

19 d that compound 53 reversed fentanyl-induced respiratory depression.

20 s is limited by the life-threatening risk of respiratory depression.

21 ain therapy with analgesic properties but no respiratory depression.

22 rious adverse effects, notably addiction and respiratory depression.

23 st and maintained even during opioid-induced respiratory depression.

24 c agonist-induced central nervous system and respiratory depression.

25 o connection between B-arrestin 2 and opioid respiratory depression.

26 cause sedation, bradycardia, hypotension or respiratory depression.

27 m of technology to counteract opioid-induced respiratory depression.

28 to high risks of dependence, tolerance, and respiratory depression.

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

30 oved therapeutic window for analgesia versus respiratory depression.

31 in ventilation that counteracts the hypoxic respiratory depression.

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

33 infants who suffer from frequent apnoeas and respiratory depression.

34 Death results from respiratory depression.

35 s side effects, including potentially lethal respiratory depression.

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

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

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

39 ciated with unwanted adverse effects such as respiratory depression.

40 n in buprenorphine-associated fatalities and respiratory depression.

41 potential treatment options for GHB-induced respiratory depression.

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

43 overdose treatment strategies on GHB-induced respiratory depression.

44 utic window for MOR-induced analgesia versus respiratory depression.

45 areas, which resembles natural sleep without respiratory depression.

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

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

48 therapeutic usefulness is their induction of respiratory depression.

49 cause of concerns about safety, particularly respiratory depression.

50 ot associated with an increased incidence of respiratory depression.

51 activation, leading to such side effects as respiratory depression.

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

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

54 appear to be devoid of side-effects such as respiratory depression, abuse liability or tolerance dev

55 identified breathing rate and post-injection respiratory depression accurately when compared to a res

56 ce of precipitated withdrawal, sedation, and respiratory depression; adverse events; length of stay;

57 ective antinociception while showing reduced respiratory depression and a lack of conditioned place p

58 as well as their unwanted actions, including respiratory depression and addiction liability.

59 , it displays several side effects including respiratory depression and addiction.

60 ling to G protein, while the side-effects of respiratory depression and analgesic tolerance are cause

61 gesia with attenuated liabilities, including respiratory depression and conditioned place preference

62 and the appearance of side effects, such as respiratory depression and constipation.

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

64 Since fentanyl can cause respiratory depression and electrolyte imbalances, in th

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

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

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

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

69 In vivo experiments in rats with respiratory depression and in those with a paralyzed hem

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

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

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

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

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

75 P135 maintains untoward side effects such as respiratory depression and reward behavior; together, th

76 uce typical MOP-related side effects such as respiratory depression and reward, whereas AT-121 appear

77 peripheral ORs in triggering heroin-induced respiratory depression and subsequent brain hypoxia.

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

79 potent analgesics, but also cause sedation, respiratory depression, and addiction risk.

80 including opioid-induced constipation (OIC), respiratory depression, and addiction.

81 nyl- and sufentanil-induced antinociception, respiratory depression, and bradycardia in mice and rats

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

83 that arrestin-3 recruitment does not impact respiratory depression, and effective arrestin-3 engagem

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

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

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

87 atory network, but the mechanisms underlying respiratory depression are poorly understood.

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

89 gnificantly contributes to secondary hypoxic respiratory depression as well as abnormalities in sleep

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

91 ity like fentanyl, it failed to produce deep respiratory depression associated with fentanyl-induced

92 taOR) is a promising target, as it lacks the respiratory depression associated with u opioid receptor

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

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

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

96 At overdose levels, opioid-induced respiratory depression becomes fatal without the adminis

97 biological effects, including analgesia and respiratory depression, but these may not be the primary

98 and protecting rats against bradycardia and respiratory depression by blocking the distribution of f

99 , but also triggered locomotion and overcame respiratory depression by opioid drugs.

100 Opioids can cause severe respiratory depression by suppressing feedback mechanism

101 impacts of hypoxaemia during opioid-induced respiratory depression can vary based on the opioid used

102 f the respiratory network and opioid-induced respiratory depression cannot be attributed to only one

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

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

105 and suggest a novel mechanism to oppose the respiratory depression caused by opioids.

106 fentanyl antinociception and the intractable respiratory depression caused by the ultrapotent opioid

107 0 mg/kg) were responsible for dose-dependent respiratory depression combining increased inspiratory (

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

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

110 Surprisingly, respiratory depression, constipation, and opioid withdra

111 antinociception, antinociceptive tolerance, respiratory depression, constipation, and reward induced

112 rive MOR-mediated antinociceptive tolerance, respiratory depression, constipation, or reward and do n

113 cts, including nausea or vomiting, sedation, respiratory depression, constipation, pruritus (itch), a

114 ith life-threatening side effects, including respiratory depression, dependence, and addiction.

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

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

117 main cause of death from opioid overdose is respiratory depression due to the activation of u-opioid

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

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

120 sia with potency similar to morphine without respiratory depression, hyperlocomotion, constipation, o

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

122 d MP, a kratom plant derivative with reduced respiratory depression in animal studies, exhibited mark

123 in KF and preBotC neurons in opioid-induced respiratory depression in awake adult mice.

124 spinal cord could antagonize opioid-induced respiratory depression in humans.

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

126 Leptin prevents respiratory depression in obesity.

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

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

129 Respiratory depression induced by an anti-nociceptive do

130 10 nmol) also attenuated the hypotension and respiratory depression induced by morphine (50 or 100 nm

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

132 apeutic window, notably for analgesia versus respiratory depression, is a result of ligand bias downs

133 Respiratory depression limits provision of safe opioid a

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

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

136 stly peripherally mediated; they produced no respiratory depression, no hyperalgesia, significantly l

137 Mild sedation, but neither respiratory depression nor ataxia, was observed for both

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

139 agonists to inhibit both antinociception and respiratory depression offering potential solutions to f

140 much greater ability to cause opioid-induced respiratory depression (OIRD) and wooden chest syndrome

141 Severe opioid-induced respiratory depression (OIRD) can be treated with intran

142 Opioid-induced respiratory depression (OIRD) causes death following an

143 opioid overdose and death is opioid-induced respiratory depression (OIRD), a life-threatening depres

144 Opioid-induced respiratory depression (OIRD), mediated by the u-opioid

145 erdose is typically caused by opioid-induced respiratory depression (OIRD).

146 risk of fatal overdose due to opioid-induced respiratory depression (OIRD).

147 morphine and fentanyl during opioid-induced respiratory depression (OIRD).

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

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

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

151 No cases of respiratory depression or sedation were reported.

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

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

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

155 morphine to map quantitative trait loci for respiratory depression, recovery time and survival time.

156 e variability in opioid-induced responses in respiratory depression, recovery time and survival time.

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

158 iazepine and opioid products about increased respiratory depression risk with simultaneous use, the U

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

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

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

162 available but are also associated with fatal respiratory depression through a pathway that remains un

163 cause MOPr-driven side effects that include respiratory depression, tolerance, addiction, and consti

164 harmful side effects of opioid drugs such as respiratory depression, tolerance, dependence, and abuse

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

166 dependence/withdrawal, reward liability, and respiratory depression versus morphine.

167 Respiratory depression was not reported.

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

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

170 , a buprenorphine metabolite associated with respiratory depression, was detected in the plasma after

171 anslational non-human primate (NHP) model of respiratory depression, we demonstrate CSX-1004-mediated

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

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

174 ependent signaling is responsible for opioid respiratory depression, whereas adenylyl cyclase inhibit

175 have serious side effects, including OUD and respiratory depression, which can lead to fatal overdose

176 erious side effects, including addiction and respiratory depression, which contribute to the ongoing

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

178 ons may lead to novel therapies that prevent respiratory depression while sparing analgesia.