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1.
Resusc Plus ; 18: 100613, 2024 Jun.
Article En | MEDLINE | ID: mdl-38549696

Objectives: Extracorporeal cardiopulmonary resuscitation (ECPR) is increasingly used due to its beneficial outcomes and results compared to conventional CPR. Cardiac arrests can be categorized depending on location: in-hospital cardiac arrest (IHCA) and out-of-hospital cardiac arrest (OHCA). Despite this distinction, studies comparing the two are scarce, especially in comparing outcomes after ECPR. This study compared patient characteristics, cardiac arrest characteristics, and outcomes. Methods: Between 2016 and 2022, patients who underwent ECPR for cardiac arrest at our institution were retrospectively analyzed, depending on the arrest location: IHCA and OHCA. We compared periprocedural characteristics and used multinomial regression analysis to indicate parameters contributing to a favorable outcome. Results: A total of n = 157 patients (100%) were analyzed (OHCA = 91; IHCA = 66). Upon admission, OHCA patients were younger (53.2 ± 12.4 vs. 59.2 ± 12.6 years) and predominantly male (91.1% vs. 66.7%, p=<0.001). The low-flow time was significantly shorter in IHCA patients (41.1 ± 27.4 mins) compared to OHCA (63.6 ± 25.1 mins). Despite this significant difference, in-hospital mortality was not significantly different in both groups (IHCA = 72.7% vs. OHCA = 76.9%, p = 0.31). Both groups' survival-to-discharge factors were CPR duration, low flow time, and lactate values upon ECMO initiation. Conclusion: Survival-to-discharge for ECPR in IHCA and OHCA was around 25%, and there was no statistically significant difference between the two cohorts. Factors predicting survival were lower lactate levels before cannulation and lower low-flow time. As such, OHCA patients seem to tolerate longer low-flow times and thus metabolic impairments compared to IHCA patients and may be considered for ECMO cannulation on a broader time span than IHCA.

3.
Prof Case Manag ; 29(3): 123-126, 2024.
Article En | MEDLINE | ID: mdl-38546494
4.
Prof Case Manag ; 29(2): 74-77, 2024.
Article En | MEDLINE | ID: mdl-38251946
6.
Prof Case Manag ; 28(5): 248-251, 2023.
Article En | MEDLINE | ID: mdl-37487160
7.
Prof Case Manag ; 28(4): 204-206, 2023.
Article En | MEDLINE | ID: mdl-37219332
9.
Prof Case Manag ; 28(3): 158-160, 2023.
Article En | MEDLINE | ID: mdl-36999768
12.
Prof Case Manag ; 27(6): 299-303, 2022.
Article En | MEDLINE | ID: mdl-36206125
13.
Prof Case Manag ; 27(2): 93-96, 2022.
Article En | MEDLINE | ID: mdl-35099424
15.
Pharmaceutics ; 13(5)2021 May 13.
Article En | MEDLINE | ID: mdl-34068263

Dopamine is crucial for neuroplasticity, which is considered to be the neurophysiological foundation of learning and memory. The specific effect of dopamine on plasticity such as long-term potentiation (LTP) and long-term depression (LTD) is determined by receptor subtype specificity, concentration level, and the kind of plasticity induction technique. In healthy human subjects, the dopamine precursor levodopa (L-DOPA) exerts a dosage-dependent non-linear effect on motor cortex plasticity. Low and high dosage L-DOPA impaired or abolished plasticity, while medium-dose preserved and reversed plasticity in previous studies. Similar dosage-dependent effects were also observed for selective D1-like and D2-like receptor activation that favor excitatory and inhibitory plasticity, respectively. However, such a dosage-dependent effect has not been explored for a nonselective dopamine agonist such as apomorphine in humans. To this aim, nonfocal and focal motor cortex plasticity induction using paired associative stimulation (PAS) and transcranial direct current stimulation (tDCS) were performed respectively in healthy participants under 0.1, 0.2, 0.3 mg apomorphine or placebo drug. Transcranial magnetic stimulation-elicited motor-evoked potentials were used to monitor motor cortical excitability alterations. We hypothesized that, similar to L-DOPA, apomorphine will affect motor cortex plasticity. The results showed that apomorphine with the applied dosages has an inhibitory effect for focal and nonfocal LTP-like and LTD-like plasticity, which was either abolished, diminished or reversed. The detrimental effect on plasticity induction under all dosages of apomorphine suggests a predominantly presynaptic mechanism of action of these dosages.

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