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001-es BibID:BIBFORM134713
035-os BibID:(scopus)105026978195 (wos)001655894700002
Első szerző:Fedor Marianna (aneszteziológus-intenzívterápiás szakorvos)
Cím:The effect of dexmedetomidine on rocuronium-induced neuromuscular blockade and its reversal by sugammadex / Fedor Marianna, Sallai Nikolett, Fülesdi Béla, Fábián Ákos I.
Dátum:2026
ISSN:2197-425X
Megjegyzések:Background Dexmedetomidine (DEX) is increasingly used in the intensive care unit for sedation and also serves as an adjuvant in general anesthesia and in procedural sedations. We tested whether dexmedetomidine at dif- ferent concentrations influences the activity of the neuromuscular junction at the diaphragm and whether DEX has an impact on the action of rocuronium at the diaphragm as well as the reversal of the neuromuscular block by sugammadex. Methods 20 male Wistar rat phrenic nerve?hemidiaphragm system was used for our experiments. The concentra- tion?response characteristics of DEX and rocuronium were quantified as the depression of the force amplitude of single twitches (ST) in response to electrical stimulation of the phrenic nerve. Rocuronium concentration?response curves were obtained with 0, 1, and 2.67 ?g/ml DEX concentration. After a single dose of rocuronium, sugammadex doses were given until additional doses of sugammadex were not accompanied by a further increase in ST force amplitude. The concentration?response curve of sugammadex was also measured in the presence of 1 ?g/ml DEX concentration. Results DEX at different doses negligibly reduces the force of the contractions and the contractility of the dia- phragm. The EC50 of rocuronium [7.74 ?M (6.99?8.57)] did not change significantly [7.18 ?M (6.58?7.84); p = 0.27] with the addition of DEX 1 ?g/ml. At 2.67 ?g/ml DEX concentration, the ED50 of rocuronium was significantly reduced [6.37 ?M (5.69?7.13); p = 0.015]. With 1 ?g/ml DEX concentration, the EC50 of the sugammadex [2.04 ?M (1.94?2.14)] needed for the reversal of rocuronium-induced neuromuscular blockade was significantly increased [2.45 ?M (2.39? 2.51); p < 0.01]. Conclusions DEX at clinically administered doses does not significantly influence the function of the neuromuscu- lar junction at the diaphragm. Under routine dosing conditions, the action of the neuromuscular blocking agents and their reversal by sugammadex are also not modified by DEX.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Dexmedetomidine
Phrenic nerve-diaphragm preparation
Neuromuscular block
Rocuronium
sugammadex
Megjelenés:Intensive Care Medicine Experimental. - 14 : 1 (2026), p. 1-7. -
További szerzők:Sallai Nikolett Fülesdi Béla (1961-) (aneszteziológus) Fábián Ákos István (1982-) (aneszteziológus)
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Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM115389
Első szerző:Szántó Dorottya (aneszteziológus, intenzív terápiás szakorvos)
Cím:Incidence and characteristics of Takotsubo cardiomyopathy in subarachnoid haemorrhage: a prospective study / Szántó Dorottya, Gál Judit, Fülöp László, Szegedi Andrea, Fülesdi Béla, Molnár Csilla
Dátum:2019
ISSN:2197-425X
Megjegyzések:INTRODUCTION. Takotsubo cardiomyopathy (TTC) is an acute, usually reversible heart failure syndrome, precipitated by emotional or physical stressors. The initial presentation of TTC has similar features to acute coronary syndrome, however, coronary angiography usually shows an absence of significant coronary artery disease. TTC has been previously described as a notable complication of SAH because of its impact on cerebral blood flow. OBJECTIVES. The aim of our prospective observational study was to investigate the incidence, predisposing factors and cardiac biomarkers of TTC associated with SAH. Our secondary goal was to evaluate its effect on outcome. METHODS. This study was conducted in our neurosugical intensive care unit between March 2015 and June 2018 (Clinical trials reg. Nr: NCT02659878). We enrolled non-traumatic SAH patients without a history of cardiac disease, who were admitted within 48 hours from symptom onset. On admission we noted the severity of the haemorrhage (modified Fisher score) and neurological state (Hunt-Hess and WFNS scores) and transthoracic echocardiogram was performed. Patients with wall motion abnormality (WMA) were diagnosed as TTC, TTC patients with ejection fraction lower than 40% were classified as severe TTC (sTTC), patients without WMA served as control group (CG). Cardiac necroenzyme detection and transcranial colour duplex was performed on a daily basis. Each patient went through follow-up echocardiograms. We evaluated Glasgow Outcome Scale (GOS) and Barthel Scale (BS) 30 days and 6 months after the onset of SAH. RESULTS. During the study period 136 patients fulfilled inclusion criteria. Incidence of TTC was 28,7% (n=39), sTTC was found in 8,1% (n=11) of the cases. TTC was more common among females than males (female/male: CG 50/47 vs. TTC 30/9, p=0,007). Higher modified Fisher score was more frequent in the TTC group (modified Fisher>2: TTC 32/39 vs. CG 54/97; p=0,004). Higher Hunt-Hess (HH> 3: sTTC 8/11 vs. CG 29/97; p=0,012) and WFNS-score (WFNS>3: sTTC 9/11 vs. CG 29/97; p=0,002) was characteristic for sTTC. Serious vasospasm had higher incidence in the sTTC group (sTTC 3/11 vs. CG 5/97; p=0,04). We found significantly elevated cTnT and NT-proBNP levels in TTC patients. On 1 and 6 month follow-up sTTC was related to increased mortality (sTTC vs. CG: 7/11 vs. 15/95, p<0,001; 8/11 vs. 24/93, p=0,004) and lower GOS score (GOS<4: sTTC vs. CG 11/11 vs 44/95, p=0,002; 9/11 vs. 32/93, p=0,007). At 30th day lower quality of life was observed in the sTTC group (BS<50: sTTC 4/4 vs. CG 23/79, p=0,016). CONCLUSION. TTC is a common cardiac complication of SAH, especially in serious SAH with severe neurological symptoms. cTnT and NT-proBNP properly signs the presence of TTC. The harmful effect of TTC on cerebral circulation may contribute to increased mortality and disability.
Tárgyszavak:Orvostudományok Klinikai orvostudományok konferenciacikk
folyóiratcikk
Megjelenés:Intensive Care Medicine Experimental. - 7 : Suppl. 3 (2019), p. 263. -
További szerzők:Gál Judit (1977-) (aneszteziológiai és ITO szakorvos) Fülöp László (1976-) (kardiológus) Szegedi Andrea (1983-) (kardiológus) Fülesdi Béla (1961-) (aneszteziológus) Molnár Csilla (1962-) (aneszteziológus)
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
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