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1.
J Clin Sleep Med ; 18(3): 885-894, 2022 Mar 01.
Artículo en Inglés | MEDLINE | ID: mdl-34725036

RESUMEN

STUDY OBJECTIVES: To assess the effectiveness of continuous positive airway pressure (CPAP) management guided by CPAP machine downloads in newly diagnosed patients with obstructive sleep apnea (OSA) using electronic health record-derived health care utilization, biometric variables, and laboratory data. METHODS: Electronic health record data of patients seen at the University of Utah Sleep Program from 2012-2015 were reviewed to identify patients with new diagnosis of OSA in whom CPAP adherence and residual apnea-hypopnea index as measured by a positive airway pressure adherence tracking device data for ≥ 1 year were available. Biometric data, laboratory data, and system-wide charges were compared in the 1 year before and after CPAP therapy. Subgroups were divided by whether patients met tracking criteria, mean nightly usage, and OSA severity. RESULTS: 976 consecutive, newly diagnosed participants with OSA (median age 55 years, 56.6% male) met inclusion criteria. There was a mean decrease of systolic blood pressure (BP) of 1.2 mm Hg and diastolic BP of 1.0 mm Hg within a year of initiation of CPAP therapy. BP improvements in the subgroup meeting CPAP tracking targets were 1.36 mmHg (systolic) and 1.37 mmHg (diastolic). No significant change was noted in body mass index, glycated hemoglobin, or serum creatinine values within a year of starting CPAP therapy, and health care utilization increased (mean acute care visits 0.22 per year to 0.53 per year; mean charges of $3,997 per year to $8,986 per year). CONCLUSIONS: An improvement in BP was noted within a year of CPAP therapy in newly diagnosed patients with OSA, with no difference in the magnitude of improvement between those meeting tracking system adherence targets. CITATION: Locke BW, Neill SE, Howe HE, Crotty MC, Kim J, Sundar KM. Electronic health record-derived outcomes in obstructive sleep apnea managed with positive airway pressure tracking systems. J Clin Sleep Med. 2022;18(3):885-894.


Asunto(s)
Registros Electrónicos de Salud , Apnea Obstructiva del Sueño , Presión Sanguínea , Presión de las Vías Aéreas Positiva Contínua , Femenino , Humanos , Masculino , Persona de Mediana Edad , Cooperación del Paciente , Sueño , Apnea Obstructiva del Sueño/terapia
2.
J Neurosci ; 24(45): 10103-10, 2004 Nov 10.
Artículo en Inglés | MEDLINE | ID: mdl-15537880

RESUMEN

Neurokinin 3 receptors (NK3-Rs) are expressed in the supraoptic nucleus (SON), and SON is innervated by substance P (SP)-expressing A1 neurons in the medulla. Because SP stimulates vasopressin (VP) and oxytocin release from explants of the hypothalamo-neurohypophyseal system (HNS), two hypotheses were tested: (1) SP-stimulated VP release is mediated by NK3-Rs, and (2) stimulation of the A1 pathway by hypotension activates SON NK3-Rs. Senktide, an NK3-R agonist, stimulated VP release from HNS explants, but neither a neurokinin 1 receptor antagonist [L732,138 (N-acetyl-L-tryptophan 3,5-bis(tri-fluoromethyl)benzyl ester)] nor two NK3-R antagonists (SB222200 and SB235375) prevented SP-stimulated VP release. Because the affinity of these antagonists for rat NK-Rs may limit their efficacy, NK3-R internalization was used to assess the ability of SP to activate SON NK3-Rs. Senktide, SP, or vehicle was microinjected above SON. The brain was perfused 5 min after injection and stained for NK3-R immunoreactivity. Using confocal microscopy, the number of NK3-R-immunoreactive (-IR) endosomes was counted in a 5.6(2) mu region of cytoplasm in SON neurons. Senktide, but not SP or vehicle, significantly increased the number of NK3-R-IR endosomes in the cytoplasm. When hypotension was induced with hydralazine, NK3-R internalization was observed within 5 min (p < 0.005). A decrease in cytoplasmic NK3-R immunoreactivity was observed within 15 min of hypotension. Unexpectedly, both senktide and hypotension resulted in translocation of NK3-R-IR immunoreactivity to the nucleus. Thus, although these studies do not identify SP as the NK3-R ligand, they do provide evidence for hypotension-induced release of an endogenous tachykinin in SON and evidence suggesting a role for NK3-Rs in transcription regulation.


Asunto(s)
Hipotensión/fisiopatología , Sistema Hipotálamo-Hipofisario/fisiopatología , Hipotálamo Anterior/metabolismo , Neuronas/metabolismo , Oxitocina/metabolismo , Receptores de Neuroquinina-3/fisiología , Sustancia P/análogos & derivados , Triptófano/análogos & derivados , Vasopresinas/metabolismo , Acetatos/farmacología , Animales , Catecolaminas/fisiología , Compartimento Celular , Núcleo Celular/química , Citoplasma/química , Endosomas/química , Hidralazina/farmacología , Hipotensión/inducido químicamente , Masculino , Microinyecciones , Microscopía Confocal , Neuronas/efectos de los fármacos , Neuronas/ultraestructura , Fragmentos de Péptidos/farmacología , Quinolinas/farmacología , Ratas , Ratas Sprague-Dawley , Receptores Acoplados a Proteínas G/efectos de los fármacos , Receptores Acoplados a Proteínas G/fisiología , Receptores de Neuroquinina-1/efectos de los fármacos , Receptores de Neuroquinina-1/fisiología , Receptores de Neuroquinina-3/efectos de los fármacos , Sustancia P/farmacología , Taquicininas/fisiología , Transcripción Genética/efectos de los fármacos , Transcripción Genética/fisiología , Triptófano/farmacología
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