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EN
The aim of this study was to evaluate the effect of ventilation on electrocardiographic time intervals as a function of the light-dark (LD) cycle in an in vivo rat model. RR, PQ, QT and QTc intervals were measured in female Wistar rats anaesthetized with both ketamine and xylazine (100 mg/15 mg/kg, i.m., open chest experiments) after adaptation to the LD cycle (12:12h) for 4 weeks. Electrocardiograms (ECG) were recorded before surgical interventions; after tracheotomy, and thoracotomy, and 5 minutes of stabilization with artificial ventilation; 30, 60, 90 and 120 seconds after the onset of apnoea; and after 5, 10, 15, and 20 minutes of artificial reoxygenation. Time intervals in intact animals showed significant LD differences, except in the QT interval. The initial significant (p<0,001) LD differences in PQ interval and loss of dependence on LD cycle in the QT interval were preserved during short-term apnoea-induced asphyxia (30–60 sec) In contrast, long-term asphyxia (90–120 sec) eliminated LD dependence in the PQ interval, but significant LD differences were shown in the QT interval. Apnoea completely abolished LD differences in the RR interval. Reoxygenation restored the PQ and QT intervals to the pre-asphyxic LD differences, but with the RR intervals, the LD differences were eliminated. We have concluded that myocardial vulnerability is dependent on the LD cycle and on changes of pulmonary ventilation.
EN
The aim of this study was to evaluate the effect of ventilation on electrocardiographic time intervals as a function of the light-dark (LD) cycle in an in vivo rat model. RR, PQ, QT and QTc intervals were measured in female Wistar rats anaesthetized with both ketamine and xylazine (100 mg/15 mg/kg, i.m., open chest experiments) after adaptation to the LD cycle (12:12h) for 4 weeks. Electrocardiograms (ECG) were recorded before surgical interventions; after tracheotomy, and thoracotomy, and 5 minutes of stabilization with artificial ventilation; 30, 60, 90 and 120 seconds after the onset of apnoea; and after 5, 10, 15, and 20 minutes of artificial reoxygenation. Time intervals in intact animals showed significant LD differences, except in the QT interval. The initial significant (p<0,001) LD differences in PQ interval and loss of dependence on LD cycle in the QT interval were preserved during short-term apnoea-induced asphyxia (30–60 sec) In contrast, long-term asphyxia (90–120 sec) eliminated LD dependence in the PQ interval, but significant LD differences were shown in the QT interval. Apnoea completely abolished LD differences in the RR interval. Reoxygenation restored the PQ and QT intervals to the pre-asphyxic LD differences, but with the RR intervals, the LD differences were eliminated. We have concluded that myocardial vulnerability is dependent on the LD cycle and on changes of pulmonary ventilation.
EN
Ambulatory blood pressure monitoring and parallel polysomnographic study were performed in 116 adult males divided into 6 groups. Thirty blood-pressure (BP) and polysomnographic variables were measured to test their usefulness for screening for both arterial hypertension and sleep apnea-hypopnea syndrome (SAHS). The development of severe breathing disorders and hypoxemia during sleep was attributed to SAHS, when compared with measurements in healthy controls and in patients with arterial hypertension. Such disorders manifested as an increased apnea-hypopnea index, apnea index, duration of arterial oxygen saturation of less than 85%, and decrease of average arterial oxygen saturation that correlated with nocturnal average diastolic BP (p=0.0049, p=0.0027, p=0.049 and p=0.0457, respectively). These respiratory disorders resulted in various nocturnal, rather than diurnal, and diastolic and systolic BP variables. The acute antihypertensive effect of continuous positive airway pressure therapy for SAHS significantly reduced the episodes of apnea and hypopnea and the secondary component of hypertension caused by excessive sympathetic stimulation. For the SAHS-induced, dose-dependent component of hypertension that responded to continuous positive airway pressure, the following variables, in decreasing significance, were useful: nocturnal average systolic and diastolic BP and 24-hour average systolic and diastolic BP, as well as percent time elevation and mean blood pressure load. The monitoring of these variables could contribute to early diagnostic and prognostic stratification of complications and adequate therapy of the secondary component of hypertension caused by SAHS.
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