RESUMEN
Positive-pressure ventilation-induced variations in arterial pressure have been related to cardiac sympathetic activity in animals. However, the effect of beta-adrenoceptor blockade on these variations in anaesthetized humans under positive-pressure ventilation has not yet been investigated. In the present study, RAPV (respiratory-related arterial pressure variability) and %SPV (percentile systolic pressure variation) were determined before and after esmolol treatment in ten mechanically ventilated patients. RAPV and %SPV decreased significantly after intravenous esmolol (1 mg/kg of body weight) treatment (maximal decrease of RAPV, 50% and %SPV, 35%). Linear regression analysis of RAPV and %SPV before and after esmolol treatment both revealed high correlation (r = 0.93 and 0.91 respectively). The amplitudes of RAPV and %SPV also significantly increased in a graded way with higher tidal volumes. Thus we propose that esmolol suppresses the variations in arterial pressure induced by positive-pressure mechanical ventilation, and we suggest that RAPV and %SPV may be alternative choices for monitoring cardiac sympathetic regulation in anaesthetized patients under positive-pressure ventilation.
Asunto(s)
Antagonistas Adrenérgicos beta , Sistema Nervioso Autónomo/efectos de los fármacos , Presión Sanguínea/efectos de los fármacos , Respiración con Presión Positiva , Propanolaminas , Anestesia General , Determinación de la Presión Sanguínea , Depresión Química , Femenino , Humanos , Periodo Intraoperatorio , Modelos Lineales , Persona de Mediana Edad , Monitoreo Fisiológico/métodos , Respiración , Procesamiento de Señales Asistido por Computador , Sístole , Volumen de Ventilación PulmonarRESUMEN
During positive pressure mechanical ventilation, percentile systolic pressure variation (%SPV) or respiratory-related arterial pressure variability (RAPV) have both been used in assessment of graded haemorrhage. We aimed to investigate whether changes in %SPV and RAPV are correlated during graded haemorrhage (by 5, 10 or 20% of the estimated blood volume) in anaesthetized positive pressure ventilated rats and to investigate the involvement of autonomic regulation. Saline vehicle or atropine produced no discernible effect on baseline %SPV or RAPV but, thereafter, %SPV and RAPV increased progressively with graded haemorrhage. Propranolol significantly decreased baseline %SPV and RAPV and changes induced in %SPV and RAPV by graded haemorrhage. Phentolamine significantly enhanced baseline %SPV and RAPV, and further enhancement of %SPV and RAPV by graded haemorrhage did not occur until 20% of the estimated blood volume was removed. RAPV was significantly correlated with %SPV in all experimental groups. We conclude that RAPV is comparable with%SPV as an indicator of graded haemorrhage and that, in anaesthetized and positive pressure ventilated rats, both are dependent on autonomic function, especially beta-adrenoceptors.
Asunto(s)
Sistema Nervioso Autónomo/fisiología , Presión Sanguínea/efectos de los fármacos , Hemorragia/diagnóstico , Respiración con Presión Positiva , Procesamiento de Señales Asistido por Computador , Antagonistas Adrenérgicos alfa/farmacología , Antagonistas Adrenérgicos beta/farmacología , Anestesia , Animales , Arterias , Atropina/farmacología , Frecuencia Cardíaca/efectos de los fármacos , Masculino , Parasimpatolíticos/farmacología , Fentolamina/farmacología , Propranolol/farmacología , Ratas , Ratas Sprague-Dawley , SístoleRESUMEN
One of the biological effects of hyperbaric oxygen (HBO) therapy in enhancing ischemia-related wound healing is the induction of angiogenesis. To elucidate the mechanism(s) underlying the HBO-induced angiogenesis, we studied the expression of several angiogenesis-related genes in human umbilical vein endothelial cells exposed to HBO. Western blot analyses showed that HBO enhanced the expression of angiopoietin-2 (Ang2) with no effect on the expression of Tie2, angiopoietin-1, and VEGF. The induction of Ang2 was further confirmed by immunohistochemistry, quantitative PCR, and Northern blot analyses. Inhibition of endothelial nitric oxide synthase blocked the HBO-induced Ang2 expression, but failed to block hypoxia-induced Ang2 expression. These data indicated that HBO-induced Ang2 expression may be through transcriptional stimulation, and requires the nitric oxide signaling pathway, which may play an important role in HBO-induced angiogenesis.