Résumé
Resumen En estudios previos se ha demostrado que la endotoxemia inducida por lipopolisacárido (LPS) produce un desacoplamiento cardiorrespiratorio (CRP) debido a los efectos fisiológicos de la inflamación sistémica. Adicionalmente se sabe que la oxitocina tiene efectos antiinflamatorios y propiedades cardioprotectoras; sin embargo, se desconoce si ésta modifica el acoplamiento CRP. El objetivo del presente estudio fue comparar diferentes métodos matemáticos lineales y no lineales para la detección del desacoplamiento cardiorrespiratorio entre series de tiempo cardiacas y respiratorias. Se estudiaron series de tiempo R-R obtenidas de electrocardiogramas de grupos de roedores macho a los cuales se les administró solución salina o vehículo (V); lipopolisacárido (LPS); oxitocina (O) y LPS + oxitocina (LPS+Ox). Las series R-R y respiratorias derivadas del electrocardiograma (EDR) se analizaron en conjunto para cuantificar su grado de acoplamiento a través de las técnicas de correlación cruzada; entropía muestral cruzada; entropía condicional; información mutua; e información mutua de Rényi para los cuatro grupos. Se observó que la oxitocina no parece favorecer el acoplamiento CRP durante la endotoxemia inducida por LPS. Finalmente, se encontró que la entropía muestral cruzada y la entropía condicional presentaron las mayores diferencias estadísticas para identificar el desacoplamiento CRP producido por el LPS.
Abstract Previous studies have shown that LPS-induced endotoxemia causes a cardiorespiratory (CRP) uncoupling owing to the physiological effects of systemic inflammation. Also, it is known that oxytocin has anti-inflammatory effects and cardioprotective properties; however, it is unknown whether it can modify the CRP coupling. This study aimed to compare different linear and nonlinear mathematics methods for the detection of cardiorespiratory uncoupling between cardiac and respiratory time series. The R-R time series of electrocardiograms of male rodents that were administered with saline solution (V); lipopolysaccharide (LPS); oxytocin (O) and LPS + oxytocin (LPS + Ox) were studied. We tested the R-R and respiratory series derived from the electrocardiogram (EDR) for the four groups to quantify the degree of coupling with cross-correlation; cross sample entropy; conditional entropy; mutual information; and Rényi's mutual information. We found that oxytocin does not seem to favor the CRP coupling during endotoxemia induced by LPS. Finally, we observed that the cross-sample entropy and the conditional entropy presented the highest statistical differences to identify the CRP uncoupling produced by LPS.
Résumé
BACKGROUND: It is a well-known phenomenon that alveolar and peritoneal macrophages exposed to bacterial lipopolysaccharide (LPS) induce a large output of nitric oxide (NO) and an inducible nitric oxide synthase (iNOS) mRNA expression. The purpose of this study is actually how much NO production and iNOS mRAN expression are effected by anesthetics (sevoflurane and propofol) on endotoxemic rats. METHODS: To examine the production of NO in peritoneal macrophages, NO concentration were measured from the rats following 2 hours exposure to LPS and 2 hours administration of sevoflurane and propofol, respectively. Culture supernatants were collected 24 hours after exposure to LPS and anesthetics and assayed by ELISA (Enzyme Linked Immunosorbent Assay) for production of NO. The iNOS mRNA expression was measured using PCR (Polymerase Chain Reaction) techniques and autoradiography. RESULTS: In the control group, the NO concentration was measured at 2 hours after infusion of LPS to rats, and showed 12 4micrometer. After insufflations of anesthetics to experimental animals, NO concentration increased in the sevoflurane and propofol groups, 37 13 (p<0.05) and 29 12micrometer (p<0.05) respectively. The size and brightness of the iNOS mRAN bands were distinct in sevoflurane and propofol in order. CONCLUSIONS: There were no different in regard of NO production and hemodynamic changes but iNOS mRNA expression between sevoflurane and propofol group in endotoxemic rats. The mechanism is not clear, but it is related to the strong stimulating effects on the respiratory tract of inhalation anesthetics.